Friday March 23, 2018

Checkpoint Protein (CHK2) Inhibitor Drug to Protect Women’s Infertility Post Cancer Treatments


Sep 02, 2017: An existing drug may one day protect premenopausal women from infertility that commonly follows cancer treatments, new research has found.

Women who are treated for cancer with radiation or certain chemotherapy drugs are commonly rendered sterile.

Women are born with a lifetime reserve of oocytes, or immature eggs, but those oocytes are among the most sensitive cells in the body and may be wiped out by such cancer treatments.

The new findings, published in the journal Genetics, raises hope of curbing infertility from cancer treatment.

The study builds on his 2014 research that identified a so-called checkpoint protein (CHK2) that becomes activated when oocytes are damaged by radiation.

Checkpoint protein functions in a pathway that eliminates oocytes with DNA damage, a natural function to protect against giving birth to offspring bearing new mutations.

When the researchers irradiated mice lacking the CHK2 gene, the oocytes survived, eventually repaired the DNA damage, and the mice gave birth to healthy pups.

Also Read: Treatment with Uterine Fibroids helps to restore Fertility in Women

The new study explored whether the checkpoint 2 pathway could be chemically inhibited.

“It turns out there were pre-existing CHK2 inhibitor drugs that were developed, ironically enough, for cancer treatment, but they turned out not to be very useful for treating cancer,” said study senior author John Schimenti, Professor at Cornell University in New York.

“By giving mice the inhibitor drug, a small molecule, it essentially mimicked the knockout of the checkpoint gene,” first author Vera Rinaldi, a graduate student in Schimenti’s lab, said.

By inhibiting the checkpoint pathway, the oocytes were not killed by radiation and remained fertile, enabling birth of normal pups, the study said.

“While humans and mice have different physiologies, and there is much work to be done to determine safe and effective dosages for people, it is clear that we have the proof of principle for this approach,” Schimenti said. (IANS)

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Nine new osteoarthritis genes discovered

The team looked for genes that were active in the progression of the disease by extracting the relevant cells from healthy and diseased tissue

Bone loss in adults. IANS
  • Researchers have discovered nine new genes responsible for osteoarthritis
  • These can help in developing new therapies
  • This research may also help in reducing the risk of the disease

Researchers have discovered nine novel genes for osteoarthritis that may open the door to new targeted therapies for this debilitating disease in the future.

Of the nine genes associated with osteoarthritis, researchers identified five genes in particular that differed significantly in their expression in healthy and diseased tissue.

These genes can help create new therapies.

The five genes present novel targets for future research into therapies, the researcher said. According to the researchers, there is no treatment for osteoarthritis. The disease is managed with pain relief and culminates in joint replacement surgery, which has variable outcomes.

“These results are an important step towards understanding the genetic causes of osteoarthritis and take us closer to uncovering the mechanism behind the disease,” said co-author of the study, Eleni Zengini from the University of Sheffield.

For the study, published in the journal Nature Genetics, researchers investigated the genetics behind osteoarthritis, as well as the diseases and traits that are linked to it.

The team studied 16.5 million DNA variations. Following combined analysis in up to 30,727 people with osteoarthritis and nearly 300,000 people without osteoarthritis in total — the controls –, scientists discovered nine new genes that were associated with osteoarthritis.

This may also help in finding ways to reduce the risk of the disease.

The researchers then investigated the role of the nine new genes in osteoarthritis, by studying both normal cartilage and diseased cartilage from individuals who had a joint replacement.

The team looked for genes that were active in the progression of the disease by extracting the relevant cells from healthy and diseased tissue, studying the levels of proteins in the tissue and sequencing the RNA — the messenger that carries instructions from DNA for controlling the production of proteins. IANS