By Admin at 30 Jan 2017, 14:31 PM

Chromosomal instability, including chromosomal damage and errors in the number of chromosomes, is common among cancer cells. Healthy cells contain built-in fail-safes causing them to self destruct amidst this type of genetic chaos, but, ironically, these abnormalities help cancer cells to grow, spread and even become resistant to treatment.

Two new studies have shed light on this phenomenon and revealed methods that might exploit points of cancer weakness to stop its spread and resistance. Lead study author professor Charles Swanton of the Francis Crick Institute in London said in a news release:

"The development and progression of cancer is fueled by an unstable genome. It can cause a high degree of diversity between cells, influencing how well treatments work and drug resistance.

If a cancer cell can cope with large scale changes to its DNA then it might gain an advantage that helps it to grow, spread and survive treatment. Until now, we knew very little about how these cancer cells kept growing and evolving.”

The first study, published in the journal Cancer Cell, focused on the BCL9L gene, which is involved in activating the caspase-2 protein when an abnormal number of chromosomes exist in a cell, causing it to self destruct.

In colorectal cancer cells, a higher number of errors in the BCL9L gene were detected, which played a role in the cancerous cells’ ability to continue thriving despite carrying an uneven number of chromosomes.

Indeed, when the BCL9L gene was inactivated, the caspase-2 protein was not activated and the cells grew normally rather than dying. Exploiting this mechanism may provide a way to limit cancer diversification and spread, the researchers noted.

In the second study, research published in the journal Cell Discovery revealed faults in cancer cells’ internal machinery, or APC/C, which slowed down their division process. Cancer cells often pass down an incorrect number of chromosomes when dividing, but seem to have a built-in mechanism that stops such errors from becoming overwhelming or life-threatening to the cell.

This mechanism may be related to faults in APC/C, as the resulting slow down in the division process ensured the cancer cells’ survival. When the APC/C was allowed to work at full speed during the study, more genetic errors were passed down as the cells divided, which could lead to cell destruction.

In cancer patients, tumor cells with chromosomal instability are more likely to develop drug resistance and evolve, which in turn is linked to decreased survival among patients. "We hope that understanding these mechanisms,” Swanton stated, “will allow us to limit drug resistance and improve the efficacy of cancer therapies."

Sources
Cancer Cell January 9, 2017
Cancer Discovery January 9, 2017
Medical News Today January 11, 2017

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