One of the most common cancer coaching questions I get from breast cancer patients, of all breast cancer types, stages and ages, is “How can I prevent a breast cancer relapse?”
Of course no one can prevent a cancer relapse 100% of the time but I can provide studies that support how I have managed my own cancer since my diagnosis in 1994 and my complete remission in 1999.
In short, I have used, and recommend a combination of both conventional/traditional therapies with the best of evidence-based non-toxic, non-conventional therapies.
Non-toxic, non-conventional nutritional supplementation is cytotoxic to breast cancer stem cells as well as integrative to conventional therapies such as cisplatin.
BC stem cells are thought to circulate in the blood system of BC patients that can grow to become a breast cancer relapse.
Yes, BC surgery, chemotherapy and radiation may have their place in the treatment of breast cancer. However, it is important for breast cancer patients to think about the long-term. All cancer survivors want to die not of their cancer but of old age.
Ginger and curcumin supplementation is one non-toxic therapy that can help you reach old age.
To learn of additional therapies, both conventional and non-conventional, to help you manage your cancer diagnosis, scroll down the page and post a question. Or click the cancer coaching button to the right.
“Cancer stem cells (CSCs) pose a serious obstacle to cancer therapy as they can be responsible for poor prognosis and tumour relapse. In this study, we have investigated inhibitory activity of the ginger-derived compound 6-shogaol against breast cancer cells both in monolayer and in cancer-stem cell-like spheroid culture…
Taxol, a drug widely used in breast cancer treatment, and curcumin, a compound earlier shown to be effective in inhibiting cancer stem-like spheroids , were used for comparison. The results showed that for both the cell types, 6-shogaol was effective in spheroids at concentrations that were 5 or 2 fold higher than the effective inhibitory concentrations in monolayer cells. In contrast, taxol, even though was highly active in monolayer cells, did not show activity against the spheroids even at 10000 fold higher concentration compared to 6-shogaol (Table 1). Curcumin was also found to be effective against MCF-7 spheroids as reported earlier …
“CONCLUSION- Recently, the potential effect of curcumin on cancer cells has been recognized by the scientific community in the world, and the molecular biological approaches help to elucidate the underlying mechanisms of actions on curcumin in tumor cells. However, the molecular mechanisms underlying the antitumor activity of curcumin have not been very clear until now. Another thing is that the molecular mechanism of curcumin on tumor cells was usually studied with tumor cell lines in vitro, and the molecular mechanisms in vivo need to be further investigated. More sophisticated technologies will have to be applied in conjunction so that curcumin derivatives could be used for rational cancer therapy.”
“Multidrug resistance (MDR) is a major obstacle to the chemotherapeutic treatment of breast cancer. The aim of this study is to investigate the mechanisms of curcumin induced increased chemosensitivity in MDR breast cancer cells.
The results of MTT and western blot showed that curcumin could sensitize MCF-7 and MCF-7/DDP cells to cisplatin and activate MCF-7/DDP cell autophagy. The levels of CCAT1, p-PI3K, p-AKT and p-mTOR detected by RT-PCR and western blot in MCF-7/DDP cells were higher than in MCF-7 cells, and curcumin downregulated their expression in a dose-dependent manner.
Moreover, we found that downregulation of CCAT1 could re-sensitize MCF-7/DDP cells to cisplatin, inactivate the PI3K/AKT/mTOR pathway and activate cell autophagy, while overexpression of it have the opposite effect in MCF-7 cells. Inactivation of autophagy by 3-MA could reverse CCAT1 knockdown-induced increased chemosensitivity and inactivation of the PI3K/AKT/mTOR pathway in MCF-7/DDP cells. PLEN-CCAT1 could reverse curcumin-increased chemosensitivity and autophagy activation, however, inactivation of the PI3K/AKT/mTOR pathway by LY294002 could reverse once more pLEN-CCAT1-decreased chemosensitivity and inactivation of autophagy.
Finally, the xenotransplant nude mouse model was used to study the effect of CCAT1 on curcumin-induced autophagy in vivo, and the results showed that curcumin inhibited tumor volume growth, downregulated CCAT1 expression and induced autophagy in vivo.
Curcumin decreased CCAT1 and inactivated the PI3K/Akt/mTOR pathway which could both activate autophagy, sensitizing MDR breast cancer cells to cisplatin…”