pharmafileAugust 10, 2017
Tag: Breast Cancer , chemotherapy
The team discovered that paclitaxel, a chemotherapy drug used as a first-line treatment, triggers changes on a molecular level which cause cancer cells to escape from the original tumour site, while creating a hospitable tissue environment for these cells in the lungs. These changes were found to be dependent on the gene Atf3, expression of which is found to be greater in those who have undergone chemotherapy.
"That chemotherapy can paradoxically promote cancer progression is an emerging revelation in cancer research. However, a molecular-level understanding of this devastating effect is not clear," said Tsonwin Hai, the study's senior author and a professor of biological chemistry and pharmacology.
"[Atf3] seems to do two things at once: essentially help distribute the 'seeds' (cancer cells) and fertilise the 'soil' (the lung)," Hai said. "I think it's an active process – a biological change in which the cancer cells are beckoned to escape into the blood – rather than a passive process in which the cancer cells get into the bloodstream because of leaky vessels."
These findings were observed in mouse models, but the study was accompanied by data taken from human breast cancer patients which suggest that these new discoveries could be relevant in human models, though Hai was keen to point out that there is much more work to be done.
"At this point, what our study and the recent literature on chemotherapy taught us is that it is prudent to keep our mind open, realising that chemo can help treat cancer, but at the same time may increase the possibility of the spread of that cancer," she said. "It's possible there could be a treatment given in conjunction with the chemo that would inhibit this problem by dampening the effect of the stress gene Atf3."
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