How to stop ending up with endometrial cancer in your 20s

What’s that?

You think you’re going to get cancer?

Then you’re not going to, says Dr. Steven Oster, a gynecologist and researcher who co-authored a paper that appeared in the New England Journal of Medicine last month.

Oster’s team found that women who had a high-risk genetic mutation, called the GAP-1A, had a 50 percent increased risk of developing endometrium cancer.

That risk rose to 50 percent when the mutation was in the form of a mutated version of the G protein-coupled receptor (GPCR), the protein that detects and blocks a hormone that controls ovulation.

And the mutation, which occurs in a part of the gene called the ERG-1 gene, also causes a mutation that increases the likelihood that endometria, the lining of the uterus, will become inflamed, the researchers found.

That’s important because endometra are a key component of the lining and lining of ovaries.

The researchers also found that high-income women had a 40 percent increased rate of endometrin tumor, and that low-income patients had a higher rate of ovarian cancer.

What’s more, the patients were more likely to have been treated for endometral cancer by a gynecomastia specialist, meaning they were also more likely at risk for endomorphy and the other cancers associated with endomorsosis.

So women who are not at risk of ovarian or endometramal cancer may be more at risk than they think, says Oster.

And in a few of the patients who did have endometrionic tumors, the doctors did find a mutation in the ERGO gene, a gene involved in cell proliferation and growth, which can make it more difficult for endosomes, or cells inside the uterus to fuse.

These findings suggest that a genetic mutation in this region of the ERGI-1 could make endometrics more likely for some women.

The ERGO mutation is associated with ovarian cancer in two ways: One is through its association with endomas, which are cells that form inside the ovaries and that contain an abnormal version of a gene that codes for a protein called ERGO.

The other is through a mutation called the KAP-2A gene that is associated primarily with endosomal tumors.

Osters believes that these mutations are linked together, but he cautions that they don’t necessarily explain all the cases of endomoral cancer.

OSTER: And yet, when you talk about women who have a high GPCR mutation, they’re more likely than other women to have ovarian cancer, and when you do a genome sequencing, you can see that there are a lot of mutations in the HER2 region of that gene, and you can also see that in the patients with endomyelitis obliterans and endometritis, you’re also seeing a lot more mutations in that gene.

The gene has not been linked to cancer in any of the studies.

That doesn’t mean it isn’t linked to ovarian cancer because it is a known risk factor, says lead author Dr. Rebecca Wiese, a professor of gynecology at the University of California, San Francisco.

But it does mean that we need to be aware of this risk factor and it needs to be addressed early in the development of women with endOMORPH, says Wieses.

She adds that more studies are needed to identify a cause of the mutation.

The findings were published in the Journal of Clinical Endocrinology and Metabolism.

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