Anti-inflammatory agents as cancer treatment

Dr. Weeks Comment:  For the past 5 years, I have lectured to my medical colleagues at conferences around the world about the critical importance of  “centsible” (safe, effective and cost effective) cancer treatment.  For example,  I have stressed that we ought not neglect treating the cancer STEM cells despite oncologists the world over ignoring these most lethal cells. Your oncologist is giving you chemo and radiation which do NOT kill cancer STEM cells but actually makes them worse (more virulent and more numerous).

(see below  ” …While chemotherapy effectively induces apoptosis, associated prostaglandin E2 (PGE2) release paradoxically promotes neighbouring CSC repopulation…”)

I have also encouraged the use of anti-inflammatory agents in order to stop the metastatic process since, quite simply,  cancer spreads using inflammatory cytokines. If you block these, then cancer has a hard time spreading!  What to use? Anti-inflammatory agents.  HOWEVER, most prescription and over the counter anti-inflammatory agents are toxic to the kidney and the liver – and can cause internal bleeding which itself can become fatal.  Hence the importance of an anti-inflammatory diet and the use of foods like black cumin seed, black raspberry seed and chardonnay grape seed  (the WHOLE SEEDS are critical here… not the seed oils!)

So don’t use the toxic NSAID recommended here when a more “centisble” option exists in Nature!  Eat the Seed!



Nature. 2014 Dec 3. doi: 10.1038/nature14034. [Epub ahead of print]

Blocking PGE2-induced tumour repopulation abrogates bladder cancer chemoresistance.


Cytotoxic chemotherapy is effective in debulking tumour masses initially; however, in some patients tumours become progressively unresponsive after multiple treatment cycles. Previous studies have demonstrated that cancer stem cells (CSCs) are selectively enriched after chemotherapy through enhanced survival. Here we reveal a new mechanism by which bladder CSCs actively contribute to therapeutic resistance via an unexpected proliferative response to repopulate residual tumours between chemotherapy cycles, using human bladder cancer xenografts. Further analyses demonstrate the recruitment of a quiescent label-retaining pool of CSCs into cell division in response to chemotherapy-induced damages, similar to mobilization of normal stem cells during wound repair. While chemotherapy effectively induces apoptosis, associated prostaglandin E2 (PGE2) release paradoxically promotes neighbouring CSC repopulation. This repopulation can be abrogated by a PGE2-neutralizing antibody and celecoxib drug-mediated blockade of PGE2 signalling. In vivo administration of the cyclooxygenase-2 (COX2) inhibitor celecoxib effectively abolishes a PGE2- and COX2-mediated wound response gene signature, and attenuates progressive manifestation of chemoresistance in xenograft tumours, including primary xenografts derived from a patient who was resistant to chemotherapy.

Collectively, these findings uncover a new underlying mechanism that models the progressive development of clinical chemoresistance, and implicate an adjunctive therapy to enhance chemotherapeutic response of bladder urothelial carcinomas by abrogating early tumour repopulation.

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