Scientists have announced this week that they’ve uncovered a genetic map that will help determine the future of ovarian cancer research for years to come. The largest undertaking of its kind to date has led to a better understanding of this “silent killer” and ways to treat it. Mapping revealed 68 genes that could become appropriate therapeutic targets for medications, either drugs already approved for cancer treatment by the U.S. Food and Drug Administration or drugs still under development.
According to the American Cancer Society, ovarian cancer is the fifth most common cancer among women, but it is especially lethal because it is often caught too late for effective treatment. Nearly 14,000 American women died of ovarian cancer in 2010, the cancer society said.
Paul T. Spellman, who conducted his research while a staff scientist at the Lawrence Berkeley National Laboratory in Berkeley, California stated:
“We have now a map that is telling the cancer research community where to look and what to work on in the future. The public should know that this is not an answer in itself. But before this we were essentially making guesses. Now we actually have a very good road map. This battery of analyses is a big step up in characterizing the many different kinds of changes that can cause cancer, in this case ovarian cancer.”
The new genomic research looked specifically at high-grade serous ovarian adenocarcinoma (HGS-OvCa), the most common form of the disease, which accounts for roughly 85% of all ovarian cancer deaths. Looking at 316 tumors, the researchers focused on what’s called “whole-exome sequencing,” examining those regions of the genome that deal with protein production. These types of examinations, along with others, were also conducted on another 173 ovarian tumor specimens.
There appear to be four different subtypes of HGS-OvCa, as well as four more additional related subtypes, based on the genetic scan. Abnormalities present in a key gene, called TP53, were found in nearly all (96%) of patients diagnosed with these tumors.
Just over one in every five of the tumors were found to have tumor mutations in the BRCA1 and BRCA2 genes, which have long been linked to risks for both ovarian and breast cancers. In this case, patients whose cancers carried these mutations had better survival rates than those who did not.
Overall, specific patterns in 108 genes were also linked to poorer survival, while those for another 85 genes were linked to better outcomes. Patients with genetic activity deemed “poor” were found to have 23% shorter survival than those without such genetic aberrations.
According to the team, as many as half of all the aggressive ovarian tumors they studied might respond to drugs that focus on genetic weaknesses in the tumor to help induce cancer cell death. Dr. Andrew Berchuck, director of the gynecologic cancer program at Duke Cancer Institute in Durham, N.C. explains further:
“What’s basically been done here is an autopsy. A forensic analysis of tumors. And what they find is that the molecular changes that occur in one case of ovarian cancer can be dramatically different from that of another in terms of what’s gone wrong in terms of cell growth and cell death. This was suspected to be the case, but no one’s ever mapped it out in extraordinary detail like this before, so that we can begin to understand the biology and root causes of what’s going on.”
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Written by Sy Kraft