Add Seeds of Eden to optimize Chemotherapy for Pancreatic Cancer

Dr. Weeks’ Comment: The opinions which oncologists typically express about what else to do (aside from simply telling the patient to show up for chemotherapy or radiation) are neither based in science nor valid.  For example,  oncologists tell patients to eat a lot, parroting “any calorie is a good calorie” (and their nurses offer cookies and sweets in the chemo chamber!)  rather than fast (eat no food) which has been scientifically proven to enhance the killing effect of chemotherapy.  Here is another article! They also tell patients to NOT take anti-oxidants like vitamin C during chemotherapy  despite all the research proving that anti-oxidants do NOT interfere with chemotherapy.  Here is another article!  In fact, they protect you while not protecting the cancer cells which minimizes your side-effects.  Finally, they say to not take herbal remedies for fear of interference with the chemo and radiation mode of action and demonstrate little if any interest when you bring to their attention articles like the following  (see below) which describe the benefits of drinking the main ingredient in Seeds of Eden prior to getting treatment.

Antitumor Activity of Gemcitabine and Oxaliplatin Is Augmented by Thymoquinone in Pancreatic Cancer

Sanjeev Banerjee, et al  Cancer Res 2009;69(13):5575-83   10.1158/0008-5472.CAN-08-4235 Published 1 July 2009

Abstract  Previous studies have shown biological activity of thymoquinone, an active compound extracted from Nigella sativa, in pancreatic cancer cells; however, preclinical animal studies are lacking. Here, we report, for the first time, the chemosensitizing effect of thymoquinone to conventional chemotherapeutic agents both in vitro and in vivo using an orthotopic model of pancreatic cancer. In vitro studies revealed that preexposure of cells with thymoquinone (25 μmol/L) for 48 h followed by gemcitabine or oxaliplatin resulted in 60% to 80% growth inhibition compared with 15% to 25% when gemcitabine or oxaliplatin was used alone. Moreover, we found that thymoquinone could potentiate the killing of pancreatic cancer cells induced by chemotherapeutic agents by down-regulation of nuclear factor-κB (NF-κB), Bcl-2 family, and NF-κB-dependent antiapoptotic genes (X-linked inhibitors of apoptosis, survivin, and cyclooxygenase-2). As shown previously by our laboratory, NF-κB gets activated on exposure of pancreatic cancer cells to conventional chemotherapeutic agents; interestingly, thymoquinone was able to down-regulate NF-κB in vitro, resulting in chemosensitization. In addition to in vitro results, here we show for the first time, that thymoquinone in combination with gemcitabine and/or oxaliplatin is much more effective as an antitumor agent compared with either agent alone. Most importantly, our data also showed that a specific target, such as NF-κB, was inactivated in animal tumors pretreated with thymoquinone followed by gemcitabine and/or oxaliplatin.
These results provide strong in vivo molecular evidence in support of our hypothesis that thymoquinone could abrogate gemcitabine- or oxaliplatin-induced activation of NF-κB, resulting in the chemosensitization of pancreatic tumors to conventional therapeutics.



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