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Aspirin the Best Cancer Drug


This is one of several recently updated articles on cancer and aspirin.  aspirin   http://healthfully.org/rc/id3.html      aspirin’s cancer protection  http://healthfully.org/rc/id18.html      Aspirin inhibits atherosclerosis  http://healthfully.org/rc/id17.html  Cancer Basics & Chemotherapy  http://healthfully.org/rc/id16.html   Cancer http://healthfully.org/rl/id4.html


There is a long list of chemicals touted as good for health.  A visit to a pharmacy and health food store reveals isles full of product, and hundreds of prescription preparation stocked behind the counter. A review of the scientific literature on drugs shows that 90% of them are minimal effective at best.  Over and over again we hear hype about safe and effective treatments.  About 5% work very effectively for specific issues.  There is just 4 drugs supported by medical science that are truly healthful (pharma has attacked all of them).  One of them significantly reduces the risk of and treats cancer, arthritis, Alzheimer’s disease, insulin resistance, and cardiovascular disease (CVD) and its assorted consequences, yet it is not prescribed for those uses, or in an ineffective dose made less effective by enteric coating. When used long-term as an anti-inflammatory drug, aspirin reduces the risk of Alzheimer’s disease 60% Parkinson 38%, and other conditions associated with inflammation including atherosclerosis[1], ALS, and arthritis.  Its anticoagulant effect reduces the risk of pulmonary embolism, stroke, heart attack and other ischemic events.  Aspirin reduces the risk of most cancers and also of it evolving into a fatal cancer by its effect upon 3 bodily defenses: as a COX-2 inhibitor, effect upon nitrous oxide (NO) system of endothelial cells, and its stimulation of the body’s system for destruction of abnormal cells.   Supporting evidence with links is at “Aspirin”, and for the basic of cancer at .  In “Aspirin” there is also a history of aspirin and a rebuttal to pharma’s assault.  For background, read “Marketing Science”, which details pharma’s tobacco ethics and their controls upon the practice of medicine.   Realizing that daily 325 mg of aspirin would cut in half their bottom line, pharma publishes its tobacco science to drum into doctors at continuing education classes that “aspirin is dangerous & ineffective”, then pitch their patented drugs.  These classes are job-training for the sales of pharma’s patented drugs.  A chorus of marginalized scientist challenge Pharma’s junk science.  The older journal literature is convincing.   As Dr. Angell:  says of pharma:  we couldn't have imagined one as bad as we have—lecture.


Molecular biological studies published in journals demonstrated that aspirin affects malignant tumors.  In Science 1994 the effects of aspirin:  “the transcription nuclear factor kappa B (NF-kappa B)[2], which is critical for inducible expression of multiple cellular and viral genes involved in inflammation and infection including interleukin-1 (IL-1), IL-6, and adhesion molecules…  This inhibition prevented the degradation of the NF-kappa B inhibitor, I kappa B.” In Journal of immunology 1999:  “In brief, NF-κB can be understood to be a protein responsible for cytokine production and cell survival…. These experiments suggest that RSK2 is a target for aspirin in the inhibition of monocyte-specific gene expression and indicate the importance of RSK2 and related kinases in cell regulation, indicating a new area for anti-inflammatory drug discovery.” Wiki” “NF-κB is a major transcription factor that regulates genes responsible for both the innate and adaptive immune response.  In Journal of Pharmacology 2002:  Aspirin targets intracellular signaling mechanisms such as kinases, including the mitogen activated protein-kinases (MAPK) cascade… inhibitory… aspirin-triggered lipoxin[3] formation are additional mechanisms that may contribute to anti-inflammatory properties”. Aspirin reduces COS-2 expression affecting colon cancer, in NEJM 2007:  aspirin use had no influence on tumors with weak or absent expression of COX-2…. Of the tumors, 423 (67%) had moderate or strong COX-2 expression…. Aspirin has other effects that are unrelated to cyclooxygenase, including inhibition of nuclear factor-κB, induction of apoptosis by activation of p38 kinase, and catabolism of polyamines. If aspirin exerts its effect on the formation of adenomas and cancers by inhibiting COX-2 or its downstream effectors, then the use of aspirin should preferentially reduce the risk of tumors for which growth depends on COX-2 function.”  Inflammation response is clearly related to many cancers’ progression.  In the Lancet 2001:  severity may be associated with functional polymorphisms of inflammatory cytokine genes, and deletion or inhibition of inflammatory cytokines inhibits development of experimental cancer.”  In British Journal of Pharmacology 2009 on Melanoma (deadly skin cancer):  In addition to the murine B16 cell line, the proliferation of SK-28 human melanoma cells was also suppressed by aspirin.  In conclusion, aspirin suppresses the proliferation of metastatic B16 cells in a JNK-dependent mechanism.”  In the Society for Endocrinology 2009, by aspirin inhibiting inflammatory action it reduces risk for prostate cancer.  Postulate that exposure to infectious agents, hormonal alterations, and dietary carcinogens could cause injury to the prostate epithelium leading to inflammation and the formation of lesions referred to as proliferative inflammatory atrophy (PIA), which are the precursors of prostatic intraepithelial neoplasia (PIN). PIN lesions are characterized by abnormalities that are intermediate between nor mal prostatic epithelium and cancer, while progression to high grade PIN is the most likely precursor of prostate carcinoma “  On COX-2 Anticancer Research, 2010:  Furthermore, COX-2 expression is high in many types of cancer and increases early on during colon carcinogenesis.”  In Cancer Research 2002 on the nitric oxide releasing effect of some NSAIDs:  This effect was due to inhibition of proliferation and induction of apoptosis and perhaps to the induction of novel cell changes, characterized by extensive DNA degradation… exposure of colonic tumor cells to 10 μM NO-ASA {aspirin] reduced the number of cells by 83% and PCNA expression by 25% and increased apoptosis at least 10-fold, not taking into account the atypical cells[4]…. For example, 48 h of exposure to 100 μM NO-ASA reduced PCNA expression by 40% and the cell number by 99%, compared with control… NO-ASA [aspirin] was the most effective of the three in inducing these changes.”  International Journal of Oncology  2002:  That NSAIDs decrease the incidence of and mortality from colon cancer has been a major advance in chemoprevention. These compounds are, however, limited by their significant side effects.  NO-releasing NSAIDs (NO-NSAIDs) are a novel class of compounds, synthesized to overcome the limitations of NSAIDs.  In general, they appear safer and much more effective than their traditional counterparts.  We review their structural features, metabolism and pharmacological actions. In vitro and in vivo studies indicate that they are much more effective than traditional NSAIDs in modulating colonocyte kinetics and the formation of premalignant colon lesions. Their mechanism of action is complex and not fully understood, including modulation of NO synthesis, signaling mediated via NF-kappaB and likely other pathways. Current early findings indicate that NO-NSAIDs may play a highly promising role in the chemoprevention of colon cancer” and by SSAT, at,   In 3 ways aspirin reduces cancer risk and improves survival:   1) a NF-kappa B inhibitor affect cell death and cell growth; 2) COX-2 inhibition affect the production of prostaglandins which mediates inflammation and cell growth; and 3)modulates nitrous oxide (NO) synthesis.  These effects of aspirin established in the laboratory were confirmed by population (epidemiological) studies.


Another way aspirin reduces cancer risk is through lowering blood glucose and the risk of insulin resistance (IR).  IR is strongly associated with cancer through insulin and ASA lowers glucose thus insulin levels..    an intensive 2-week course of aspirin [5 gm daily] abolished glycosuria and lowered the fasting blood sugar to normal… to moderately severe diabetics” BMJ-1953 also 2001, and review.  Chronic hyperinsulinemia, in affected individuals, may promote cancer, as insulin can exert its oncogenic potential via abnormal stimulation of multiple cellular signaling cascades, enhancing growth factor dependent cell proliferation and/or by directly affecting cell metabolism’ at 2012[5]. IGF—1 (insulin like growth factor) affect upon cell proliferation including cancers is well documented.  Insulin is the main regulatory hormone for IgF-1, and thus is downstream of elevate insulin.  .Whether through this affect alone are in combination with other effects of IR has not been


The clue to aspirin’s anti-cancer activity was uncovered in rodent studies during the 80s on colon tumors induced by chemical carcinogens and testing effects of NSAIDs, such as aspirin.  These studies revealed that that aspirin suppressed tumor cell proliferation through an immune response.  Small studies in humans in 83, 88, and 89 confirmed this.  In 1991 the NEJM published a prospective mortality study of 1,185,239:  Rates of death from colon cancer decreased with more frequent aspirin use among both men and women in the overall cohort.  For those who took 6 or more aspirin per month for at least 1 year the relative risk was 0.59 [a 41% reduction].”  After the widely publicized NEJM article, a number of epidemiological studies were published for the most common cancers.  In a 2005 review of 91 epidemiological studies “Daily intake of NSAIDs, primarily aspirin, produced risk reductions of 63% for colon, 39% for breast, 36% for lung, and 39% for prostate cancer. Significant risk reductions were also observed for esophageal (73%), stomach (62%), and ovarian cancer (47%). NSAID effects became apparent after five or more years of use and were stronger with longer duration.”  In the Oxford Journal 2002, “The multivariate-adjusted relative risk of pancreatic cancer associated with any current use of aspirin versus no use was 0.57 [43% risk reduction]…. use six or more times per week compared with no use for 1993–1999 was 0.39 [61% reduction]…. and 1.21 for women who used only non-aspirin NSAIDs [21% increase].”  A clinical trial of 17.285 participants published in the Lancet 2012 found that those who took 75 mg or greater of aspirin, that of the 987 cancers, aspirin users cancers were 36% less likely to be metastatic (fatal).   Those initially diagnosed not metastatic, the risk of it proven to be metastatic later was reduced by 55%.  Moreover, of those allocated aspirin following diagnosis of non-metastatic cancer, their survival rate was 50% higher than those who didn’t take aspirin.  Oxford Journal 2003, with 2 aspirins per week for 5 years is associated with a 40% risk reduction for Hodgkin’s lymphoma, but not with other NSAIDs, and increased 72% with acetaminophen. Given the design of these studies, results would be higher than those obtained if it included only those who took daily 325 mg or more of aspirin.   Oxford Journal 2010 on breast cancer survival found a 67% reduction in deaths for stages 1-3 with daily aspirin.  Benefits on high does are not published:  those with arthritis until the late 1990s were treated with 2.5 grams or more of aspirin, Merck Manual 1987, p 960.  Populations studies since the late 80s included those who took the very low dose (under 100 mg) aspirin for cardio-protection; too low for cancer protection. Pharma’s makes use of these flawed studies.    


 




[1] Atherosclerosis  starts with an inflammatory response by lymphocytes and macrophages to damaged LDL--see paragraph 2.

[2]   NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens.  NF-κB plays a key role in regulating the immune response to infection (κ light chains are critical components of immunoglobulins). Incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection…. In addition to roles in mediating cell survival, studies by Mark Mattson and others have shown that NF-κB has diverse functions in the nervous system including roles in plasticity, learning, and memory.  I In addition to roles in mediating cell survival, studies by Mark Mattson and others have shown that NF-κB has diverse functions in the nervous system including roles in plasticity, learning, and memory.  Elevated NF-κB has also been associated with schizophrenia. Recently, NF-κB activation has been suggested as a possible molecular mechanism for the catabolic effects of cigarette smoke in skeletal muscle and sarcopenia.   Ben-Neriah and others has highlighted the importance of the connection between NF-κB, inflammation, and cancer, and underscored the value of therapies that regulate the activity of NF-κB.  Aberrant activation of NF-κB is frequently observed in many cancers.  Moreover, suppression of NF-κB limits the proliferation of cancer cells. In addition, NF-κB is a key player in the inflammatory response” Wiki.  For example aspirin has been shown through this pathway to inhibit the growth of colon cancer, at PLOS 2012.  Hence aspirin’s methods of inhibiting NF-κB signaling has potential therapeutic application in cancer and inflammatory diseases of which atherosclerosis is the most important.

[3]  Lipoxins are members of the family of bioactive products generated from Arachidonic Acid (AA). They have a number of immunomodulatory and anti-inflammatory actions… During inflammation, cells die by apoptosis.  As part of resolution, lipoxins signal macrophages to the remains of these cells (phagocytosis)“ Wiki.

[4] For colon in another study (Anticancer Research supra) approximate 35% of cancer cells were resistant to the COX-2 mediated--in the Aspirin Handbook, mechanism of apoptosis.   Most cancers involve stem cells or pluripotent cells which cause variation in gene expression and cells shape.  Thus sometimes there are some cells in the tumor that are resistant to a particular immune mechanism; these select cells will proliferate.  

[5] This is a seminal paper that could well had been ghost written by pharma. For example ample space is given to insulin stimulating the production of estrogen, yet in table 1, on the increased risk for type-2 diabetics, the increase in breast cancer is the lowest of the 10 cancers listed.  For several reasons, I doubt that estradiol increases the risk of breast cancer and its spread. A similar claim is made for prostate cancer, yet there is no shown increase, in table 1.  Since testosterone and estradiol are so similar in structure and function it like wasn’t increase for type 2 diabetics, the population with the greatest degree of IR. Harvard Professor Morgantaler has shown the accepted belief about the role of testosterone in prostate cancer if based on a flawed sample of 1 castrated patient, at 2006.   This divergence of content and conclusion, when it supports pharma’s position, is common in their journal literature. 


There is a long list of chemicals touted as good for health.  A visit to a pharmacy and health food store reveals isles full of product, and hundreds of prescription preparation stocked behind the counter. A review of the scientific literature on drugs shows that 90% of them are minimal effective at best.  Over and over again we hear hype about safe and effective treatments.  About 5% work very effectively for specific issues.  There is just 4 drugs supported by medical science that are truly healthful (pharma has attacked all of them).  One of them significantly reduces the risk of and treats cancer, arthritis, Alzheimer’s disease, insulin resistance, and cardiovascular disease (CVD) and its assorted consequences, yet it is not prescribed for those uses, or in an ineffective dose made less effective by enteric coating. When used long-term as an anti-inflammatory drug, aspirin reduces the risk of Alzheimer’s disease 60% Parkinson 38%, and other conditions associated with inflammation including atherosclerosis[1], ALS, and arthritis.  Its anticoagulant effect reduces the risk of pulmonary embolism, stroke, heart attack and other ischemic events.  Aspirin reduces the risk of most cancers and also of it evolving into a fatal cancer by its effect upon 3 bodily defenses: as a COX-2 inhibitor, effect upon nitrous oxide (NO) system of endothelial cells, and its stimulation of the body’s system for destruction of abnormal cells.   Supporting evidence with links is at “Aspirin”, and for the basic of cancer at .  In “Aspirin” there is also a history of aspirin and a rebuttal to pharma’s assault.  For background, read “Marketing Science”, which details pharma’s tobacco ethics and their controls upon the practice of medicine.   Realizing that daily 325 mg of aspirin would cut in half their bottom line, pharma publishes its tobacco science to drum into doctors at continuing education classes that “aspirin is dangerous & ineffective”, then pitch their patented drugs.  These classes are job-training for the sales of pharma’s patented drugs.  A chorus of marginalized scientist challenge Pharma’s junk science.  The older journal literature is convincing.   As Dr. Angell:  says of pharma:  we couldn't have imagined one as bad as we have—lecture.

Molecular biological studies published in journals demonstrated that aspirin affects malignant tumors.  In Science 1994 the effects of aspirin:  “the transcription nuclear factor kappa B (NF-kappa B)[2], which is critical for inducible expression of multiple cellular and viral genes involved in inflammation and infection including interleukin-1 (IL-1), IL-6, and adhesion molecules…  This inhibition prevented the degradation of the NF-kappa B inhibitor, I kappa B.” In Journal of immunology 1999:  “In brief, NF-κB can be understood to be a protein responsible for cytokine production and cell survival…. These experiments suggest that RSK2 is a target for aspirin in the inhibition of monocyte-specific gene expression and indicate the importance of RSK2 and related kinases in cell regulation, indicating a new area for anti-inflammatory drug discovery.” Wiki” “NF-κB is a major transcription factor that regulates genes responsible for both the innate and adaptive immune response.  In Journal of Pharmacology 2002:  Aspirin targets intracellular signaling mechanisms such as kinases, including the mitogen activated protein-kinases (MAPK) cascade… inhibitory… aspirin-triggered lipoxin[3] formation are additional mechanisms that may contribute to anti-inflammatory properties”. Aspirin reduces COS-2 expression affecting colon cancer, in NEJM 2007:  aspirin use had no influence on tumors with weak or absent expression of COX-2…. Of the tumors, 423 (67%) had moderate or strong COX-2 expression…. Aspirin has other effects that are unrelated to cyclooxygenase, including inhibition of nuclear factor-κB, induction of apoptosis by activation of p38 kinase, and catabolism of polyamines. If aspirin exerts its effect on the formation of adenomas and cancers by inhibiting COX-2 or its downstream effectors, then the use of aspirin should preferentially reduce the risk of tumors for which growth depends on COX-2 function.”  Inflammation response is clearly related to many cancers’ progression.  In the Lancet 2001:  severity may be associated with functional polymorphisms of inflammatory cytokine genes, and deletion or inhibition of inflammatory cytokines inhibits development of experimental cancer.”  In British Journal of Pharmacology 2009 on Melanoma (deadly skin cancer):  In addition to the murine B16 cell line, the proliferation of SK-28 human melanoma cells was also suppressed by aspirin.  In conclusion, aspirin suppresses the proliferation of metastatic B16 cells in a JNK-dependent mechanism.”  In the Society for Endocrinology 2009, by aspirin inhibiting inflammatory action it reduces risk for prostate cancer.  Postulate that exposure to infectious agents, hormonal alterations, and dietary carcinogens could cause injury to the prostate epithelium leading to inflammation and the formation of lesions referred to as proliferative inflammatory atrophy (PIA), which are the precursors of prostatic intraepithelial neoplasia (PIN). PIN lesions are characterized by abnormalities that are intermediate between nor mal prostatic epithelium and cancer, while progression to high grade PIN is the most likely precursor of prostate carcinoma “  On COX-2 Anticancer Research, 2010:  Furthermore, COX-2 expression is high in many types of cancer and increases early on during colon carcinogenesis.”  In Cancer Research 2002 on the nitric oxide releasing effect of some NSAIDs:  This effect was due to inhibition of proliferation and induction of apoptosis and perhaps to the induction of novel cell changes, characterized by extensive DNA degradation… exposure of colonic tumor cells to 10 μM NO-ASA {aspirin] reduced the number of cells by 83% and PCNA expression by 25% and increased apoptosis at least 10-fold, not taking into account the atypical cells[4]…. For example, 48 h of exposure to 100 μM NO-ASA reduced PCNA expression by 40% and the cell number by 99%, compared with control… NO-ASA [aspirin] was the most effective of the three in inducing these changes.”  International Journal of Oncology  2002:  That NSAIDs decrease the incidence of and mortality from colon cancer has been a major advance in chemoprevention. These compounds are, however, limited by their significant side effects.  NO-releasing NSAIDs (NO-NSAIDs) are a novel class of compounds, synthesized to overcome the limitations of NSAIDs.  In general, they appear safer and much more effective than their traditional counterparts.  We review their structural features, metabolism and pharmacological actions. In vitro and in vivo studies indicate that they are much more effective than traditional NSAIDs in modulating colonocyte kinetics and the formation of premalignant colon lesions. Their mechanism of action is complex and not fully understood, including modulation of NO synthesis, signaling mediated via NF-kappaB and likely other pathways. Current early findings indicate that NO-NSAIDs may play a highly promising role in the chemoprevention of colon cancer” and by SSAT, at,   In 3 ways aspirin reduces cancer risk and improves survival:   1) a NF-kappa B inhibitor affect cell death and cell growth; 2) COX-2 inhibition affect the production of prostaglandins which mediates inflammation and cell growth; and 3)modulates nitrous oxide (NO) synthesis.  These effects of aspirin established in the laboratory were confirmed by population (epidemiological) studies.

Another way aspirin reduces cancer risk is through lowering blood glucose and the risk of insulin resistance (IR).  IR is strongly associated with cancer through insulin and ASA lowers glucose thus insulin levels..    an intensive 2-week course of aspirin [5 gm daily] abolished glycosuria and lowered the fasting blood sugar to normal… to moderately severe diabetics” BMJ-1953 also 2001, and review.  Chronic hyperinsulinemia, in affected individuals, may promote cancer, as insulin can exert its oncogenic potential via abnormal stimulation of multiple cellular signaling cascades, enhancing growth factor dependent cell proliferation and/or by directly affecting cell metabolism’ at 2012[5]. IGF—1 (insulin like growth factor) affect upon cell proliferation including cancers is well documented.  Insulin is the main regulatory hormone for IgF-1, and thus is downstream of elevate insulin.  .Whether through this affect alone are in combination with other effects of IR has not been

The clue to aspirin’s anti-cancer activity was uncovered in rodent studies during the 80s on colon tumors induced by chemical carcinogens and testing effects of NSAIDs, such as aspirin.  These studies revealed that that aspirin suppressed tumor cell proliferation through an immune response.  Small studies in humans in 83, 88, and 89 confirmed this.  In 1991 the NEJM published a prospective mortality study of 1,185,239:  Rates of death from colon cancer decreased with more frequent aspirin use among both men and women in the overall cohort.  For those who took 6 or more aspirin per month for at least 1 year the relative risk was 0.59 [a 41% reduction].”  After the widely publicized NEJM article, a number of epidemiological studies were published for the most common cancers.  In a 2005 review of 91 epidemiological studies “Daily intake of NSAIDs, primarily aspirin, produced risk reductions of 63% for colon, 39% for breast, 36% for lung, and 39% for prostate cancer. Significant risk reductions were also observed for esophageal (73%), stomach (62%), and ovarian cancer (47%). NSAID effects became apparent after five or more years of use and were stronger with longer duration.”  In the Oxford Journal 2002, “The multivariate-adjusted relative risk of pancreatic cancer associated with any current use of aspirin versus no use was 0.57 [43% risk reduction]…. use six or more times per week compared with no use for 1993–1999 was 0.39 [61% reduction]…. and 1.21 for women who used only non-aspirin NSAIDs [21% increase].”  A clinical trial of 17.285 participants published in the Lancet 2012 found that those who took 75 mg or greater of aspirin, that of the 987 cancers, aspirin users cancers were 36% less likely to be metastatic (fatal).   Those initially diagnosed not metastatic, the risk of it proven to be metastatic later was reduced by 55%.  Moreover, of those allocated aspirin following diagnosis of non-metastatic cancer, their survival rate was 50% higher than those who didn’t take aspirin.  Oxford Journal 2003, with 2 aspirins per week for 5 years is associated with a 40% risk reduction for Hodgkin’s lymphoma, but not with other NSAIDs, and increased 72% with acetaminophen. Given the design of these studies, results would be higher than those obtained if it included only those who took daily 325 mg or more of aspirin.   Oxford Journal 2010 on breast cancer survival found a 67% reduction in deaths for stages 1-3 with daily aspirin.  Benefits on high does are not published:  those with arthritis until the late 1990s were treated with 2.5 grams or more of aspirin, Merck Manual 1987, p 960.  Populations studies since the late 80s included those who took the very low dose (under 100 mg) aspirin for cardio-protection; too low for cancer protection. Pharma’s makes use of these flawed studies.    

 



[1] Atherosclerosis  starts with an inflammatory response by lymphocytes and macrophages to damaged LDL--see paragraph 2.

[2]   NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex that controls transcription of DNA. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens.  NF-κB plays a key role in regulating the immune response to infection (κ light chains are critical components of immunoglobulins). Incorrect regulation of NF-κB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection…. In addition to roles in mediating cell survival, studies by Mark Mattson and others have shown that NF-κB has diverse functions in the nervous system including roles in plasticity, learning, and memory.  I In addition to roles in mediating cell survival, studies by Mark Mattson and others have shown that NF-κB has diverse functions in the nervous system including roles in plasticity, learning, and memory.  Elevated NF-κB has also been associated with schizophrenia. Recently, NF-κB activation has been suggested as a possible molecular mechanism for the catabolic effects of cigarette smoke in skeletal muscle and sarcopenia.   Ben-Neriah and others has highlighted the importance of the connection between NF-κB, inflammation, and cancer, and underscored the value of therapies that regulate the activity of NF-κB.  Aberrant activation of NF-κB is frequently observed in many cancers.  Moreover, suppression of NF-κB limits the proliferation of cancer cells. In addition, NF-κB is a key player in the inflammatory response” Wiki.  For example aspirin has been shown through this pathway to inhibit the growth of colon cancer, at PLOS 2012.  Hence aspirin’s methods of inhibiting NF-κB signaling has potential therapeutic application in cancer and inflammatory diseases of which atherosclerosis is the most important.

[3]  Lipoxins are members of the family of bioactive products generated from Arachidonic Acid (AA). They have a number of immunomodulatory and anti-inflammatory actions… During inflammation, cells die by apoptosis.  As part of resolution, lipoxins signal macrophages to the remains of these cells (phagocytosis)“ Wiki.

[4] For colon in another study (Anticancer Research supra) approximate 35% of cancer cells were resistant to the COX-2 mediated--in the Aspirin Handbook, mechanism of apoptosis.   Most cancers involve stem cells or pluripotent cells which cause variation in gene expression and cells shape.  Thus sometimes there are some cells in the tumor that are resistant to a particular immune mechanism; these select cells will proliferate.  

[5] This is a seminal paper that could well had been ghost written by pharma. For example ample space is given to insulin stimulating the production of estrogen, yet in table 1, on the increased risk for type-2 diabetics, the increase in breast cancer is the lowest of the 10 cancers listed.  For several reasons, I doubt that estradiol increases the risk of breast cancer and its spread. A similar claim is made for prostate cancer, yet there is no shown increase, in table 1.  Since testosterone and estradiol are so similar in structure and function it like wasn’t increase for type 2 diabetics, the population with the greatest degree of IR. Harvard Professor Morgantaler has shown the accepted belief about the role of testosterone in prostate cancer if based on a flawed sample of 1 castrated patient, at 2006.   This divergence of content and conclusion, when it supports pharma’s position, is common in their journal literature. 


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Disclaimer:  The information, facts, and opinions provided here is not a substitute for professional advice.  It only indicates what JK believes, does, or would do.  Always consult your primary care physician for medical advice, diagnosis, and treatment.