A close look at a tumor’s or patient’s genetics can provide important, possibly lifesaving clues to preventing and treating cancer. So say scientists who outlined their research Tuesday in five presentations at the American Association for Cancer Research’s annual conference, in Denver.”That is an interesting group of presentations,” John S. Witte, a professor in the Institute for Human being Genetics at the University of California, San Francisco, said throughout a midday press conference. “All the studies impact on the potential to predict risk or recurrence or response to treatment,” he said. In the 1st study, researchers led by Dr. Charles Mullighan, an assistant member at St. Jude Children’s Research Hospital, Memphis, discovered that children with severe lymphoblastic leukemia (ALL) who have mutations in the JAK tyrosine kinase gene generally possess poor outcomes, including an increased risk of recurrence of their cancer. The selecting suggests the gene is actually a potential diagnostic tool and a fresh therapeutic focus on. Despite improvements in treatment, some children with ALL will relapse, Mullighan told reporters. For the analysis, the Memphis team analyzed the genes of 221 children with the condition. Although JAK mutations weren’t previously known to occur in children with ALL, they were discovered in 10 percent of these sufferers. The mutations were associated with a deletion of the genes IKZF1 and CDKN2A/B and poor end result. And, over four years, 71 percent of the kids with JAK and IKZF1 alterations had a relapse of their disease, weighed against just 23 percent for sufferers without these genetic alterations, the researchers found.
But there was good news, too. “When we treated the cancer cells with a JAK inhibitor, the cells died,” Mullighan stated. “This shows that these JAC mutations certainly are a new therapeutic focus on in this subtype of leukemia.” Another research on leukemia discovered that a set of genetic variants escalates the risk for chronic lymphocytic leukemia (CLL). The findings of the study add more pieces to the puzzle and could lead to better avoidance and prognosis of the disease, in accordance to lead researcher Susan Slager, associate professor of biostatistics at the Mayo Clinic in Rochester, Minn.
Regarding 15,000 Americans will develop CLL every year, and 4,000 will die, so that it is among the rarer cancers, Slager said during the teleconference. However, “for those who have a member of family with chronic lymphocytic leukemia, your chances of getting the disease are eight times greater than that of the general population,” she noted. An earlier analysis identified seven DNA sequencing aberrations known as “solitary nucleotide polymorphisms” (SNPs) that might result in chronic lymphocytic leukemia. In today’s study, researchers confirmed these results in another sample of sufferers. They discovered the strongest genetic association for the condition was for a SNP on the 11q24 gene, where the risk was 50 percent higher. This is followed by a 39 percent increased risk with a separate SNP on the 6p25 gene.”Our results will ideally understand the biology of the condition, which may help us predict the condition, and it may help all of us develop better remedies and prognostic markers,” Slager said. Outcomes of another research presented at the conference showed that genetic variants in what’s known as the microRNA digesting pathway may predict a woman’s risk for ovarian cancer.”Ovarian cancer may be the fifth leading reason behind cancer in women in the United States, and among the major risk factors is a family group history of ovarian cancer, indicating that a genetic component plays a part in ovarian cancer risk,” Dr. Xifeng Wu, a professor in the department of epidemiology at the University of Texas M. D. Anderson Cancer Center in Houston, said through the teleconference. For the analysis, Wu’s and team evaluated 70 SNPs in eight microRNA pathway genes. They were extracted from 380 ovarian cancer cases, and also from 146 healthy ladies.
The researchers found 16 SNPs which were predictive of ovarian cancer risk. Individuals who carried five or fewer of the SNPs were at low risk for ovarian cancer. However, sufferers with six and seven SNPs got greater than a twofold increased risk, and those with eight or more experienced over a fivefold increased risk. Furthermore, as the number of these SNPs increases, so does resistance to treatment and poorer survival, Wu said.
This information, and also other genetic and lifestyle risk factors, could possibly be used to develop an ovarian cancer risk-prediction model, Wu said. In a fourth study, experts led by Dr. Gangning Liang, a co-employee professor of analysis in the department of urology at the University of Southern California, reported
locating a DNA modification called a “methylation pattern,” that may diagnosis bladder cancer and detect patients at risk designed for recurrence of the disease.
“Bladder cancer may be the fifth most common cancer in men and the sixth most common in women,” Liang said during the teleconference. “It is mainly within smokers.”DNA methylation is an activity in which genes could be either silenced or activated in malignancy. For the study, experts measured DNA methylation in 12 patients who did not have bladder cancer, 52 patients with noninvasive bladder tumors and 39 patients with invasive bladder tumors.
Comparing cancerous cells with normal bladder tissue, they discovered 158 “hypermethylated” loci and 366 “hypomethylated” locations. Furthermore, they found 21 locations that were hypermethylated in the normal-appearing bladder cells in individuals with bladder cancer.
These loci could be markers for identifying people at risk for bladder malignancy, the researchers said. Furthermore, the scientists discovered that noninvasive tumors had a definite pattern of hypomethylation weighed against invasive tumors. This obtaining supports the idea that two types of bladder malignancy develop along different paths. Bladder cancer can simply recur, Liang noted. “It requires frequent and invasive monitoring. We think these results are clinically useful and have benefits for the patient, because we can identify these methylation adjustments in the patient’s urine,” he explained.
“So, we are able to use a noninvasive method to monitor the individual and may also be able to display for bladder cancer in high-risk populations, like smokers,” he said. In your final report, researchers led by Sunita Setlur, an instructor in pathology at Brigham and Women’s Hospital and Harvard Medical School, found simply no association between the gene variant UGT2B17 and the chance of prostate cancer. Although this gene had been from the risk for prostate cancer in two earlier studies, this new study found no such association. For the study, researchers looked at 269 males of whom 156 got prostate cancer. The researchers looked at the amount of copies of the UGT2B7 gene and discovered that although deletion patterns for UGT2B17 and UGT2B28 genes were between 3.4 percent and 19.9,
this did not increase the risk for prostate cancer.”We did not see any association between polymorphism of UGT2B17 and UGT2B28 with malignancy,” Setlur stated during Tuesday’s teleconference.