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Aspirin mechanism cancer survival

Aspirin reduces cancer risk through promoting death of abnormal cells (apoptosis) and through effect upon prostaglandins (COX-1 & COX-2).  . Overexpression of cyclooxygenase-2 (COX-2) and increased prostaglandin biosynthesis correlates with carcinogenesis and metastasis at most anatomic sites.  Several mechanism for promoting death of abnormal cells have been found including the activiation of NF-B signaling pathway

Aspirin and Salicylate Induce Apoptosis and Activation of Caspases in B-Cell Chronic Lymphocytic Leukemia Cells


We analyzed the effect of aspirin, salicylate, and other nonsteroidal antiinflammatory drugs (NSAIDs) on the viability of B-chronic lymphocytic leukemia (B-CLL) cells. Aspirin induced a decrease in cell viability in a dose- and time-dependent manner. The mean IC50 for cells from 5 patients was 5.9 1.13 mmol/L (range, 4.4 to 7.3 mmol/L). In some cases, 2.5 mmol/L aspirin produced an important cytotoxic effect after 4 days of incubation. No effect was observed with other NSAIDs, at concentrations that inhibit cyclooxygenase, such as ketorolac (10 μmol/mL), NS-398 (100 μmol/mL), or indomethacin (20 μmol/mL), thus suggesting the involvement of cyclooxygenase-independent mechanisms in aspirin-induced cytotoxicity. Salicylate also produced dose-dependent cytotoxic effects on B-CLL cells and the mean IC50 for cells from 5 patients was 6.96 1.13 mmol/L (range, 5 to 7.8 mmol/L). Both aspirin and salicylate induced DNA fragmentation and the proteolytic cleavage of poly(ADP(adenosine 5′-diphosphate)-ribose) polymerase (PARP), demonstrating that both compounds induce apoptosis of B-CLL cells. Finally, inhibition of caspases by Z-VAD.fmk blocked proteolytic cleavage of PARP, DNA fragmentation, and cytotoxicity induced by aspirin. Mononuclear cells from normal donors showed a lower sensitivity than cells from B-CLL patients to aspirin as determined by analysis of cell viability. B and T lymphocytes from normal donors and T lymphocytes from CLL patients are more resistant to aspirin-induced apoptosis, as determined by analysis of phosphatidylserine exposure. These results indicate that aspirin and salicylate induce apoptosis of B-CLL cells by activation of caspases and that this activation involves cyclooxygenase-independent mechanisms.

1998 by The American Society of Hematology.

  • Submitted August 4, 1997.  Accepted April 17, 1998.   Copyright 1998 American Society of Hematology


Several mechanisms of prostaglandin promotion of cancer growth have been discovered.  Below is just one.  Aspirin inhibits prostaglandins and thus slow the growth of cancer.  Along with apoptosis aspirin acts to significantly increase cancer survival.--jk

Nature Medicine  8, 289 - 293 (2002) doi:10.1038/nm0302-289

Prostaglandin E2 transactivates EGF receptor: A novel mechanism for promoting colon cancer growth and gastrointestinal hypertrophy

Rama Pai, Brian Soreghan, Imre L. Szabo, Meredith Pavelka, Dolgor Baatar & Andrzej S. Tarnawski

Medical Service, Department of Veterans Affairs Medical Center, Long Beach, California, and the Department of Medicine, University of California, Irvine, California, USA

Correspondence should be addressed to Andrzej S. Tarnawski




Prostaglandins (PGs), bioactive lipid molecules produced by cyclooxygenase enzymes (COX-1 and COX-2), have diverse biological activities, including growth-promoting actions on gastrointestinal mucosa1, 2, 3, 4, 5. They are also implicated in the growth of colonic polyps and cancers6. However, the precise mechanisms of these trophic actions of PGs remain unclear. As activation of the epidermal growth factor receptor (EGFR) triggers mitogenic signaling in gastrointestinal mucosa, and its expression is also upregulated in colonic cancers and most neoplasms7, 8, 9, we investigated whether PGs transactivate EGFR. Here we provide evidence that prostaglandin E2 (PGE2) rapidly phosphorylates EGFR and triggers the extracellular signal-regulated kinase 2 (ERK2)−mitogenic signaling pathway in normal gastric epithelial (RGM1) and colon cancer (Caco-2, LoVo and HT-29) cell lines. Inactivation of EGFR kinase with selective inhibitors significantly reduces PGE2-induced ERK2 activation, c-fos mRNA expression and cell proliferation. Inhibition of matrix metalloproteinases (MMPs), transforming growth factor-Description: alpha (TGF-Description: alpha) or c-Src blocked PGE2-mediated EGFR transactivation and downstream signaling indicating that PGE2-induced EGFR transactivation involves signaling transduced via TGF-Description: alpha, an EGFR ligand, likely released by c-Src-activated MMP(s). Our findings that PGE2 transactivates EGFR reveal a previously unknown mechanism by which PGE2 mediates trophic actions resulting in gastric and intestinal hypertrophy as well as growth of colonic polyps and cancers.



NSAIDs block prostaglandin synthesis, a growth factor frequently overexpress in cancer tumors.


Anti-Cancer Drugs:

February 2002 - Volume 13 - Issue 2 - pp 127-137

COX-2 inhibitors in cancer treatment and prevention, a recent development


Epidemiological and experimental studies have demonstrated the effect of non-steroidal anti-inflammatory drugs (NSAIDs) in the prevention of human cancers. NSAIDs block endogenous prostaglandin synthesis through inhibition of cyclooxygenase (COX) enzymatic activity. COX-2, a key isoenzyme in conversion of arachidonic acid to prostaglandins, is inducible by various agents such as growth factors and tumor promoters, and is frequently overexpressed in various tumors. The contribution of COX-2 to carcinogenesis and the malignant phenotype of tumor cells has been thought to be related to its abilities to (i) increase production of prostaglandins, (ii) convert procarcinogens to carcinogens, (iii) inhibit apoptosis, (iv) promote angiogenesis, (v) modulate inflammation and immune function, and (vi) increase tumor cell invasiveness, although some studies indicated that NSAIDs have COX-2-independent effects. A number of clinical trials using COX-2 inhibitors are in progress, and the results from these studies will increase our understanding of COX-2 inhibition in both cancer treatment and prevention. The combination of COX-2 inhibitors with radiation or other anti-cancer or cancer prevention drugs may reduce their side effects in future cancer prevention and treatment. Recent progress in the treatment and prevention of cancers of the colon, esophagus, lung, bladder, breast and prostate with NSAIDs, especially COX-2 inhibitors, is also discussed


NSAIDs inhibit the proliferation rate, alter the cell cycle distribution, and induce apoptosis in colon cancer cell lines

Biochemical Pharmacology

Volume 52, Issue 2, 26 July 1996, Pages 237–245


Effects of nonsteroidal anti-inflammatory drugs on proliferation and on induction of apoptosis in colon cancer cells by a prostaglandin-independent pathway


Nonsteroidal anti-inflammatory drugs (NSAIDs) decrease the incidence of and mortality from colon cancer. We observed that NSAIDs inhibit the proliferation rate, alter the cell cycle distribution, and induce apoptosis in colon cancer cell lines. We evaluated whether the inhibition by NSAIDs of prostaglandin (PG) synthesis is required for their effects on colon cancer cells by studying two human colon cancer cell lines: HCT-15 and HT-29. HCT-15, which lacks cyclooxygenase transcripts, does not produce PGs even when exogenously stimulated, whereas HT-29 produces PGE2, PGF, and PGI2. HCT-15 and HT-29 cells, when treated for up to 72 hr with 200 μM sulindac sulfide (an active metabolite of sulindac) or 900 μM piroxicam, showed changes in proliferation, cell cycle phase distribution, and apoptosis. Treatment with PGE2, PGF, and PGI2, following a variety of protocols, and at concentrations between 10−6 and 10−11 M, failed to reverse the effects of NSAIDs on these three parameters of cell growth. We concluded that NSAIDs inhibit the proliferation rate of the two colon cancer cell lines independent of their ability to inhibit PG synthesis. Thus, alternative mechanisms for their activity on tumor cell growth must be entertained. These observations may be relevant to the mechanism of colon tumor inhibition by NSAIDs. two colon cancer cell lines independent of their ability to inhibit PG synthesis. Thus, alternative mechanisms for their activity on tumor cell growth must be entertained. These observations may be relevant to the mechanism of colon tumor inhibition by NSAIDs.

Aspirin induces necrosis factor for abnormal cell death.  Detailed article at 

Wikipedia aspirin

Discovery of the mechanism

In 1971, British pharmacologist John Robert Vane, then employed by the Royal College of Surgeons in London, showed aspirin suppressed the production of prostaglandins {such as COX-1 and COX-2} and thromboxanes.[114][115]

Aspirin reduces the effects of vasopressin[123] upon the secretion of ACTH and cortisol by the hypothalamic-pituitary-adrenal axis (HPA axis), which has been suggested to occur through an interaction with endogenous prostaglandins and their role in regulating the HPA axis.[123]


Vasopressin is a peptide hormone that controls the reabsorption of molecules in the tubules of the kidneys by affecting the tissue's permeability. It also increases peripheral vascular resistance, which in turn increases arterial blood pressure. It plays a key role in homeostasis, and the regulation of water, glucose, and salts in the blood.

Aspirin reduces fever and headaches

Although aspirin has been used to combat fever and pains associated with common cold for more than 100 years, its efficacy in this role was only recently confirmed in controlled clinical trials on adults. One gram of aspirin, on average, reduced the oral body temperature from 39.0 C (102.2 F) to 37.6 C (99.7 F) after three hours. The relief began after 30 minutes, and after six hours, the temperature still remained below 37.8 C (100.0 F). Aspirin also helped with "achiness", discomfort and headache,[36] and with sore throat pain, for those who had it.[37] The effects of aspirin were indistinguishable from those obtained using paracetamol {acetaminophen, which is toxic to the liver} in any respect, except for, possibly, a slightly higher incidence of sweating and gastrointestinal side effects.[36]

Fever and joint pain of acute rheumatic fever respond extremely well, often within three days, to high doses of aspirin. The therapy usually lasts for one to two weeks; and only in about 5% of the cases it has to continue for longer than six months. After fever and pain have subsided, the aspirin treatment is unnecessary, as it does not decrease the incidence of heart complications and residual rheumatic heart disease.[38]

A 2010 study by Oxford University involving over 25000 patients showed taking a small (75 mg) daily dose of aspirin for between four and eight years substantially reduces death rates from a range of common cancers by at least a fifth and the reduction of risk continued for 20 years in both men and women. For specific cancers the, reduction was about 40% for bowel cancer, 30% for lung cancer, 10% for prostate cancer and 60% for oesophageal cancer, while the reductions in pancreas, stomach, brain, breast and ovarian cancers were difficult to quantify because there were not enough data, but other studies are in progress. However, taking aspirin doubles the annual risk of major internal bleeding that normally has a very low incidence (about 1 in 1000) in middle age, but increased dramatically after 75 years old.[68]

  ^ "Small daily aspirin dose 'cuts cancer risk". BBC News Health (2010), available at



Adult aspirin tablets are produced in standardised sizes, which vary slightly from country to country, for example 300 mg in Britain and 325 mg in the USA. Smaller doses are based on these standards; thus, 75- and 81-milligram tablets are used; there is no medical significance in the slight difference. It is of historical interest that the US 325 mg dose is almost exactly equivalent to the historic 5 grain aspirin tablet that preceded the metric dosage.


Wikipedia prostaglandin

A prostaglandin is any member of a group of lipid compounds that are derived enzymatically from fatty acids and have important functions in the animal body.  Every prostaglandin contains 20 carbon atoms, including a 5-carbon ring.

They are mediators and have a variety of strong physiological effects, such as regulating the contraction and relaxation of smooth muscle tissue.[1] Prostaglandins are not hormones, but autocrine or paracrine, which are locally acting messenger molecules. They differ from hormones in that they are not produced at a discrete site but in many places throughout the human body. Also, their target cells are present in the immediate vicinity of the site of their secretion (of which there are many).

The prostaglandins, together with the thromboxanes and prostacyclins, form the prostanoid class of fatty acid derivatives, a subclass of eicosanoids.

The diversity of receptors means that prostaglandins act on an array of cells and have a wide variety of effects such as:


Wikipedia Thromboxane

Thromboxane is a member of the family of lipids known as eicosanoids. The two major thromboxanes are thromboxane A2 and thromboxane B2. The distinguishing feature of thromboxanes is a 6-membered ether-containing ring.

Thromboxane is named for its role in clot formation (thrombosis).



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 any medical advice, diagnosis, and treatment.