tumeric appears to boost folfox effectiveness, read this study and make your own decision
I have made my decision.
To all on FOLFOX and thinking about natural supports. Please read the discussion paper below.
Should this be a separate post as I want it to focus on folfox and tumeric.
I think this post is at a tangent to the originating post re tumeric and aspirin and is specifically focused on the tumeric and chemo folfox for most questions.
If this paper is scientifically valid I would ask the question why we are not advised about this natural support.
Based on this paper and the advice from Naturopaths research group I am taking tumeric on folfox.
The summary about the effectiveness of folfox to kill all the colorectal cancer cells I found a little depressing. Its exactly what I was told by TCM ONC.
The lack of effectiveness I had raised with ONC which she claimed was rubbish.
So below is a study that backs up TCM ONC view of folfox effectiveness. I am glad I have not put all my faith in folfox, when it appears to me that folfox needs help.
I feel extreme frustration when these types of research are advised and clearly discussed means we suffer while taking folfox and get only some of the benefit when it appears a more complete and effective response as at our finger tips. Its certainly a cost effective option. If you do tumeric with diet you need it with pepper according to anticancer. I do tumeric by supplement now. Just having my first.
Feel free to argue and debate this , I feel its worthy of a complete and frank discussion. Again my thanks to Blake whose initial warning about tumeric got me researching topic and to pepe for his copy and paste skills.
While the MD anderson tumeric advice is interesting but now I have more specific studies and advice from my naturopathic research team I will follow on the path of enhancing folfox effectiveness. I hope this is ok said one guineapig to the next!
My naturopath response is at the end.
hugs and love to all,
Chemotherapy produces incomplete responses in a vast majority of cancer cases particularly of colorectal cancer (2). This leads to survival of a population of cells within the tumor resulting in subsequent chemotherapy-resistant relapses. The precise mechanism of this phenomenon of chemo-survival remains unknown.
Abnormal activity of EGFRs has been associated with the development and progression of many malignancies, including that of the colon. In particular, overexpression of EGFR and HER2 in colorectal cancer correlates with an extremely poor clinical prognosis (20, 21). The majority of solid tumors, including those of the colon, overexpress one or more members of the EGFR family and coexpression of EGFR with HER-2 or HER-3 results in the development of enhanced drug resistance (9, 22). More recently, IGF-1R is also emerging as an important pathway responsible for the development and progression of colorectal cancer. In addition, there is crosstalk between EGFRs and IGF-1R, resulting in therapeutic resistance with targeting individual pathways (23). EGFR inhibitors have been successfully incorporated in the therapeutic armamentarium of colon cancer. However, the benefits appear to be modest and the complete responses are rare (24). One of the mechanisms of resistance to EGFR inhibitors is their hetrodimerization with IGF-1R receptor (25). Hence, co-targeting of EGFR and IGF-1R would likely result in greater therapeutic efficacy. In our model of chemo-surviving colon cancer cells, we show that not only EGFR and its family members, but also IGF-1R, are significantly activated, confirming their involvement in survival of these cells. Therefore, targeting them may provide beneficial effect in terms of reversing chemotherapy resistance. Recently a report by Dallas et al., who demonstrated inhibition of growth of oxaliplatin-resistant colon cancer cells by inhibiting IGF-1R, further supports the contention that certain growth factor receptors play a critical role in cells surviving chemotherapy insult (11). However, one of the major concerns with combining various biological agents is an increase in overall toxicity. Hence, the development of pleiotropic agents with minimal toxicity is highly desirable in combating the emergence of chemo-surviving cells and the resultant subsequent relapse. Our current data demonstrate that one can target these survival pathways with non-toxic pleiotropic agents such as curcumin for therapeutic gains.
Human epidemiological and laboratory animal model studies have suggested that nonsteroidal antiinflammatory drugs reduce the risk of development of colon cancer and that the inhibition of colon carcinogenesis is mediated through the alteration in cyclooxygenase metabolism of arachidonic acid. Curcumin, which is a naturally occurring compound, is present in turmeric, possesses both antiinflammatory and antioxidant properties, and has been tested for its chemopreventive properties in skin and forestomach carcinogenesis.
BELOW IS AN ANSWER FROM MY NATUROPATH RE TUMERIC AND FOLFOX CHEMO
> Animal studies indicate that curcumin may inhibit cyclophosphamide in
> treating breast cancer, but results from a phase I trial found a
> combination of curcumin and docetaxel to be safe. I didn't find any
> information that specifically pertains to using turmeric during
> chemotherapy for bowel cancer. The Sloan Kettering Cancer Centre
> recommend that more research is necessary and that it is advisable for
> cancer patients undergoing chemotherapy to limit intake of turmeric.
> The information that we have collated for our safety database has lead
> us at Metagenics to 'caution' the use of turmeric during chemotherapy.
> Whilst curcumin has been shown to enhance chemotherapy in ovarian
> cancer, it may suppress chemotherapy-induced apoptosis in breast
> cancer: curcumin was found to inhibit chemotherapeutic effects by
> reducing camptothecin-,
> mechlorethamine- or doxorubicin induced apoptosis in breast cancer
> cells, and reduce the effectiveness of cyclophosphamide in an in vivo
> mouse model. In contrast, curcumin has also been shown to augment the
> cytotoxic effects of other chemotherapeutic drugs, including
> doxorubicin, tamoxifen, cisplatin and camptothecin, doxorubicin,
> 5-fluorouracil, paclitaxel, daunorubicin, vincristine, and melphalan,
> with no effect on the toxicity of etoposide, daunorubicin, and idarubicin.
GENERAL SUMMARY ARTICLE
Despite the use of surgical resection and aggressive chemotherapy, nearly 50% of patients with colorectal carcinoma develop recurrent disease, highlighting the need for improved therapies. Curcumin (diferuloylmethane), the major active ingredient of turmeric (curcuma longa) with no discernable toxicity, has been shown to inhibit the growth of transformed cells and colon carcinogenesis at the initiation, promotion, and progression stages in carcinogen-induced rodent models. In a Phase I clinical trial, curcumin has been found to be extremely well tolerated and effective. In this review, we summarized the current status of our knowledge about the effectiveness of curcumin when given in combination with current chemotherapeutics such as 5-fluorouracil, oxaliplatin, and gemcitabine in treatment of gastrointestinal cancers with particular reference to colorectal cancer. Existing data suggest that curcumin in combination with chemotherapy is a superior strategy for treatment of gastrointestinal cancer.
5-Fluorouracil (5-FU) or 5-FU plus oxaliplatin (FOLFOX) remains the backbone of colorectal cancer chemotherapeutics but with limited success. This could partly be due to the enrichment of cancer stem cells (CSCs) that are resistant to conventional chemotherapy. Therefore, validation of a nontoxic agent that can either cause reversal of chemoresistance or promote the killing of CSCs would be highly desirable. The current study examines whether curcumin, the major active ingredient of turmeric, either alone or together with FOLFOX, would be an effective strategy to eliminate colon CSCs. Exposure of colon cancer HCT-116 or HT-29 cells to FOLFOX that inhibited their growth led to the enrichment of CSC phenotype as evidenced by increased proportion of CD133-, CD44-, and/or CD166-positive cells and epidermal growth factor receptor (EGFR) levels. Treatment of FOLFOX-surviving colon cancer cells with either curcumin alone or together with FOLFOX resulted in a marked reduction in CSCs, as evidenced by the decreased expression of CD44 and CD166 as well as EGFR and by their ability to form anchorage-dependent colonies. They also caused disintegration of colonospheres. Increased expression of EGFR in FOLFOX-surviving cells could be attributed to hypomethylation of the EGFR promoter, whereas an opposite phenomenon was observed when the FOLFOX-surviving cells were treated with curcumin and/or FOLFOX. These changes were accompanied by parallel alterations in the levels of DNA methyltransferase 1. In conclusion, our data suggest that curcumin by itself or together with the conventional chemotherapeutic could be an effective treatment strategy for preventing the emergence of chemoresistant colon cancer cells by reducing/eliminating CSCs.
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