Michael Retsky (Ph.D. in physics from University of Chicago) made a career change from physics to cancer research. He is Editor-in-Chief of Journal of Bioavailability and Bioequivalence, on staff at Harvard School of Public Health, faculty at University College London, and Prof Adj at UANL, Monterrey, Mexico. He was on Judah Folkman’s staff at Harvard Medical School for 12 years. He is on the board of directors of the Colon Cancer Alliance and has published more than 60 papers in physics and cancer. He has a patent pending for treatment of early stage cancer.


In developed countries, metastatic relapse aft er diagnosis of early stage breast cancer is the common pathway leading to mortality from the disease. How to prevent relapses remains perhaps the most important unsolved problem in oncology. Mechanisms are not well understood. It would be helpful to know more about mechanisms to aid our discussions on bioequivalence and bioavailability in oncology. As my colleagues and I recently reported, analysis of clinical breast cancer relapse data aft er mastectomy suggests most distant relapses occur within 4 years of surgery and are precipitated or accelerated by something that happens around the time of surgery. Sudden growth from single cells and angiogenesis of avascular micrometastases are indicated. Late relapses are not accelerated by surgery. Many clinical characteristics of breast cancer can be explained with this hypothesis. Recent retrospective analysis of clinical data from one Brussels hospital indicates early relapse events were reduced 5-fold when an NSAID was used as perioperative analgesic. Combining the surgery induced metastatic activity hypothesis with these data suggests transient systemic inflammation following primary tumor removal, that has been identifi ed by markers in serum, may facilitate most metastatic activity and was eff ectively blocked by the NSAID. While breast cancer is a disease that runs its course in over a decade, most of the damage seems to occur in the week or two aft er surgery. Th is suggests new mechanisms for metastatic initiation and possibly an eff ective nontoxic, low cost intervention that may signifi cantly reduce mortality from breast cancer.

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