The extra or missing chromosomes—also called aneuploidy—in 90% of cancer cells may be a factor in treatment resistance, a new study shows. Researchers reported the findings in Developmental Cell.
In their lab study, researchers triggered chromosomal instability in melanoma cells to cause them to develop more aneuploidy. Using a comparison sample of standard melanoma cells, the researchers exposed both sets of samples to either vemurafenib or paclitaxel. They also left cells from both samples unexposed to cancer therapies to watch how they grow in the absence of treatment.
They found that the aneuploidy cells that received no cancer treatment grew slower than standard melanoma cells. However, exposure to vemurafenib or paclitaxel caused accelerated growth and treatment resistance in the aneuploidy cells.
They also linked specific chromosomal anomalies to separate treatment resistance. The tumors that resisted vemurafenib had extra copies of chromosomes 11 and 18, whereas those that resisted paclitaxel were missing copies of chromosomes 16, 19, and 20.
Similar studies have already confirmed the results, but additional research is needed to identify strategies to exploit those mechanisms for more effective cancer treatments.
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