Tuesday July 16, 2019

Girls may inherit ovarian cancer gene from fathers

The researchers collected information about pairs of granddaughters and grandmothers and sequenced portions of the X-chromosome from 186 women affected by cancer

0
//
A mutation on the X-chromosome may also advance ovarian cancer's age of onset by more than six years. Wikimedia Commons
A mutation on the X-chromosome may also advance ovarian cancer's age of onset by more than six years. Wikimedia Commons

Scientists have found a gene responsible for ovarian cancer that can be passed down from fathers to their daughters.

The study found that genes on the X-chromosome get potentially passed down through the father to his daughter, thus increasing the risk of ovarian cancer in girls.

A mutation on the X-chromosome may also advance ovarian cancer’s age of onset by more than six years.

“Our study may explain why we find families with multiple affected daughters: because a dad’s chromosomes determine the sex of his children, all of his daughters have to carry the same X-chromosome genes,” said Kevin H.

Also Read: Surgical Infections More Common in Low-Income Countries, Study Finds

Eng, Assistant Professor at Roswell Park Comprehensive Cancer Centre in Buffalo, the US.

The study, published in the journal PLOS Genetics, stated that the genetic mutation inherited from the paternal grandmothers were also associated with higher rates of prostate cancer in fathers and sons as well.

The study found that genes on the X-chromosome get potentially passed down through the father to his daughter, thus increasing the risk of ovarian cancer in girls. Wikimedia Commons
The study found that genes on the X-chromosome get potentially passed down through the father to his daughter, thus increasing the risk of ovarian cancer in girls. Wikimedia Commons

The researchers collected information about pairs of granddaughters and grandmothers and sequenced portions of the X-chromosome from 186 women affected by cancer.

The results proposed that a gene on the X-chromosome may contribute to a woman’s risk of developing ovarian cancer, independently of other known susceptibility genes, such as the BRCA genes.

This observation suggests that there may be many cases of seemingly sporadic ovarian cancer that are actually inherited, and may lead to improved cancer screening and better genetic risk assessment.

Also Read: Tips That Will Help In Recovery From Surgery

However, future studies will be needed to confirm the identity and function of this gene.

“What we have to do next is make sure we have the right gene by sequencing more families. This finding has sparked a lot of discussion within our group about how to find these X-linked families,” Eng said.

“It’s an all-or-none kind of pattern: A family with three daughters who all have ovarian cancer is more likely to be driven by inherited X mutations than by BRCA mutations,” Eng noted. (IANS)

Next Story

Researchers Find Way to Make Cancer Cells Self-destruct

It also shows that ATF4 turns on the genes MYC needs for growth and also controls the rate at which cells make specific proteins called 4E-BP

0
Cancer, Patients, Invasive
Traditional treatments often include chemotherapy or radiation to kill cancer cells and shrink tumors. Pixabay

In a new hope for cancer patients, researchers have found a way to cause some cancer cells to self-destruct.

The research team has identified a new pathway that works as a partner to a gene called MYC which controls normal cell growth, but when it is mutated or amplified in cancer, it sets off a chain reaction that helps tumours grow uncontrollably.

The pathway involves a protein called ATF4, and when it’s blocked, it can cause cancer cells to produce too much protein and die.

Published in the journal Nature Cell Biology, the study done on mice points the way towards a new therapeutic approach as inhibitors that can block synthesis of ATF4 already exist.

Cancer
Cancer Ribbon. Pixabay

“What we’ve learned is that we need to go further downstream to block tumour growth in a way that cancer cells can’t easily escape, and our study identifies the target to do just that,” said Constantinos Koumenis, Professor at the University of California.

According to researchers, this finding shows the alternative approach is to target ATF4 itself, since it’s the point where both signal pathways converge, meaning there’s less redundancy built in to allow cancer to survive.

Also Read: Consuming this Bacteria May Cut Risk of Heart Diseases

It also shows that ATF4 turns on the genes MYC needs for growth and also controls the rate at which cells make specific proteins called 4E-BP.

This study also found that when tumours in humans are driven by MYC, ATF4 and its protein partner 4E-BP are also overly expressed, which is further evidence that these findings may point to an approach that could work for humans. (IANS)