Dr. Weeks’ Comment: Aspirin, a common drug (Acetylsalicylic acid) extracted originally from willow bark is anti-inflammatory and anti-platelet aggregation. Too much of it over time is toxic to liver and kidneys which is why doctors used say “Take it until your ears ring, then cut back.” I have reported how Max Wicha, a leaning cancer researcher has recommended anti-inflammation for the treatment of cancer STEM cells and a recent article in NATURE confirms but recommends the toxic drug celebrex. So, in this publication, we have another example of the importance of taking an anti-inflammatory (like the organic non-GMO 3 seed drinks) if you or a loved on has cancer. Does your oncologist recommend aspirin?
“…We find that ASA not only prevents breast tumor cell growth in vitro and tumor growth in nude mice xenograft model through the induction of apoptosis, but also significantly reduces the self-renewal capacity and growth of breast tumor-initiating cells (BTICs)/breast cancer stem cells (BCSCs) and delays the formation of a palpable tumor…”
Laboratory Investigation , (13 April 2015) | doi:10.1038/labinvest.2015.4
Aspirin blocks growth of breast tumor cells and tumor-initiating cells and induces reprogramming factors of mesenchymal to epithelial transition
Gargi Maity, Archana De, Amlan Das, Snigdha Banerjee, Sandipto Sarkar and Sushanta K Banerjee
Abstract
Acetylsalicylic acid (ASA), also known as aspirin, a classic, nonsteroidal, anti-inflammatory drug (NSAID), is widely used to relieve minor aches and pains and to reduce fever. Epidemiological studies and other experimental studies suggest that ASA use reduces the risk of different cancers including breast cancer (BC) and may be used as a chemopreventive agent against BC and other cancers. These studies have raised the tempting possibility that ASA could serve as a preventive medicine for BC. However, lack of in-depth knowledge of the mechanism of action of ASA reshapes the debate of risk and benefit of using ASA in prevention of BC. Our studies, using in vitro and in vivo tumor xenograft models, show a strong beneficial effect of ASA in the prevention of breast carcinogenesis. We find that ASA not only prevents breast tumor cell growth in vitro and tumor growth in nude mice xenograft model through the induction of apoptosis, but also significantly reduces the self-renewal capacity and growth of breast tumor-initiating cells (BTICs)/breast cancer stem cells (BCSCs) and delays the formation of a palpable tumor. Moreover, ASA regulates other pathophysiological events in breast carcinogenesis, such as reprogramming the mesenchymal to epithelial transition (MET) and delaying in vitro migration in BC cells. The tumor growth-inhibitory and reprogramming roles of ASA could be mediated through inhibition of TGF-β/SMAD4 signaling pathway that is associated with growth, motility, invasion, and metastasis in advanced BCs. Collectively, ASA has a therapeutic or preventive potential by attacking possible target such as TGF-β in breast carcinogenesis.