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WNT16B, acting in a cell nonautonomous manner, promotes the survival of cancer cells after cytotoxic therapy.

Consistent with previous studies, transcripts encoding matrix metalloproteinases such as MMP1, chemokines such as CXCL3 and peptide growth factors such as amphiregulin were substantially elevated in PSC27 fibroblasts after genotoxic damage,.

Notably, the expression of WNT16B increased between eightfold and 64-fold as a result of these treatments (P < 0.005)

In other words, chemotherapy causes cancer.

Treatment-induced damage to the tumor microenvironment promotes prostate cancer therapy resistance through WNT16B

WNT16B protein was substantially and significantly increased after chemotherapy in the periglandular stroma, which included fibroblasts and smooth muscle cells (P < 0.01)

We confirmed these findings in breast and ovarian carcinomas, two other malignancies commonly treated with cytotoxic chemotherapy.

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

Click here to add your own text  The news comes after it was previously ousted by similarly-breaking research that expensive cancer drugs not only fail to treat tumors, but actually make them far worse. The cancer drugs were found to make tumors ‘metasize’ and grow massively in size after consumption. As a result, the drugs killed the patients more quickly