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Cancer basics and chemotherapy

For a concise covering of cancer.

I have rewritten the section on cancer based up discovering that cancer is dependent upon glucose, and therefore can be starved into remission or better.  Sadly, though I have been reading the technical journals and summation articles I hadn't discovered the Warburg Theory (1924) until 2016.  The science is solid; I have spent 6 months examining it.  As a consequence I have rewritten one of my 2 summation articles on cancer and its dietary fix.  What follows is that work.  I have left my older work up, much of its is valid.  I simply didn't want to spend the time on rewriting both.  I have other trees to chop.  



This applies to 95% of all cancer patient, that chemotherapy cannot alter significantly the course of the disease--a few cancers it can. 


CANCER basics & CHEMOTHERAPY- 11 pgs –

1/13/17  http://healthfully.org/rc/id16.html & long version rl/id4

Complying with laws, below reflects my views and is not a recommendation for others to follow. 

Key points:  Moved to NT-Summation-cancer-diet-fasting in diet > KD diet.

That all cancers have defective metabolisms because of mutations in their mitochondria.

While each cancer is unique, the norm is for the mitochondria to have lost the ability to metabolize fat and to metabolize glucose aerobically; via., the mitochondria make ATP by a fermentation process.

Without ATP cells soon die, thus cutting off glucose by dietary restriction will kill cancer

Since there are minor secondary sources of energy such as glutamine, the cancer will likely shrink due to apoptosis and become dormant thus requiring a life-long ketogenic diet.

An indolent cancer becomes metastatic because of fusion of their mitochondria to a microphage.

Because of damage to the immune system and side effects, I would forgo all chemotherapies that can’t cure.

I would use fasting and ketogenic diet prior to excision (at least 2 weeks of fasting prior). 

I would use diet and fasting for all cancers, reliance upon which depends on initially findings and lab reports on the tumor:  A likely metastatic neoplasm, even if local, such as small cell lung, requires maximum dietary treatment, a cancerous polyp removed from the colon minimal.   

[If the cancer is stage I-III, excision is sufficient unless there is a significant chance to there being distant clumps of cells (metastatic cells) such as with small cell lung cancer.[1]  Therefore, I would forgo for stage I-III chemotherapy, unless in clinical trials it can produce a cure in over 30% of metastatic cancers.] 


There is a reason why the war on cancer, started under President Nixon has very few bright spots, though of course pharma claims much more.  Maximizing profits is at conflict with understanding the disease. Preventing it, and when that fails curing it.  It is essential to understand the inroads made upon medical science by corporate medicine: Corporate medicine is market driven; medical science evidence driven.  These two approaches result in different explanations concerning cancer.  The goal here is to understand the general basic biology of cancer, and then its treatment options based quality scientific evidence—without market considerations.  What follows is based upon sound science with sources.  Marketing science is driven by profits, & thus promotes aggressive drug cocktail for everyone with cancer.  Prevent is given deceptive lip service.  With a couple exception, chemotherapy does more harm than good.  Pharma’s marketing ploys confirms Harvard Prof. Dr. Marcia Angell’s  observation that we have “the worst system we could imagine.”  To learn more read Marketing Science & Side Effects, and you will learn how doctors are taught by Pharma to be pill pushers, and why they are.  It is as Prof. Goldacre writes:  A perverse system produces perverse results.

“A benign tumor is a mass of cells (tumor) that lacks the ability to invade neighboring tissues or metastasize.  These characteristics are required for a tumor to be defined as cancerous and therefore benign tumors are non-cancerous.  Also, benign tumors generally have a slower growth rate than malignant tumors and the tumor cells are usually more differentiated (cells have normal features).  Benign tumors are typically surrounded by an outer surface (fibrous sheath of connective tissue) or remain with the epithelium.  Common examples of benign tumors include moles, colon polyps,[2] and uterine fibroids.   Although benign tumors will not metastasize or locally invade tissues, some types may still produce negative health effects…. [Some types of] benign tumors can become malignant….  invade adjacent tissues or spread to distant sites by metastasizing.  For this reason, benign tumors are not classed as cancer Wiki.  Bad pharma has blurred the distinction between benign and malignant by calling benign tumors “carcinoma”, then aggressively treat with surgery and chemotherapy.  Critics point out in journal articles the negative consequences of treating benign (small local) tumors of the breast prostate, thyroid cancers, and others tissues with adjunct chemotherapy following excision. Yet pharma ignores this and through their KOLs (Key Opinion Leaders) sets up guidelines for aggressive treatment which includes chemotherapy. Their KOLs write medical textbooks, run the clinical trials, and instruct physicians in mandated continuing education classes.  In this and other ways pharma shapes the practice of medicine.  One ways is that on an average over half the revenues in a cancer clinic is derived from the spread of the cost of a drug and what they receive for administering it in their office.  This topic is covered at Cancer long version and in the Journal of the British Medical Association, Nov. 2016, Cancer Drugs, Survival and Ethics.  This link is to a sampling of articles in leading journals on bad pharma.

With regulatory capture, the FDA often grants patents to drugs that are not in the best interest of the patient.  Moreover pharma’s role in the production of journal articles entails bias.  For Industry funded trials positive bias averaged 32% (range 11 to 69%) for clinical trials based on a comparison of the raw data submitted to the FDA to the journal articles.  And it is worse, FDA approval is flawed.  Surrogate endpoints of shrinkage of tumor and/or duration in which tumor doesn’t grow are used by the NIH in a very select population of terminal patients (younger patients who have not undergone prior chemotherapy).  Unfortunately those with no treatment if they have more than a year to live would do better than the chemo cohort.  This is because the cancer cells that have thrived during the chemo, now that the frail cells have been eliminated, are getting all the energy molecule glucose and tumors are very glucose hungry, up to 200 times more than a normal tissue--to be explained later.  Moreover, the quality of life is reduced based upon the often horrendous side effects.  And it gets worse, for it is the norm to use the chemo on those without metastatic cancer, and depending on type most have been cured by excision, thus no benefit from chemo.  More on this later under Hope’s Hypothesis.  Typically in those with terminal cancer it translates into an average life extension of 1 to 3 months—general the duration of the chemo therapy.  Once stopped the vigorous remaining tumors cells resume growing.  Not surprisingly, a 2015 study Published in the BMJ (one of the 5 top English medical journals) found that most cancer drugs in the real world population “do not increase survival”, at.  And it gets worse, industry funded studies are always biased in favor of industry.  A study which relied upon the raw data found all 74 clinical trials journal articles industry produced were biased; its average 32%.  It as Prof. Goldacre said, “The devil is in the details.”  This makes good advice and informed decision unlikely. 

“Cancer (malignant neoplasm) is a broad spectrum of diseases involving improperly regulated cell growth.  For that cell growth to become life-threatening it must be capable of sufficient reproduction so as to disrupt essential bodily processes.  Over 80% of fatal cancers spread to more distant part of the body through the lymphatic or blood systems—some such as cerebral cancer destroy a vital organ, and others such as  liver, and pancreatic simply grow beyond the margins of the tissue into other organs.  With the exception of blood and lymphatic cancers, they form hard tumors.  One of the most important factors in classifying a tumor as benign or malignant is its invasive potential” Wiki.   A microscopic examination of a biopsy by itself is insufficient to prove that the tissue is malignant, for it doesn’t reveal the properties of being invasive and/or metastatic.  Lab reports often numerical grade the tissue based on shape of cells, the heterogeneity of cells in tumor to produce a probability rating.  Lab write up of a biopsy very often use cancerous and carcinoma though it should be prefixed with an adjective such as likely or unlike.  Cancerous can only be definitively determined with additional imagining, such as MRI and CAT scan.  Depending on lab findings, removal often is the best choice, and but subsequent chemotherapy often isn’t necessary.

Oncogenesis (carcinogenesis):  literally the creation of cancer. It is a process by which normal cells are transformed into cancer cells. According to the standard theory (which I no-longer hold), “there is a progression of changes at the cellular genetic and epigenetic [regulate the expression of other genes] that ultimately reprogram a cell to undergo uncontrolled cell division, thus forming a malignant mass.  Over 98% of potential mutations and epi-mutations will have no bearing on cancer” Wiki.  There are 3 theories of how a tumor becomes malignant (invasive).  It is important for me to understand which theory fits best the evidence, and also how cancers produce the energy molecule ATP, for as you shall see, it affects my treatment choices.

Three theories on conversion of a tumor into cancer:  Standard theory is that there are typically seven essential types of mutations such as the cell line becoming immortal, fooling the immune system, etc. necessary to convert a benign tumor.  The second theory is that the tumor signals stem cells to become involved, and they give the tumor cells the properties needed to become cancerous.  The third is similar but having the changes brought about by M2 macrophages.  It seems that the only essential mutation for a cancer occurs in the mitochondria, known as the Warburg Hypothesis (1924 observation) which limits the metabolism of glucose in the mitochondria to fermentation (anaerobic).  This I will develop at the end since it entails way to starve cancer by having the body switch to fat metabolism—now lacking in cancer cells.  Yes, starve cancer!

A)    Six-mutation theory:  This is the theory favored by pharma (and once I too with the aid of stem cells until Dec. 2016).  It holds that 6 mutations are necessary for a tumor to become invasive, and these gradually accumulate among the many other mutations in the cell’s nucleus DNA (see Scientific American, July 2003) .  The theory holds that random mutation, whose rate is increased through exposure to mutagenic substance, radiation, or other forms of stress, and/or if a gene which checks the reduction of DNA during mitosis is switched off or damaged, such as the P53, BRAC1, or BRAC2 genes—being the best known and studied.  Common mutations it is held as causes (1) the cell to replicate at a high rate, (2) fail to respond to signals to return to the normal rate,   (3) evasion of apoptosis signals (programmed cell dismantling), (4) angiogenesis (causing new blood vessel to nourish the expanding tumor, (5) to reproduce bypass the telomerase system which limits replication to about 50 division, (6) not appear as foreign to immune cells when the tumor cells break off and invade different tissue type and/or migrate to distant locations using the lymph or blood circulatory systems for transport.  To this, I would add is the ability to penetrate membranes which form barriers.  This explanation ignores other essential changes in a cancer:  (1) the loss of the ability for aerobic metabolism of glucose using an inefficient system producing lactate anaerobic fermentation, (2) deformed mitochondria (the vacuoles engines produce over 90 of the ATP used by the body for energy) being deformed, (4) the inability to metabolize fatty acids (fats) (3) the involvement of the mitochondria.  of For most tissues, 7 or more mutations are required to create a malignant tumor.  Less than 10% of all cancers involve inherited mutations, the remainder is a result of environmental factors and bad luck.  Over half the cancers are attributable to carcinogens.  Excluding skin cancer, only about half of all cancers prove fatal.    

B)   Role of Stem cells theory:  A way to explain the properties of a cancer without so many mutations.  There must be some, otherwise there wouldn’t be a benign tumors consisting of what once was normal cells.  Most significant are mutations that diminish the ability of cells to produce an exact copy of the parent cell DNA.  This increases the lineage’s number of mutation typically about 10 fold.  In the stem-cell theory, stem cells in their reproductive-healing role then step in to convert some of the tumor’s benign cells to cancerous cells. An April 2006 article in Scientific American and another in July (also at) claimed that stem cells were what was turning a cancer into metastatic phase.[3]  On stem cells Wiki:  “they are  undifferentiated  biological cells, that can differentiate into specialized cells and can divide through mitosis to produce more stem cells, which are found in various tissues.  In adult organisms, stem cells and progenitor cells act as a repair system for the body, replenishing adult tissues. Stem cells maintain the normal turnover of regenerative organs, such as blood, skin, or intestinal tissues.  Stem cells possess two properties:  self-renewal (to maintain through cell division the undifferentiated state) and potency (to give rise to any mature cell type).  Induced pluripotent, these are not adult stem cells, but rather adult cells (e.g. epithelial cells) reprogrammed to give rise to pluripotent capabilities of forming more than one type of tissue.  A progenitor cell is a biological cell that, like a stem cell, has a tendency to differentiate into a specific type of cell, but is already more specific than a stem cell and is pushed to differentiate into its "target" cell… and can divide only a limited number of times.”  The occasional finding of stem cells in malignant tumors, and the heterogeneity of cells in most malignant tumors is held to demonstrates their role:  it fit the evidence; but a neat theory was shot down by facts, some below. 

C)   Role of type tumor associated macrophages[4] (TAM):  This is similar to the stem-cell hypothesis only the role is filled by macrophages; the supporting evidence is strongest (the extent of this evidence is to be found at a review journal article link to my published version, on line, and summarized 2012 Allevena.  Contrary to expectations, in malignancies, tumour-associated macrophages (TAM) promote disease progression by supporting cancer cell survival, proliferation and invasion. TAM and related myeloid cells…. also promote tumour angiogenesis and suppress adaptive immune responses.  Dr. Seyfried in his lecture points that experiments show that the DNA from the nucleus of cancer isn’t the cause of the cancer, but rather the mutations in the mitochondria which cause inefficient glucose metabolism. In experiments by inserting the mitochondria of a cancer cell into a normal cell, that cell will become cancerous—a event that won’t happen if the DNA of the cancerous cell is inserted.  Macrophages which are immune cells which engulf foreign substances including bacteria and viruses, help dispose of the products of cell apoptosis, and stimulate the growth of new tissue in the repair process on very rare occasions will attach to a tumor and acquire the defective mitochondria of the cancerous tumor.  This will turn the macrophage into a cancer cell.  In established tumours, TAM resemble M2-like macrophages… in the context of a growing tumour they may favour disease progression. [42,50–54]. Cancer-related inflammation is now recognized as a hallmark of cancer [55,56]. Macrophages are key initiators of the subtle chronic inflammation present in the tumour microenvironment, as they are major producers of inflammatory mediators.  IL-6 is a key growth-regulating and anti-apoptotic cytokine, having tumour-inducing activities on both malignant and stromal cells.  In mouse models of colitis, IL-6 is produced mainly by macrophages in response to intestinal injury and in an NF-kB-dependent manner.  Tumour cells exploit the ECM degradation mediated by TAM to invade locally, penetrate into vessels and disseminate to give distant metastasis. The chemokine CCL18 produced by TAM has been shown recently to play a critical role in promoting breast cancer invasiveness by activating tumour cell adherence to ECM. Tumour macrophages have the ability to suppress the adaptive immune response, thus contributing directly to the phenomenon of immune evasion of cancer. in the majority of human tumours high numbers of infiltrating TAM have been associated significantly with advanced tumours and poor patient prognosis [11,15,42,111],  TAM are present in large numbers in tumour tissues and are key promoters of cancer-related inflammation.” Summary article 2012 Supra.  The six mutation theory and the role of stem cells fall far short in evidence to TAM.

 On treatment and prognosis is about the typical, common cancers 

For the 5 common cancers (lung, colorectal, breast, prostate & pancreatic), 3 of them if assumed not metastatic on initial diagnosis can be successfully be treated by excision (over 70% at 10 years will not have died from that cancer).  Two of them small cell lung cancer (the most common type) and prostate over 90% die in the first 2 years.  Pancreatic cancer is locally invasive and cannot be entirely removed by surgery, and small cell lung cancer has metastasized by the time it can be seen with imaging.  For each there type of cancer there is a bell curve of variation for rate of growth.  Rate of growth can only be determined on subsequent imaging.

FIVE KEY FACTORS AFFECTING PROGNOSIS (the benign tumor that a TAM has converted into a cancer:  

 One factor is the stage I-IV, which is based upon the degree of invasiveness of the cell line and size of cancer.  A larger tumor, spread to adjacent tissue, or is found in lymph nodes is more likely to have undergone the changes involving TAM and become metastatic (lethal).   For an example 5-year survival of breast cancer, if greater than 5 cm 65%, for less than 2 cm 96%—tissue of origin makes only a small difference.  Each tissue type percentage figures is different. How fast the cancer invades adjacent tissue and spreading through the tissue of origin can only be determined by a successive examinations months apart.  Second, is the primary tissue.  Each tissue has its own prognosis.  Pancreas has 3 common primary tissues; however, all tissues produce a very high percentage of aggressive malignancies (the 5-year survival rate is 2%).  The third is the variation in cells within the tumor the more likely a M2 obtained a mitochondria from the tumor that will cause the mitochondria to become caner.  And if it still is mutating at a higher, the less like that all the cancer sell will be removed or respond to dietary restriction or radiation.  Fourth is the degree of differentiation from the tissue of origin.  The closer the tumor resembles the parent tissue the more likely is it that it won’t be cancerous or if cancerous will be indolent and thus easy to cure with excision and diet.  The complex processes involving many genes, their control mechanism, the also way the M2 macrophages (TAM) and other immune cells respond to the benign and later malignant tumors, all this makes each cancer unique.  Fifth, the presences and involvement of M2 macrophages.  But for a few experimental settings, the lack of awareness entails that lab reports don’t contain this information.

On Staging: While the stage of cancer development is important as to survival (success of excision in curing cancer) the early detection yields no survival benefit.  Yes finding a cancer early doesn’t improve the patient’s chances versus findi later.  Theory behind early detection is that the clock is running, and at some point the cancer will have a mutation that will allow to spread to distant tissues.  Allow me to explain, if it is really a cancer, not a benign in situ tumor, then by the time it has gone invaded other tissues, it has already done a fusion with a macrophage, and what properties that tumor has gained have determined it properties; viz., weather the cancer is deadly or not.  So removing a pea size tumor is already too late if mitochondria fusion has occurred.  Only a certain percentage of fusions are deadly, and that percentage is determined by the tissue type.  Some tissues have most of the cancers progress slowly while others like small cell lung tissue are very likely metastatic rapid growth. This theory of early detection was shot down in the fifties when a program of screen with X-rays was adopted. Since death typically occurs within 9 months, answers to this question was in hand by the end of the second year.  The program was stopped because there wasn’t a statistically significant benefit.  It was in an era when most trials were ran by a university, even those funded by pharma, their further involvement was minimal.  That has all changed with the changes made by the Republicans during Reagan’s administration.  Others like breast cancers are in between.  Thus a so called breast cancer of 2 cm or less has only a 4% chance of killing the woman; while one of 5 cm has a 35% chance.  The point is that with a regular checkup only 11% of the metastatic cancers haven’t progressed from small to 5 cm.  Some of those are indolent and the new colonies will take years to show up, but most aren’t.  Early discovery doesn’t change the nature of the cancer.  This has again been confirmed with breast cancer.  The harm done by early detection, treating tumors that aren’t cancer.  In a study published in 2017 in the BMJ, article drawing attention to the article published in the Annals of internal Medicine found that one in 3 women was over-diagnosed (a polite way of saying they didn’t have cancer, just a benign tumor).  Seventeen years of organised breast screening in Denmark has not reduced the incidence of advanced tumours but has markedly increased the incidence of non-advanced tumours [not cancer] and ductal carcinoma in situ” BMJ, 2017.   This is the same for other detection methods which lead to a biopsy.  I was diagnosed with prostate cancer based on a biopsy in 2006, and didn’t go back for further screening after reading the lab report which call it “carcinoma”.  The percentages were the same for biopsy following a high PSA as for mammogram.  Millions have had their lives shortened by treating a phantom cancer:  they poison called chemotherapy, made all the worse by chemical castration (block estradiol or testosterone).  But pharma who miss-educates doctors benefits.

FOUR KEY PROBLEMS WITH MOST CHEMOTHERAPIES, LACK OF SELECTIVITY, DEPRESSION OF IMMUNE SYSTEM, SUMPRESSION OF TUMOR GROWTH SHORT-TERM DOES NOT PRODUCE A CURE, DEVELOPMENT OF RESISTANCE AND ELIMINATION OF WEAKER MALIGNANT CELLS:  1) Cancer cells are nearly identically to body cell; their genes and thus proteins are identical.  Thus unless the tissue type can be eliminated without dire consequences (as with testicular cancer) it is unlikely that the chemo will produce a cure.  Thus very few chemotherapies harm only cancerous tissues.  2) The common cancer drugs function by blocking functions vital to cells and tissues (and thus the patient) such as the production of new blood vessels, cellular reproduction, etc.  “Thus chemotherapy also harms normal cells especially those that divide rapidly, most notably in the bone marrow,  digestive tract, and hair follicles.  This results in the most common side-effects of chemotherapy:  myelo-suppression    (decreased production of blood cells, hence also immuno-suppression),  mucositis (inflammation of the lining  of the digestive tract), and  alopecia (hair loss).  Virtually all chemotherapeutic regimens can cause depression of the immune system, often by paralysing the bone marrow and leading to a decrease of white blood cells, red blood cells, and platelets Wiki.  Thus since macrophages have vital functions to develop a chemo to suppress their functions would soon prove fatal.   This explains why chemo therapies (with a few exceptions) can be given only short term, and often not continuously but every week or two for a couple of months.  3) The surrogate endpoint of tumor shrinkage and progress-free period is used by the FDA for drug approval.  This is a very low hurdle that can extend the life of a terminal patient near death a few weeks or months, but doesn’t translate into benefit for patients whose death from cancer is a year or more out, or who were cured by surgery.[5]  Causing damage throughout the body is why most chemotherapies are given only short term intermittently (such as biweekly) and stopped after a couple of months.  They at best for the terminal patient near death prolongs life on average 2 months for metastatic cancers.[6]  This explains why there is a lack of long-term studies with the end point of death for those with stage I, III, and III cancers.[7]  And if stage IV, I wouldn’t want to have the decline of my health in my last few months.  4) If the chemo proves toxic to the weaker malignant cells, those that survive are both resistant to the chemo, and now are not competing with the weaker tumor cells for the limited supply of glucose, their energy molecule.  Thus once the chemo has stopped the malignant cell typically then reproduce at an accelerated rate.  Moreover since the immune system often plays a key role in suppressing a cancer, to weaken the immune system for many also contributes to the growth and spread of the cancer.  If I was likely to be cured by excision or radiation, the use of chemo subsequent or prior is a choice I would never make--see Hope’s hypothesis below.   A recent of new drugs (2003 to 2013) showed them on an average no better than old drugs at Jan 4, 2017. Of course pharma exaggerates the benefits and downplays the side effects.  

Evolution works for the survival of the most vigorous cancer cells.  This is why in most cases when a cancer returns the same treatment is not repeated, or if repeated has little positive effect.  The very high rate of mutation for most aggressive cancer gives an evolutionary resistance that entails survival of some of the cells during chemotherapy.  (That is why the greater the variation in appearance seen under a microscope of the tumor cells is associated with an increased risk of the cancer proving to be metastatic.)  Thus for a chemotherapy that reduces tumor size, some of the cells will survive, and continue to reproduce.  “Those resistant cells reproduce at the highest rate will make up most of the new tumor.… Over a sufficiently long period of time there always are metastases that share little with their tumor of origin…. But the sad reality is that the current cure rates for metastatic-disease still sit where they have been throughout the history of humankind—in a neighborhood near zero” (Slipping Past Cancer’s Barriers, Mauro Ferrari, American Scientist, Vol. 101, p. 430 12/2013).  These three issues entail that for nearly all chemotherapies entail the net result is not in the best interest of the patient. 

THE PROBLEM OF DESTROYING CELLS THAT HAVE ALL OF THAT PERSON’S GENES:  A metastatic cancer is as stated a line of cells from a person’s body that have undergone mutations in the mitochondria the result of reactive chemical the products of metabolism and glycation that disables its ability to metabolize fats and glucose aerobically.  (Mitochondria have their own genes.)  The macrophages in a rare fusion process acquire the abnormal mitochondria with its genes to become cancerous.  Instead of growth of lung tissue to repair damage from an accident or infection, the mitochondria now function like aberrant lung tissue.  This cancer is from that person’s body cells with all its genes.  How can a chemical destroy those body cells without also destroy other lung cells, or other tissue throughout the body?  It can’t.  Consider how different a bacteria is or the protozoan Malaria from human cells, different in many ways, yet there isn’t for Malaria a chemotherapy that will destroy the disease.  And with bacteria, the antibiotics must be given in low dose so as not to kill the patient.  The antibiotic only helps the immune system destroy the bacteria generally by slowing the reproduction of the bacteria.  Once the immune system is damaged by chemotherapy, survival is shortened if the cancer turns out NOT to be metastatic, or if metastatic and indolent.  How much is a guess because population data banks are not open to the academic community; these include records by major insurers and hospital chains such as Kaiser, and by our government (Veterans Hospitals). Informed consent requires the patient and being given valid figures on the endpoint results of all causes of death and side effect in a real world population, and his oncologist needs access to these figures for giving advice.  But pharma, the global trillion dollar gorilla is very good at market.

What of cancer cells which no longer are held in check by white blood cells, as they once were before TAM modified it in a way that permits the cancer cells to spread to distant tissues.  The chemo must somehow destroy the cancer without now the aid of the white blood cells; it can’t.  Oncologist use the term “survival” to sell patients on a poison that for most chemotherapies extends life of a terminal patient under 3 months; that is not “survival”, only modest extension of the patient’s suffering.  The poison is used short term because if it is used continuously it will kill the patient.  And even short term, most patients have a major reduction in the quality of life.  If oncologist weren’t merchants of false hope, and patients knew the meaning of their use of “survival”, most would refuse chemotherapy.

SHOULD CHEMOTHERAPY BE GIVEN TO A STAGE I, II, OR III CANCER?  Typical 5 year survival for breast cancer  is 97% for stage I, 85% for stage II, and 65% for stage III.[8]  (The very higher survival rate for stage 1 comes from treating many benign tumors, called malignant).  If chemotherapy is given to those who will remain cancer free, it is life shortening and affects quality of life.  This negative effect is very significant in cancers of the prostate and breast because of hormone blocking (castrating) drugs are included in the chemotherapy.  Yes, sex hormones not only increase libido, but also promote health, which is why pharma and the NIH do tobacco science to claim the opposite (see Natural HRT and Testosterone links).  Without estrogen, total morality was double at 10 years.  Moreover, if the surgery misses some of the cancer, the chemo won’t destroy that tumor.  Once observed it can be removed.  If the cancer has evolved to be metastatic in the interim period, it would have with or without the chemo.  Chemo, since it can’t destroy the missed tumor it doesn’t change the course of events.  Thus for stage III breast cancer (cancer found in nearby lymph nodes), 65% of patients must endure chemotherapy when they don’t need it and its horrible side effects, which persist for years for about 40%.  And for the 35% who will die of cancer, they are gaining nothing but side effects.  Since they are not near death, the cancer is more likely to be more aggressive now that the febrile tumor cells have been eliminated, and all the glucose absorbed is used by the surviving cells.  Rather than treat every one, it would be better to treat only those who have progressed to stage IV (metastatic) cancer if they want to be poisoned.  And given the small benefit of chemo, why prolong the illness with costly treatment that lowers the quality of life?  Yes, pharma is very good at marketing

Hope’s Hypothesis (pharma’s deceptive logic):  that chemo could make me a survivor.  Chemotherapy in clinical trials doesn’t have a placebo group.  It is given to terminal patients, thus avoiding long-term following with its side effects.  Remission is measured by imaging observations of the tumors size.  Typically the tumor stops growing or shrinks for 3 months.  Suppose the average death occurs at 12 months and that 20% die in 3 months; and 5% are live 2 years—the length of the trial.  That does not prove that a few patients had an atypical positive response to the drugs.  Rather a few patients had indolent metastatic cancer and would have lived that long without the chemo.  In the 60s, prior to chemo some survived for years with metastatic cancer.  Today the patients receiving a poisonous cocktail (typically 3 drugs) some will die from side effects such as opportunist diseases for stage II and III, and many also for stage I, even when the literature cautions against aggressive treatment.  These patients believe that the chemo will destroy all the cancer missed by surgery, and the oncologist promotes this belief.  Moreover, the horrible side effects will be downplayed.  Instead the oncologist sells Hope Hypothesis; pharma makes billions; and the patients suffer.  The evidence basis always is biased in favor or pharma.  For an account of trial distortions read Bad Pharma by Dr. Ben Goldacre.  Pharma’s clinical trials are not about uncovering side effects or indolent metastatic cancer, but about marketing.  I certainly would fall for Hope’s Hypothesis, unless the cancer I had could be for some be cured based upon clear published evidence.  Remission isn’t a cure!

IF CHEMO CAN’T CURE METASTATIC CANCER, THEN IT CAN’T CURE INDOLENT CANCER.  They are essentially the same but for the ability to fool the immune system. There is not an atypical positive response for a subgroup; those terminal patients have an indolent form of the cancer.  The term “Survival” applied to chemo means “delays death” a few months.  Like soldiers, doctors are believers, thus they sell their faith in chemo.


 Side effects:  because chemotherapy consists of chemicals that blocks essential processes, major side effects are the norm.  Among the effects, an assortment of sickness symptom (nausea, pain, weakness, etc.) that is sufficient for about half to modify or forgo full treatment.   There is a significant mortality risk because of suppression of the production of red and white blood cells.  Typhlitis is an intestinal infection with a “very poor prognosis”.    Anemia and bleeding are blood suppression consequence along with fatigue.  Long-term consequences include weakness and fatigue, an increased risk for new cancers, heart attack, infertility, & damage to the heart, kidney, liver, intestines, hearing, brain, skin, and other organs.  Chemo brain (PCCI) is a significant cognitive dysfunction; for some “lasting 10 years or more” Wiki,   A 1980 study of various cancers found, “…this was surprising, due to the fact that a majority of the drugs administered in this study are known to not cross the blood brain barrier (BBB)…  Commonly describe as affecting vision, memory, coordination, attention, understanding…”  Other studies have added a psychiatric dimension.  In a 2013 summation of imaging studies both brain volume and neural activities were down--both short and long-term.  Increased mortality is grossly under reported, only cancer deaths are counted, quality of life reduced and years lost.  

JK’s Hope’s Hypothesis--Positive Choices

In 1924 Otto Warburg one of the leading biochemists of the 20th century and Nobel Laurette published his findings that cancers have abnormal glucose metabolism and abnormal mitochondria.  Since as described above cancer is dependent essentially on glucose fermentation, I would starve the cancer.  I would start with a water fast[9] of 14 days or longer. At the end of the fast, I would go on a ketogenic diet and even limit fiber.[10]  Protein limited to 25-35 grams a day to prevent loss of muscle mass.  The amino acid glutamine is another fuel for cancer, thus the low protein diet.  With its calories limited, for mot the growth stops and the cancer shrinks.  How effective depends to a large extent on how crippled the mitochondria is, and if some can still metabolize fat to some extent.  I would also become current on the latest work on diet.  Currently work is being done to limit glutamine (another functional metabolic substrate), and supply cancer with a optical isomer of glucose that it can’t metabolize.  It would be a high fat diet since cancer with their defective mitochondria can’t metabolize fats.  Hyperbolic oxygen has also been shown to promote the death of cancer cells.  I would also have the tumor removed as soon as possible.  I would be less aggressive in staving the cancer if it was a local stage 1 cancer with a favorable biopsy report.  Assuming it is stage 2 or in a tissue that has a high mortality rate, I would adhere strictly to the diet and go on repeated fasts using fat for energy or try alternate day fasting.  I would also take 2 grams of aspirin daily.  Aspirin has the highest cure rate of all chemotherapies for stage I, II, and III, and aspirin prevents cancer.  (Oncologists hear a much different account at pharma’s continuing education classes.)  Breast cancer survival is up 66% by stimulating necrosis factor TNF; colon cancer survival up 74%, & others for stages I, II & III; but does not increase survival of metastatic cancer, yet should lengthen survival.  Aspirin reduces risk of cancer evolving into a fatal cancer by its effect upon 3 bodily defenses: as a COX-2 inhibitor, upon nitrous oxide (NO) system of endothelial cells, and stimulation of the body’s system for destruction of abnormal cells (apoptosis).  Aspirin increases survival of glandular, blood, & epithelial cancers.  Also aspirin reduces the risk for most cancers by promoting various necrosis factors and inhibition of JNK which “regulates several important cellular functions including cell growth, differentiation, survival and apoptosis” Wiki.  Risk various tissues:   reduction of63% colon, 39% breast, 36% lung, and 39% prostate cancer, also for esophageal 73%, stomach 62%, and ovarian cancer 47%” also Hodgkin's disease, and adult leukemia, melanoma 55%.  Other studies have shown that aspirin promotes the death of abnormal cells through the natural mechanism of apoptosis by stimulating tumor necrosis factor NF-B, by p38 & JNK.  Long term, but low dose is insufficient because of drug tolerance.  Moreover the increase risk of ulcer is in the US Physician’s Study 1 per 1780 patient years with 325 bi-daily.  At dose of 975 mg daily, the ulcer risk is about 1 per 300 patient years.  In the Physician’s Study the rate of heart attack was reduced 44%.   With higher dose of 325 mg daily, it has an inhibitory effect upon atherosclerosis that would be statistically significant after 3 years-- and also its inhibitory effect upon cancer.  The positive results in journal articles are based on general population studies.  For example a study published in 1991 on cancer prevention based on lifestyle of 662,424 adults found that those who took 16 or more aspirin a month had a 50% reduction in colon-cancer deaths (measured 1982-88).   Similar study using nurses found similar benefits for breast prevention & survival.  Pharma of course doesn’t fund clinical trials for aspirin except to “demonstrate” its risk and ineffectiveness.  The positive information sits in journals, while pharma friendly organizations using marketing studies produce treatment guidelines on cancer and prevention of heart attacks which warn about the grave risk of stomach bleeds that counters the modest benefits of low dose aspirin; a message repeated in continuing education classes.  I would also take testosterone (and if a woman estradiol with progesterone) since the sex hormones like other steroid promote healing.  One study found HRT subsequent to breast cancer resulted in a substantial reduction in cancer mortality.  This is what I would do and advise my wife to do.

Recommended lectures

***** Targeting Energy Metabolism in Brain Cancer 21 min, 113,000 views by Prof Thomas Seyfried, leading research to audience of fellow scientists on how to starve cancer which depends on glucose metabolism and thus cause its apoptosis through ketogenic diet. Cancer cells have damaged mitochondria that metabolized glucose & glutamine-- read his Cancer as a Metabolic Disease s. https://www.youtube.com/watch?v=sBjnWfT8HbQ&hd=1 Excellent

*****Cancer as a Mitochondrial Metabolic Disease, 60 min, 13,000 views by Prof Thomas Seyfried, similar to the above, but with more such as the role of macrophages, more on diet, glutamine, and how current standard treatment kills their patients. https://www.youtube.com/watch?v=dm_ob5u9FdM Excellent

***** The Ketogenic Diet and Cancer 152,000 views, 30 minutes Dr. John Bregman radiologist recommends intermittent fasting, with 8 hour window for eating and ketogenic diet misses glutamine, critical of standard treatment.  https://www.youtube.com/watch?v=Q9socQcwPIs Excellent.

For more go to section 4 of this link Part 7 Videos food, drugs, health YouTube


[1] As of now I don’t know enough about lymphomas and leukemias to predict the effects of energy restriction. 

[2] "Most hyperplastic polyps are found in the distal colon and rectum.[3].  They have no malignant potential, [3] which means that they are no more likely than normal tissue to eventually become a cancer” Wiki.  See also Controversy about removing benign bowel lesions.

[3] “Only a small subset of tumor cells has the power to proliferate and expand… share treats with stem cells….  Spring forth from regulator failures in damaged stem cells… cancer treatments must target cancer-stem cells” at p, 42 As per above, not stem cells but TAM in which macrophage has turned on certain oncogenic genes in the tumor. 

[4] Macrophages are large immune cells which function to clean up cell debris, engulf foreign substance, microbes, cancer cells, stimulate immune system, decrease immune reaction, encourage repair (M2 macrophage)  signal for other immune cells

[5] Most stage I. II, & III cancers are cured by excision; commonly estimated at 85% or more according to several journal articles. 

[6] If we dropped the few cancers that lives are saved (testicular, some leukemia-s and lymphomas) the average would be 2 months.

[7] As mentioned prior bias is the norm for pharma-funded studies.  For example those who die during the period of chemo treatment are doped out of the study as too those who drop out because of severe side effects, and their side effects are not included in the journal article.  Moreover, the post-marketing studies (after a patent has been granted) are of the lowest quality.  Read Ben Goldacre’s Bad Pharm and Marcia Angell How Drug Companies Deceive Us—and on YouTube.  


[8] Stage I is local, stage II is invading adjacent tissue, and stage III is also found in lymph nodes; stage IV is metastatic, found in other tissues such as the liver, bone, brain, etc. 

[9] This would include tea with lemon juice and possible bone broth (See Fung, Obesity Code P. 265)

[10] As much as half the calories from fiber are made available through the metabolism by intestinal bacteria.  Though it doesn’t raise insulin because of low quantity it supplies glucose to the cancer.  

CHEMO THAT CAN’T CURE METASTATIC CANCER, THUS IT CAN’T CURE INDOLENT CANCER.  They are essentially the same but for the ability to fool the immune system. There is not an atypical positive response for a subgroup; those terminal patients have an indolent form of the cancer.  The term “Survival” applied to chemo means “delays death” a few months.  Like soldiers, doctors are believers, thus they sell their faith in chemo.


There is a sales pitch for chemotherapy based upon bad logic.  An example will make it clear.  The 2 year survival for untreated small cell lung cancer average is 9 month, with 95 dying within 2 years.  Chemo therapy adds to the bell curve 2 months.  Thus average survival is 11 months, and 95% die within 2 years 2 months.   Gertrude has small cell breast cancer, and would untreated live average of 9 months.  If she elects treatment, she will be dead in the 11th month.  Treatment doesn’t place Gertrude in the fortunate group of living over 2 years. 

If, for example a  stage 3 breast cancer (65% chance that it is metastatic) turns out to be metastatic  the results is the same with chemo, only now that person lives 2 months longer.  Chemo doesn’t convert doesn’t change the course of events.  Metastatic cancer is like a time bomb, set to kill its host after so many months.  For those who have an indolent non-metastatic cancer, the operation entails they are a cancer survivor.  If she is a survivor without chemo, electing chemotherapy, she shortened her life by years.  I estimate at least 4.5 years.  Millions of people undergo pointless chemo that shortens their lives, and most of them falsely believe they are a survivor because of the chemo.     

Currently 3/14 there is a problem with the Google Chrome and the Internet Explorer browsers of page width, but not with Mozilla.

CANCER basics & CHEMOTHERAPY– 13 pgs  --  10/18/13 

 1) While beyond the scope of this paper, it is essential to understand the inroads made upon medical science by corporate medicine.   Corporate medicine is market driven; medical science evidence driven.    These two approaches result in different explanations concerning cancer. The goal here is to understand the general basic biology of cancer and its treatment options based quality scientific evidence—without market considerations. What follows is based upon sound science with sources.  Marketing science is driven by profits, & thus promotes aggressive treatments.   Pharma’s marketing ploys confirms Harvard Prof. Dr. Marcia Angell’s  observation that we have “the worst system we could imagine.”  To learn more read Marketing Science and its links.


2)  The primary goal of this explanation of the biology concerning cancer is to understand the benefits and limitations of chemotherapy.   This requires an explanation of the biology of cancer, a topic I have long studied.[1]  Since cancer involves a broad group of diseases, the exceptions to the generalities are often excluded (the object is to understand what cancer is; thus not to bury the reader in details).  Cancer is a line of body cells that have through mutations and often stem cells developed the ability to spread rapidly. There are 7 essential types of mutations for turning a cell into a cancerous cell line, and they involve over a hundred biochemical cellular activities.  Most chemotherapies hinder one of these essential processes, and thus it must be applied short term—only a few chemotherapies are curative (see paragraph 16).  With corporate medicine, this treatment of cancer is sold as effective, but most aren’t.   Radiation and excision, by removing an indolent cancer, reduces the risk of mutating into metastatic cancer.   If the tumor is in fact a cancer and has already metastasized, the prognosis is very, very poor:  excision, radiation, and chemotherapy are ineffective at preventing the fatal outcome.  Metastatic cancer can be indolent and take years to be diagnosed.  Chemotherapy does not destroy either the indolent or aggressive cancers, though pharma and physicians will try to persuade you otherwise.  Chemotherapies shut temporarily off an essential bodily process, and thus effects also cancer cells.  Once therapy has been stopped, the essential process, such as making new capillaries, resumes.   Life extension from chemotherapy in terminal patient averages 2 to 3 months.  It is not a magic bullet that destroys cancer cells.[2]   It affect upon non-metastatic cancer is not worth the side effects.   Chemotherapy won’t prevent an indolent cancer from at some future date becoming metastatic.  It is all a matter of numbers, and clinical trials for FDA approval are on terminal cancer patients, and are barely better than a placebo (no treatment).  Once approved, they are marketed using tobacco science for all stages of cancer.  Pharma manipulation of the results,  is the norm because effective peer review is impossible.[3]  When administered in office, the oncologist receives a spread between what is billed insurance and their bulk price for the drugs, plus a fee for treatment.  For the reasons just stated early only excision and irradiating the cancer are effective.  This paper in it discussion of the biology cancer reveals why chemotherapy fails to cure.     


 3)   “A benign tumor is a mass of cells (tumor) that lacks the ability to invade neighboring tissues or metastasize. These characteristics are required for a tumor to be defined as cancerous and therefore benign tumors are non-cancerous. Also, benign tumors generally have a slower growth rate than malignant tumors and the tumor cells are usually more differentiated (cells have normal features). [1][2][3]  Benign tumors are typically surrounded by an outer surface (fibrous sheath of connective tissue) or remain with the epithelium.[4]  Common examples of benign tumors include moles (nevi), colon polyps,[4] and uterine fibroids (leiomyomas).   Although benign tumors will not metastasize or locally invade tissues, some types may still produce negative health effects.  The growth of benign tumors produce a "mass effect" that can compress tissues and may cause nerve damage, reduction of blood to an area of the body (ischaemia), tissue death (necrosis) and organ damage.  The mass affect of tumors are more prominent if the tumor is within an enclosed space such as the cranium, respiratory tract, sinus or inside bones.  Tumors of endocrine tissues may overproduce certain hormones, especially when the cells are well differentiated.  Examples include thyroid adenomas  and  adrenocortical adenomas.[1]    Although most benign tumors are not life-threatening, many types of benign tumors can become malignant through a process known as tumor progression.[5]  For this reason and other possible negative health effects, some benign tumors are removed by surgery.[6]Wiki.  Unfortunately pharma who profit from overtreatment of benign tumors, promotes guidelines that are contrary to the best interests of patients.  This practice has been exposed for the prostate, breast, thyroid,  cervix, uterus and ovaries, where studies have shown that aggressive treatment causes more harm than good—and undoubted for other tissues.                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                     


4)   Cancer (malignant neoplasm) is a broad spectrum of diseases involving improperly regulated cell growth.  For that cell growth to become life-threatening it must be capable of sufficient reproduction so as to disrupt essential bodily processes.  Over 80% of fatal cancers spread to more distant part of the body through the lymphatic or blood systems—some such as cerebral cancer often don’t.  With the exception of blood and lymphatic cancers, they form hard tumors.  One of the most important factors in classifying a tumor as benign or malignant is its invasive potential” Wiki.  “If a tumor lacks the ability to invade adjacent tissues or spread to distant sites by metastasizing then it is benign, whereas invasive or metastatic tumors are malignant.[1]  For this reason, benign tumors are not classed as cancer”[2] Wiki. The degree of dysplasia (abnormal development of tumor & it’s cells) does not make a tumor cancerous.   To be cancer it must be invasive.  Not all tumors are cancerous, benign tumors do not invade neighboring tissues and do not metastasizeWiki.  Unfortunately based on biopsy and microscopic examination of tissue and corporate medicine, many of these benign tumors are called cancerous.  The removal of a few benign tumors can be justified because of the high risk of becoming cancerous; however, in most cases low-risk benign tumors are removed.  Often both are mislabeled “carcinoma”.  Guideline then require excision (or irradiation) and chemotherapy.   A number of quality studies have shown that this aggressive approach does more harm than good.[5] The 800 pound gorilla (pharma), using marketing science, has worked the treatment-guideline committees, and thus compel physicians to treat tumors aggressively—compel though hospital administrators, and the risk of litigation based on failure to follow guidelines.      

5)  “Cancer cells are cells that grow and divide at an unregulated,[6] quickened pace.  Although cancer cells can be quite common in a person they are only malignant when the other cells (particularly natural killer cells, cytotoxic lymphocytes) fail to recognize and/or destroy them.[1]  The failure to recognize cancer cells is caused by the lack of particular co-stimulated molecules that aid in the way antigens react with lymphocytes.[2]  Other factors pay a role including viruses, immune system issues, genetics, environmental pollutants including radiation which promote random mutations of the DNA code, age, and too much of SP2 protein which may turn stem cells into cancer cells” Wiki.  Genetic and epigenetic[7] changes can occur at many levels, from gain or loss of entire chromosomes, to a mutation affecting a single DNA nucleotide, or to silencing or activating a microRNA that controls expression of 100 to 500 genes.[4][5] 

6)  Oncogenesis (carcinogenesis): is literally the creation of cancer. It is a process by which normal cells are transformed into cancer cells. It is characterized by a progression of changes at the cellular genetic and epigenetic that ultimately reprogram a cell to undergo uncontrolled cell division, thus forming a malignant mass.  Cell division is a physiological process that occurs in almost all tissues and under many circumstances.  Under normal circumstances, the balance between proliferation and programmed cell death, usually in the form of apoptosis, is maintained by tightly regulating both processes to ensure the integrity of organs and tissues. Only certain mutations and epimutations [genes that regulate the expression of other genes[8]] in DNA that disrupt the orderly process can lead to cancer.  These changes may remain through cell divisions for the remainder of the cell's life and may also last for multiple generations. The majority of potential mutations and epimutations will have no bearing on cancer” Wiki.

7)   “A proto-oncogene is a normal gene that can become an oncogene due to mutations or increased expression. The resultant protein may be termed an oncoprotein.[10]  Proto-oncogenes code for proteins that help to regulate cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through their protein products. Upon activation, a proto-oncogene (or its product) becomes a tumor-inducing agent, an oncogene.[11]   The proto-oncogene can become an oncogene by a relatively small modification of its original function” Wiki.

[1] In 1983 I bought from the University of Colorado, Cancer Biology by Raymond Ruddon, Oxford Press 1981; a great foundation.  In 1999 Science devoted an issue to cancer and cutting edge developments.  I spent about 30 hours studying the article I deemed relevant to bring me current on the topic.  Cancer remained a topic which I kept current. 

[2] The few exceptions, magic bullets such as for testicular cancer and non-Hodgkin’s lymphoma; they are widely known. 

[3] Impossible because the raw data is never included with the submission for journal publication in pharma-funded studies.  Pharma owns the material, and they de facto control the journal through advertising dollars.  Positive bias averaged 32% (range 11 to 69%) in a study which compared to the raw data submitted to the FDA in drug submissions for approval, a 2008 NEJM article revealed.   The raw was obtained from the FDA through the Freedom of Information Act.  http://healthfully.org/index/id9.html;.  

[4] "Most hyperplastic polyps are found in the distal colon and rectum.[3] They have no malignant potential,[3] which means that they are no more likely than normal tissue to eventually become a cancer” Wiki.  See also Controversy about removing benign bowel lesions.

[5].  Instituting treatment for indolent benign tumors, called cancerous cancers of the thyroid, breast, uterus, and prostate have drawn sharp criticism from scientists, because the treatment causes more harm than good.   

[6] Cancer cells are immortal because they cause telomerase reverse transcriptase (TERT) to lengthen telomeres in DNA strands, thereby allowing senescent cells that would otherwise become post-mitotic and undergo apoptosis to exceed the Hayflick limit and become potentially immortal. 

[7]  Epigenetics is the study of changes in gene expression or cellular phenotype, caused by mechanisms other than changes in the underlying DNA sequence—hence the name epi- (Greek: επί- over, above, outer) -genetics. Some of these changes have been shown to be heritable.  Examples of such modifications are DNA methylation and histone modification, both of which serve to regulate gene expression without altering the underlying DNA sequenceWiki.

[8] Does not involve changes to the underlying DNA sequence.  Gene expression can be controlled through the action of repressor proteins that attach to silencer regions of the DNA {introns]. This is a way for cells to be responsive to environmental changes. 

8)  Stem cells

Stem Cell

Progenitor Cell

Self-renewal in vivo



Self-renewal in vitro





Unipotent, sometimes oligopotent

Maintenance of self-renewal




Reaches maximum number of cells before differentiating

Does not reach maximum population

Stem cells are undifferentiated biological cells, that can differentiate into specialized cells and can divide (through mitosis) to produce more stem cells.  In mammals, there are two broad types of stem cells: embryonic stem cells, which are isolated from the inner cell mass of blastocysts,[1]  and adult stem cells, which are found in various tissues.  In adult organisms, stem cells and progenitor cells act as a repair system for the body, replenishing adult tissues. Stem cells maintain the normal turnover of regenerative organs, such as blood, skin, or intestinal tissues.  Stem cells possess two properties:  self renewal (to maintain through cell division the undifferentiated state) and potency (to give rise to any mature cell type).   For example, the defining test for a bone marrow or hematopoietic stem cell (HSC) is the ability to transplant one cell and save an individual without HSCs. In this case, a stem cell must be able to produce new blood cells and immune cells over a long term, demonstrating potency.[2]   Stem cells can also be isolated by their possession of a distinctive set of cell surface markers.  Most adult stem cells are lineage-restricted (multipotent) and are generally referred to by their tissue origin (mesenchymal stem cell, adipose-derived stem cell, endothelial stem cell, dental pulp stem cell, etc.).[28][29]  Induced pluripotent, these are not adult stem cells, but rather adult cells (e.g. epithelial cells) reprogrammed to give rise to pluripotent capabilities. Using genetic reprogramming with protein transcription factors, pluripotent stem cells equivalent to embryonic stem cells have been derived from human adult skin tissue.[53][54][55]   Adult stem cells (somatic stem cells)


9)  A progenitor cell is a biological cell that, like a stem cell, has a tendency to differentiate into a specific type of cell, but is already more specific than a stem cell and is pushed to differentiate into its "target" cell. The most important difference between stem cells and progenitor cells is that stem cells can replicate indefinitely, whereas progenitor cells can divide only a limited number of times.  The majority of progenitor cells lie dormant or possess little activity in the tissue in which they reside. They exhibit slow growth and their main role is to replace cells lost by normal attrition. In case of tissue injury, damaged or dead cells, progenitor cells can be activated. Growth factors or cytokines are two substances that trigger the progenitors to mobilize toward the damaged tissue. At the same time, they start to differentiate into the target cells. “Symmetric division gives rise to two identical daughter cells both endowed with stem cell properties. Asymmetric division, on the other hand, produces only one stem cell and a progenitor cell with limited self-renewal potential” Wiki.


10)  A transcription-n factor (sometimes called a sequence-specific DNA-binding factor) is a protein that binds to specific DNA sequences, thereby controlling the flow (or transcription) of genetic information from DNA to messenger RNA.[1][2]  Transcription factors perform this function alone or with other proteins in a complex, by promoting (as an activator), or blocking (as a repressor) the recruitment of RNA polymerase(the enzyme that performs the transcription of genetic information from DNA to RNA) to specific genes.[3][4][5] A defining feature of transcription factors is that they contain one or more DNA-binding domains(DBDs), which attach to specific sequences of DNA adjacent to the genes that they regulate.[6][7] Additional proteins such as coactivators, chromatin remodelers, histone acetylases, deacetylases, kinases, and methylases, while also playing crucial roles in gene regulation, lack DNA-binding domains, and, therefore, are not classified as transcription factors.[8]  Many transcription factors are either tumor suppressors or oncogenes, and, thus, mutations or aberrant regulation of them is associated with cancer. Three groups of transcription factors are known to be important in human cancer: (1) the NF-kappaB andAP-1 families, (2) the STAT family and (3) the steroid receptors.[73] 


11)  Cancerous Stem Cells (CSCs):  The role of stems cells is complex, varied, only partially revealed, and very uncertain.  A number of factors support their role, but just what it is need elucidation.  A major problem consists of identification; viz., differentiating between stoma cells turned cancerous and that of stem cells turned cancerous.  A number of paths involving stem cells as the source of the malignant tumor, or as the driving force behind progenitor cells, or functioning in the healing process to stimulate the growth of benign tumors that emit an appropriate signal for this process.  Whatever way or ways, CSC would explain the variability of cell lines in cancerous tumors and their rapid growth.  A third issue clouding the research is that that only a small percentage of CSCs have the ability of generating a tumor.  In human acute myeloid leukemia the frequency of these cells is less than 1 in 10,000[9].  Many tumors are very heterogeneous and contain multiple cell types native to the host organ. Heterogeneity is commonly retained by tumor metastases. This implies that the cell that produced them had the capacity to differentiate into multiple cell types. In other words, it possessed multi-differentiative potential, a classical hallmark of stem cells[9]  One important distinction that will often be raised is that the cell of origin for a tumor cannot be demonstrated using the cancer stem cell as a model. This is because cancer stem cells are isolated from end-stage tumors. Therefore, describing CSCs as a cell of origin is often an inaccurate claim, even though a cancer stem cell is capable of initiating new tumor formation.  Tissues with high rates of turnover, such as skin and colon are likely to involve CSCs, since they are more active in such tissues. Like normal stem cells, CSCs can have “the ability to form anchorage-independent spheres.”  Metastatic cancer stem cells:  Metastasis causes 80% of tumor lethality in patients.  Since cancerous tumors are made up of different cells (see illustration above), not every tumor cell has the ability to metastasize. This “potential depends on factors that determine  growth,  angiogenesis [growth of new blood vessels], invasion and other basic processes of tumor cells.  Many tumors are very heterogeneous and contain multiple cell types native to the host organ. Heterogeneity is commonly retained by tumor metastases. This implies that the cell that produced them had the capacity to generate multiple cell types. In other words, it possessed multi-differentiative potential, a classic hallmark of stem cells[9]Wiki.  “To date, researchers have reported findings evidence of cancerous stem cells in tumors of breast, brain, skin, colon prostate, pancreas, and liver, among others…. At least some cancers follow the stem cell model… Nor do researchers understand how cancer stem cells originate;, how often they derive from normal stem cells, or whether each tumor has just a few or many of the cells.  Some of the latest study results suggest that a complex mix of both the standard model [one cell line] and the cancer stem cell idea comes closest to elucidating how cancers form.”  Cassandra Willyard, Scientific American Aug, 2011, p. 34)

12) Mechanisms for preventing a cell line from becoming malignant: 

Cancer is the result of a series of mutations that confer on one cell line (from a single cell) a number of properties for which various biological constraints on proliferation have been modified.  In most cases the cell line continues to mutate rapidly and presents when examined presents significant variation in physical form, function, and mutations.  Nevertheless, the tissue from which the cancerous cell line is derived very significant effects prognosis.  Oncogenesis involves typically 7 basic families of changes (leukemia 4) which are governed by many genes.  Typical of most cancer cell lines is an oncogene failing to limit the rate of mutations thus causing an abnormally high rate of mutations.  This increases the probability of a lethal cancer.  Thus in addition to transformation into oncogenes, there are many other noncancerous mutations which affect the cancerous cell line.  Thus most tumors under the microscope show a high degree of abnormal cells (see illustration above).  A second key to malignancy is the involvement of stem cells.  A few stems cells are found in benign tumors, in metastatic, and in invasive cancers.  Their important roles have been an object of intensive research for over 3 decades (see section below).  While the tumor is small, most ultimately fatal cancers develop the ability to metastasize.  Nevertheless, an indolent invasive cancer as it ages can evolving into a fatal cancer.  Early detection has been oversold (a topic developed below with breast cancer used as an example), and the removal benign potentially cancerous tumors has for most tissues minimal effect upon lethality.  Such benign tumors are too often called stage I cancers.  Under 10% of all cancers involve an inherited genetic mutation disabling a gene which promotes the accurate reproduction of the DNA during mitosis, and thereby accelerating the rate of ocogenetic mutation and subsequent cancer.  Those with the inherited defect have a cellular mutation rate of around 10 fold that of the norm.  Another common way the rate of mutation accelerates is through the exposure of tissues to radiation or chemicals which promote mutations.  Tobacco smoke contains such chemicals, and increases the risk of cancer in most tissues; for example pancreatic cancer 250%.  Counting environment including infectious causes, they account for about 50% of all cancers; the rest are a matter of chance including the 10% inherited oncogenes.  There are 15 general types of functional alterations that contribute to turning a single cell line into a life-threatening cancer; however, not all 15 types of are essential. 

[1] The blastocyst is a structure formed in the early gestation of vertebrates. It is preceded by the morula. It possesses an inner cell mass (ICM), or embryoblast, which subsequently forms the embryo, and an outer layer of cells, or trophoblast, surrounding the inner cell mass and a fluid-filled cavity known as the blastocoele. The human blastocyst comprises 70-100 cells.


[2] Cell potency is a general term which describes a stem cell's ability to differentiate into different cell types.[1] [2] The more cell types a stem cell can differentiate into, the greater its potency.   Potency is also described as the gene activation potential within a cell which like a continuum begins with totipotency to designate a cell with the most differentiation potential, pluripotency, multipotency, oligopotency and finally unipotency.


13)  Changes: 

1.  Rapid cell division by turning on the chemical signals for mitosis and leaving it on.  VERY COMMON

2.   Angiogenesis: Stimulating the formation of new capillaries to assure adequate oxygen supply for continued growth of the abnormal cells. ESSENTIAL but for leukemia

3.   Limitless replication of one cell line by turning on telomerase, which adds telomeres to make the cell line immortal.  Cell divisions in normal cells are limited to about 50 replications.  ESSENTIAL

4.  Mutations affecting adhesiveness[1], to free the cells from the matrix which holds them in place. VERY COMMON

5.   Invade adjacent tissues:  Organs are enveloped in a membrane (muscle, intestine, lung, etc).  Most cancers fairly early develop the ability to grow through the membrane and invade adjacent tissues.  VERY COMMON

6.  Metastasize:  have microscopic colonies of the tumor relocate in other sites.  This involves mutations affecting the ability to enter capillaries, which thus permits single cells to migrate.  ESSENTIAL for the 80% that are metastatic cancers.

7.  Fool immune system for migration to distant tissues: change markers on the cell wall so cells do not appear as foreign to the immune system, which will destroy those cells.  Which tissues a cancer migrates to is highly dependent upon the markers.  ESSENTIAL for metastatic cancer.

8.  Being able to both enter and leave blood vessels like the way lymphocytes do by secreting a factor which allows them to enter a capillary and then at another site to pass out of the capillary again--a class of compounds known as SRC kinase. ESSENTIAL for metastatic cancer.

9.     Infection including oncovirus can increase risk of cancer.  The WHO estimates that 18% (1/6th) of cancers have as a causal vector an infection, of which two thirds are viral.

10.  Some cancers have abnormal DNA due to gross changes in the chromosome that consist of translocation, duplication, deletion, or inversion.  This type of abnormality results in the imperfect expression of genes on that chromosome. MODERATELY COMMON

11. Environment causes, exposure to carcinogens and ionizing radiation by causing mutation—for a large population, a causal factor in about 30% of cancer.

12.   Disabling of the gene that check the accuracy of replication of DNA during mitosis, such as p53, BRAC1, BRAC2, etc. Given the number of mutations required for cancer, most cancerous cell lines have this system disable to some extent.  Not all mutations disable the checking process, thus the risk factor depends on the mutation.[2]  When a specific cancer runs in a family, the cause could be an inherited mutation. Of one of these genes.  COMMON

13.  Programmed cell death (apoptosis) is disabled.  Cancers are immortal:  not limited to about 50 cell division.  ESSENTIAL


14.  Heterogeneity results from the high rate of mutation in most cancers, “tumor population exhibit functional, and tumors are formed from cells with various proliferative and differentiate capacities” Wiki, and.[3]  VERY COMMON

15.  Excrete growth factors which enable the cancer to attract stem cells which then help support the growth of the tumor by stimulating the growth of capillaries and other structures needed to support a large tumor.  ESSENTIAL

16.  Natural selection favors the uncontrolled reproduction of the cancerous cell line.[4]

17.  Pluripotent cells created by action of stem cells create from stoma cells.  COMMON

This is a list of the key types of mutations On average, for example, “15 driver mutations" and 60 "passenger" mutations are found in colon cancers.[2] Mutations in those certain types of genes that play vital roles in cell division, apoptosis (cell death), and mutations and epimutations (see article Genome instability) in DNA repair genes will cause a cell to lose control of its cell proliferation.  This mass alternation of genetic code in malignant tissue is essential to the understanding of why cancer can develop resistance to chemotherapy, and why invasive cancer given a couple of years has a guestimate 20% chance of becoming metastatic.  Natural selection favors the cell line which can resist chemotherapy and spread to distant organs. This raises the question against the backdrop of orderly low rate of mutation stoma cells[5] and while others form tumors that are quite indolent; why is there a modest percentage that are mutating at very high rates?  How is this possible?  One answer is mutations in genes which promote accurate replication of DNA.  Another is the involvement of stem cells.   Stems cells have the ability to convert stoma cells into progenitor cells as a way to promote re-growth are undifferentiated cells, found throughout the body after development, that multiply by cell division to replenish dying cells and regenerate damaged tissues.


14.   Complexity—some examples

Chemical stimulation of angiogenesis is performed by various angiogenic proteins, including several growth factors.


Overview  http://en.wikipedia.org/wiki/Angiogenesis (genes involved in the production of new blood vessels): 




Promotes proliferation & differentiation of endothelial cells, smooth muscle cells, and fibroblasts


Affects permeability


Integrate survival signals

Ang1 and Ang2

Stabilize vessels

PDGF (BB-homodimer) and PDGFR

recruit smooth muscle cells

TGF-β, endoglin and TGF-β receptors

extracellular matrix production



Integrins αVβ3, αVβ5 (?[6]) and α5β1

Bind matrix macromolecules and proteinases

VE-cadherin and CD31

endothelial junctional molecules.


Determine formation of arteries or veins

plasminogen activators

remodels extracellular matrix, releases and activates growth factors

plasminogen activator inhibitor-1

stabilizes nearby vessels

eNOS and COX-2


regulates angioblast differentiation


Regulates endothelial transdifferentiation



This table is illustrative of the number of orchestrated genes that are involved the production of new blood vessels.  Thus an epigenetic switch is responsible for angiogenesis.  That for most tumors this switch is off, then at some point turned is evidence for the role of stem cells.     

[1]  In most cervical cancer, for example, a mutation causes the cell-to-cell adhesive molecule E-carherin to be digested, and as a consequence the cancerous cervical cell line can spread to distant tissues.


[2] For the BCA1 & BRAC2 mutation can increase the frequency of ovarian, breast, and fallopian tube cancers. If cancers of these tissues run in the family, than blood relatives are at very significant increased risk—depending on the mutation’s effect upon the DNA checking process.  Since there is no data bank based on code mutation of a gene, stats for these mutations are given in averages.  A mother with a BRAC2 mutation having breast cancer doesn’t prove cause. Not all BRAC mutations are equal, and other causes could be determinate for the daughter.  

[3] “It  is now appreciated that cancers can be composed of multiple clonal subpopulations of cancer cells which differ among themselves in many properties, including karyotype, growth rate, ability to metastasize, immunological characteristics, production and expression of markers, and sensitivity to therapeutic modalities….Heterogeneity is not a unique property of malignancy.  Prenoplastic tumors, as well as normal tissues, are also composed of cellular subpopulations” Tumor heterogeneity.     

[4] Thus for example an intestinal polyp can undergo a mutation that results in the growth of new capillaries permitting that cell line to form a section of the colon.  Now a large colony the chances of one cell in that line to undergo the remaining couple of mutations necessary to form a metastatic cancer has been greatly increased. See supra for discussion with photo. 

[5] Adult stem cells (somatic stem cells) are undifferentiated cells, found throughout the body after development, that multiply by cell division to replenish dying cells and regenerate damaged tissues

17)  WHY MOST CHEMOTHERAPIES DO NOT AFFECT THE LETHALITY OF METASTATIC CANCER: The fundamental problem is how to poison or make dormant long-term, bodily cells that are malignant without also poisoning or making dormant normal bodily cells.  The difficulty arises because cancerous cells are nearly identical to normal cells.  There are a few very effective chemical therapies; most often in a tissue for which major damage is not life threaten, such as testicles.  A unique marker on the cell wall or a unique chemical process in that cell line can permit the development of a chemotherapy that will destroy the metastatic distant tumors without destroying the adjacent tissue.  For the other types of tissue where this is unlikely, pharma relies upon chemicals that are disrupting cell division (reproduction).  Most cancers divide rapidly.   “Thus chemotherapy also harms normal cells that divide rapidly in the bone marrow, digestive tract, and hair follicles, and to a lesser extent slow dividing cells.  This results in the most common side-effects of chemotherapy:  myelo-suppression (decreased production of blood cells, hence also immuno-suppression),  mucositis (inflammation of the lining of the digestive tract), and alopecia (hair loss).  Virtually all chemotherapeutic regimens can cause depression of the immune system, often by paralysing the bone marrow and leading to a decrease of white blood cells, red blood cells, and platelets Wiki.   Indolent cancers tend to respond much more modestly to chemotherapy.  Causing damage and shut-down are why most chemotherapies are given short term.  Thus for aggressive cancers, the chemotherapy does not eliminate the cancer, but rather produces a short remission and thus prolongs life on average a few months.  


18)  PROBLEMS WITH RESEARCH, JOURNAL PUBLICATIONS, and AND GUIDELINES:  Drug companies push that everyone with cancer should be on chemotherapy at the greatest dose for the longest time, and they do the research to “prove” it (see Marketing Science and Side Effects).   Given that positive bias is the norm (average 32%), and guidelines heavily rely upon junk science, a starting point would be to look for published clinical trials show major advantages to the treated cohort, and remember that side effects are always under-reported, and long-term ones don‘t become statistically significant during the period of most studies and often are not within the study’s protocol.[1]     The standard testing for FDA patent of exclusivity is on terminal metastatic cancer patients, compared to a placebo generally after the standard chemotherapy’s temporary remission has ended and further chemotherapy is contra-indicated.  If there is an average life extension of a couple of months for the treated cohort, the FDA grants a patent of exclusivity.  And though the FDA receives the raw data during the approval process, they do not make it public, nor do they review for accuracy the journal articles published based these submissions.  The 32% bias referred to above was found in a study comparing the raw data submitted to the FDA compared to its journal publication (raw data obtained through the Freedom of Information Act).  Such short-term testing in terminal patients does not reveal most side effects.  Unfortunately the treatment is not tested on those mostly likely to receive it, Stage I-III cancers.  But should they, and how to decide?   Remember the marketing department of pharma is involved in all aspects of their clinical trials and they own the results.  Given this, major benefits must be demonstrated, as it is for the treatment of non-Hodgkin’s lymphoma.  Bias, junk science, junk guidelines, and junk continuing education of doctors are the norm. 


18)  SHOULD CHEMOTHERAPY BE GIVEN TO A STAGE I, II, OR III CANCER?  Except for the most lethal cancers, all too often the chemotherapy is life shortening, because of its side effects upon those who were cured through invasive treatment.  Aggressive treatment of stages I & II shorten life, for breast cancer an average of 2.5—and this is not taught oncologists in continuing education classes.  The journal article that documented this has been lost in the sea of time and pharma sponsored articles.  Besides most  doctors follow treatment guidelines even when skeptical of its application. 


Following radiation or surgery, how beneficial is adjunct chemotherapy, maintenance (long-term) chemotherapy, and neo-adjunct (prior to radiation/surgery)?   A combination of factors is germane:  1) the life expectancy of the patient following excision of the cancer.  2) The health consequences of the chemotherapy both on quality of life and duration.  3) The cost of the chemotherapy and the recommended subsequent drugs. 4) The effectiveness of the chemotherapy upon the indolent excised cancer with in vitro chemo-sensitivity testing.[2]  5) The effectiveness of the chemotherapy upon the malignant tissue found in adjacent lymph nodes.[3]  6) The result of study of a matching or placebo controlled study on the value of adjunct chemotherapy for stage I, II, III cancers.  Most studies are not placebo control, so duration of cancer growth suppression (termed “remission”) is the best substitute information.  Typically it averages the duration of the chemotherapy.  Since the manufacturer most likely funded the study the results are biased over 30%, thus increased survival needs to be adjusted.[4]   An informed choice is not easy, made more difficult by the system of corporate medicine and the vest interest the oncologist has in aggressive treatment.[5]  Serving the patient’s best interest is lost in the corporate system.  Thus for example chemotherapy as an adjunct treatment is pushed on patients without in vitro testing of the drugs.  There are more profits in treating everyone.  Moreover, the costs of treatment upon the healthcare system and the need for a better allocation of resources, this is not figured into the short-term maximization of corporate profits.  


19)  Three special cases for chemotherapy:

1)       Salvage chemotherapy or palliative chemotherapy is given without curative intent, but simply to decrease tumor load and increase life expectancy. For these regimens, a better toxicity profile is generally expected. 

2)       Curative chemotherapy, such as for non-Hodgkin’s lymphoma and testicular cancer.

3)       Some newer anticancer drugs (for example, various monoclonal antibodies) are not indiscriminately cytotoxic, but rather target proteins that are abnormally expressed in cancer cells and that are essential for their growth.  Such treatments are often referred to as targeted therapy (as distinct from classic chemotherapy).   Their lower immediate and obvious side effects, doesn’t entail that there aren’t major long-term ones.  And being able to target the cancer does ipso facto make them curative.  Their use with traditional chemotherapy should be carefully evaluated to remove business bias. 

20)  Deciding what to do

Read Marketing Science then start with the journal literature, oncology textbooks, http://www.wikipedia.org/, https://www.worstpills.org/, http://www.rxlist.com, http://www.mayoclinic.com/, http://www.cochrane.org/, and the http://www.merckmanuals.com/.  Be skeptical of the advice given by the oncologist.  If you can’t find strong evidence of major advantage in all the articles for the chemotherapy than forgo such treatment.  Write out key point which promotes rational analysis rather than a decision by a gut feeling, for which social considerations play a major role.  Treatment choices ought to be solely based on the evidence.    


For the few patients who research the issues.  Learn to recognize the 1) unmerited positive enthusiasm in journal articles.    Bias is often found in the conclusion and abstract sections that does not follow from the results of the study.  Convert results to the number of patients that must be treated for 1 patient to show major life extension, Calculate the average life extension of treated group.  One common fallacy is to conclude that a 2) subgroup will benefit atypically from the chemotherapy and be cured or have a prolonged remission.  This is the result of a statistical fallacy:  by simple chance a few small groups will do better than the average (and a few will do worse).  Without clear proof, don’t assume that slowing down the rate of mitosis (cell division) for a few months will produce a cure for a subgroup of patients.     Look for 3) obvious issues that should be measured but aren’t; all too often they aren’t because the results aren’t in the interest of pharma.[6]  Most studies don’t follow long-term patients or list all causes of death because pharma doesn’t like those results.  It is very convenient that they use terminal patients, since side effects are very poorly reported and long-term ones don’t occur.   4) Pharma actively downplays and hides side effects.  After FDA approval for which pharma must submit the raw data, the subsequent marketing studies are of a significant lower standard since there is no review of the raw data.  Many of these studies are on non-metastatic cancer.  Don’t assume that there is an honest evaluation of side effects.   Most studies do not have a placebo group, which make evaluation of net benefit impossible.

Remember only those who are pharma “friendly” receive funds for research, and pharma’s marketing department is actively involved in all aspects of the project, and they often ghost write the journal articles. 5)  Don’t assume that there isn’t substantial favorable bias  for the reported benefits of chemotherapy.  There are many ways to create positive bias.  Remember that this is the way business is done.


Especially, search for articles by critics published in a major medical journal.  These articles often review the literature and perform a meta-study on the published clinical trials that meet a higher standard.  But they can’t rise above pharma’s hold upon research, favorable bias is the norm.  Sometimes an article will glean out of pharma funded studies the negative results. These critical articles meet a higher standard that marketing studies to be published in a major journal.   Also in general older wisdom is not false, especially when it stands in the way of profits for pharma.  For example in our article of natural estrogen there is listed 8 articles with links showing that estrogen lowers the risk of metastatic  breast cancer deaths, the incidents of breast cancer,  and the relapse.  Also shown is that using certain progestins in HRT the opposite consequences—with 4 links to journal articles.  The 800 pound gorilla has rewritten the book on HRT and breast cancer.   Question treatment guidelines, they are all pharma friendly.  Remember “The pharmaceutical industry is the most lucrative, the most cynical and the least ethical of all the industries.  It is like an octopus with tentacles that has infiltrated all the decision-making bodies:  world health organizations, government agencies, parliaments, high administrations in health and hospitals and the medical profession." Dr. Evan with Debre authors of Guide Des 4,000 Medicaments Sept. 2012.  There they list half the drugs that are useless and dangerous.   Population studies show that cancer, if it is metastatic, chemotherapy and regular checkups[7] make minor differences, not enough to justify chemotherapy or frequent follow-up examinations.   


21)  Atypical cures, Hope’s hypothesis:

Chemotherapy is sold on the hope that a few will undergo long-term remission. Case histories don’t prove that point, only large studies can show that a treatment works just for a few patients.  And that is because it is compared to a population who were given that chemotherapy.    It is Hope’s hypothesis to believe that the benefit for a few terminal patients who live much longer than the average, that it was because of treatment.  For terminal lung cancer if 90% of the placebo cohort survival averages 6 months and 10% live longer than 1 year, and the chemotherapy cohort lived an average of 3 months longer, the logical conclusion is that for each treated patient 3 moths is the benefit.  Thus a patient living 16 months, the logical conclusion is untreated death would come at 13 months..  There is no reason to assume atypical benefits, and if there are, then some had no benefits at all, thus giving the 3-motnh average.   Pharma often teases out of a trial a subgroup that benefits, and argues for approval from FDA on that basis when their drug’s results are the same as the placebo.  This is a statistical fallacy, especially in smaller trials.  Create sufficient subgroups and some will by chance come at better than the matching control group.   Repeat the trial, and different results will be obtained. 

The treatment of cancer has usually been aimed at destroying the primary tumor or at least in stopping its growth. Even though, major improvements in the methods of surgery, radiation and chemotherapy have taken place, often there have not been corresponding improvements in patient survival.[8] Treatment methods that focus on the primary cancer typically fall short in aiding the patient after the cancer has metastasized[1]Wiki.  How can there be major improvements if it doesn’t result in a corresponding improvement in patient survival?  The razzle-dazzle has improved.  In other words, survival has been determined upon excision and radiation.  If the cancer has already metastasized, it is a leathel.  The chemotherapy won’t change the course, at best delay it.  Given this most chemotherapy are not worth the side effects. 

[1] For example very few long-term studies of statins record the incidence of cancer, though animal studies show them to be a carcinogen.  And if record, the standard for recording events is very important.  For example Warfarin & Plavix count as a serious stomach bleeding only those who require a transfusion of 2 or more pints of blood.  

[2] Like the testing of an antibiotic on a patient’s bacterial culture, the chemotherapy should be tested on in vitro tumor samples. 

[3] Heterogeneity entail variation, the cancer capable of spreading to lymph nodes can be different than the cancer in the primary tissue.

[4]   Don’t look at percentage of benefit, but rather the number of patients that must be treated for 1 to show the major benefit--and find out what counts as major benefit.  If after one year 15 in the chemotherapy group die of cancer and 20 in the placebo group die, then it likely will be written up as increased survival of 33% {5/15}, but if there were 100 in the treated group then 20 {5/100}must undergo chemotherapy for to extend one life beyond the 1 year marker.   And that doesn’t report what happened at the 2 and 5 year markers.  Also, what is the total death rate, all causes   If 5 treated died from MI, then the net benefit is zero, made wore tan zero when included are those who survived their heart attack.  All too often the missing information is unfavorable—such as total deaths. 

[5] Besides direct pay for visits, he receives for in office chemotherapy the spread between what he bills the patient and the discount price he obtains the chemotherapy. 

[6] An example of such (10/13 BMJ article) in a large epidemiological study of breast cancer screening where they only considered the increased incidence of invasive breast cancer.  They didn’t indicate lives save, thought that data was available.  A review of the journals shows that mammograms Prestigious Cochrane Review, ”the studies which provided the most reliable information showed that screening did not reduce breast cancer mortality.”  By over treating mammograms shorten lives an average of 2.5 years because of pharma’s chemically castrating women with breast cancer,  Subsequent to treatment, estrogen increases survival and longevity of women, but for those who have ER positive metastatic breast cancer.      

[7] A five-state study found, “The percentage of patients who died from breast cancer was 45.4% with standard follow-up, versus 45.8% without follow-up. In older women, the gain was even less… and recent observational studies show more over diagnosis than in the trials and very little or no reduction in the incidence of advanced cancers with screening.” Removing an invasive or local cancer does not affect metastatic cancer which is always fatal.  Early detection is too late.  The same was found for lung 55 years ago.   

[8] Alluded to is the fact that for a given stages II, III, IV of cancer the survival rate differs little over the last 6 decades.  In most cases, stats which show an improvement there is an increases derived from benign, indolent, small tumor being treated and counted as stage I cancer cures.  Prostate, breast, thyroid, and cervical cancer stats are illustrative of this trend to over diagnose and over treat Stage I.  


^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^  Non-technical summation

Cancer is distinguished from a benign tumor by its ability to invade neighboring tissue and sometimes spread to distant tissues (metastasize).  Also benign tumors generally have a slower growth rate and are more differentiated (more normal cell features).  This is the first area where business has blurred the distinction between benign and malignant and thus aggressively treats with surgery and chemotherapy benign tumors, by calling them “carcinoma”.  Critics have pointed out the negative consequences from such treatment of benig tumors of the breast prostate, and thyroid cancers, and others by the adjunct chemotherapy following excision.  Benign breast tumors, called “cancer”, when treated shorten life over 2.6 years.  Another line crossed is to treat a stage I & II cancers aggressively where the risk for it being metastatic cancer is low and the chemotherapy offers minor benefit.  With a few exceptions, chemotherapy doesn’t cure cancer, but rather shuts down an essential biological process that affects the rate of cell reproduction, including the cancers’.  This toxicity entails a limit to the chemotherapy.  The average remission for such treatments is 3 months.  Both in the treated and untreated groups there will be people who last years past the average (they have indolent cancers); therefore consider only the average life extension.

Three special cases for chemotherapy:

1)       Salvage chemotherapy or palliative chemotherapy is given without curative intent, but simply to decrease tumor load and increase life expectancy. For these regimens, a better toxicity profile is generally expected. 

2)       Curative chemotherapy, such as for non-Hodgkin’s lymphoma and testicular cancer.  Only a few cell lines of metastatic cancers can be cured. By chemotherapy.  

3)      Some newer anticancer drugs (for example, various monoclonal antibodies) are not indiscriminately cytotoxic, but rather target proteins that are abnormally expressed in cancer cells and that are essential for their growth.  Such treatments are often referred to as targeted therapy (as distinct from classic chemotherapy).   But being able to target the cancer doesn’t make them curative. 

The choice of chemo and target therapy should be carefully evaluated to remove business bias and the oncologist sales pitch.  Oncologists make the spread between what they bill and the discount price.  Remember that excision produces over 95% of the cures for the common types of cancer.   

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