Dr. Weeks’ Comment: As I clarified in the prior post about radiation making your cancer worse, same with chemotherapy. And here is the science:
2012 Research has documented that chemotherapy, far from ridding anyone of cancer actually feeds the growth and spread of cancer.
- Scientist Peter Nelson of the Fred Hutchinson Cancer Research Center in Seattle in a write-up of a study of why cancer cells were so easy to kill in the lab but not inside our bodies, found that healthy cells damaged by chemotherapy secreted more of a protein called WNT16B which boosts cancer cell survival. “The increase in WNT16B was completely unexpected,” Nelson told AFP.
He added that,“WNT16B, when secreted, would interact with nearby tumor cells and cause them to grow, invade, and importantly, resist subsequent therapy.” That would explain why in cancer treatment, tumors often respond well initially, followed by rapid regrowth and then resistance to further chemotherapy.
The study was conducted by a team of scientists from different cancer research centers, universities as well as from the Lawrence Berkeley National Laboratories. It was published online in August 2012 in the journal Nature Medicine. Among their alarming conclusions was that, “The expression of WNT16B in the prostate tumor microenvironment attenuated the effects of cytotoxic chemotherapy in vivo, promoting tumor cell survival and disease progression.”
HERE’S the actual STUDY : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3677971/
EXCERPT : We confirmed these findings in breast and ovarian carcinomas, two other malignancies commonly treated with cytotoxic chemotherapy. Genotoxic treatments induced the expression of WNT16B protein in primary human fibroblasts isolated directly from breast and ovarian tissues and in the prostates, breasts and ovaries of mice treated with MIT (Supplementary Fig. 2a–d). WNT16B protein expression was significantly elevated in the stroma of human breast and ovarian cancers treated with neoadjuvant chemotherapy compared with tumors from patients that did not receive treatment (P < 0.001) (Fig. 2). Notably, in each of the tumor types evaluated, a range of absent to robust WNT16B expression was evident. Because responses to chemotherapy also varied, we evaluated whether WNT16B expression was associated with clinical outcome. In patients with prostate cancer treated with neoadjuvant chemotherapy, higher WNT16B immunoreactivity in prostate stroma after treatment was associated with a significantly greater likelihood of cancer recurrence (P = 0.04) (Fig. 2d). We next sought to determine the mechanism(s) by which WNT16B could contribute to treatment failure.
WNT16B promotes cancer cell proliferation and invasion