Monday February 19, 2018

Indian-origin scientist Ravi Majeti, turns cancer cells into harmless cells

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By Anurag Paul

An Indian-origin researcher at the Stanford University in the US has found a method that can cause dangerous leukemia cells to mature into harmless immune cells known as macrophages.

Assistant professor of medicine Ravi Majeti made the key observation after collecting leukemia cells from a patient and trying to keep the cells alive in a culture plate.

During the study, Majeti and post-doctoral scholar Scott McClellan found that some of the cancer cells in culture were changing shape and size into what looked like macrophages.

The team confirmed that the methods shown to have altered the destiny of the mouse progenitor cells years ago could be used to transform these human cancer cells into macrophages which can engulf and digest cancer cells and pathogens.

“We were giving everything at them to help them hold out,” said Majeti in a report that appeared in the journal Proceedings of the National Academy of Sciences. B-cell leukemia cells are in many ways progenitor cells that are forced to stay in an immature state.

B-cell acute lymphoblastic leukemia with a variation called the Philadelphia chromosome is a especially aggressive cancer with poor results.

“So finding potential treatments is especially exciting,” Majeti added.

Majeti and his colleagues have some reason to hope that when the cancer cells become macrophages, they will not only be neutralized but may actually assist in fighting the cancer.

“Because the macrophage cells came from the cancer cells, they will already carry with them the chemical signals that will distinguish the cancer cells, causing an immune attack against the cancer more likely,” Majeti explained.

The researchers’ next steps would be to find out if they can discover a drug that will incite the same reaction and that could function as the groundwork for a therapy for the leukemia.

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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

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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.

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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.

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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)

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