A close look at a tumor’s or patient’s genetics can offer important, potentially lifesaving clues to stopping 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.”This is an interesting set of presentations,” John S. Witte, a professor in the Institute for Human being Genetics at the University of California, SAN FRANCISCO BAY AREA, said throughout a midday press conference. “All of the studies have an impact on the potential to predict risk or recurrence or response to treatment,” he stated. In the initial study, researchers led by Dr. Charles Mullighan, an assistant member at St. Jude Children’s Study Hospital, Memphis, found that children with acute lymphoblastic leukemia (ALL) who’ve mutations in the JAK tyrosine kinase gene generally have got poor outcomes, including an increased risk of recurrence of their cancer. The obtaining suggests the gene is actually a potential diagnostic device and a fresh therapeutic focus on. Despite improvements in treatment, some children with Most will relapse, Mullighan told reporters. For the study, the Memphis team analyzed the genes of 221 children with the condition. Although JAK mutations weren’t previously recognized to occur in children with ALL, these were discovered in 10 percent of these sufferers. The mutations were connected with a deletion of the genes IKZF1 and CDKN2A/B and poor result. And, over four years, 71 percent of the kids with JAK and IKZF1 alterations got a relapse of their disease, weighed against just 23 percent for individuals without these genetic alterations, the researchers found.
But there was very good news, too. “Whenever we treated the cancer cellular material with a JAK inhibitor, the cells died,” Mullighan stated. “This shows that these JAC mutations are a new therapeutic focus on in this subtype of leukemia.” Another study on leukemia found that a set of genetic variants escalates the risk for chronic lymphocytic leukemia (CLL). The findings of this study add more pieces to the puzzle and could lead to better avoidance and prognosis of the condition, according to lead researcher Susan Slager, associate professor of biostatistics at the Mayo Clinic in Rochester, Minn.
About 15,000 Americans will develop CLL every year, and 4,000 will die, so that it is among the rarer cancers, Slager said through the teleconference. However, “if you have a member of family with chronic lymphocytic leukemia, your likelihood of obtaining the disease are eight times higher than that of the general population,” she noted. A youthful analysis determined seven DNA sequencing aberrations known as “solitary nucleotide polymorphisms” (SNPs) that might lead to chronic lymphocytic leukemia. In the current study, experts confirmed these results in another sample of individuals. They found 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 hopefully understand the biology of the disease, which may help us predict the condition, and it could help us develop better remedies and prognostic markers,” Slager said. Outcomes of another research presented at the meeting demonstrated that genetic variants in what’s known as the microRNA processing pathway may predict a woman’s risk for ovarian cancer.”Ovarian cancer is the fifth leading cause of cancer in ladies in the usa, and among the major risk factors is a family history of ovarian malignancy, indicating 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 study, Wu’s and team evaluated 70 SNPs in eight microRNA pathway genes. These were extracted from 380 ovarian cancer cases, and also from 146 healthy women.
The researchers found 16 SNPs which were predictive of ovarian cancer risk. Individuals who carried five or fewer of these SNPs had been at low risk for ovarian malignancy. However, patients with six and seven SNPs experienced greater than a twofold increased risk, and those with eight or even more experienced over a fivefold increased risk. In addition, as the amount of these SNPs increases, so does resistance to treatment and poorer survival, Wu said.
This information, along with other genetic and lifestyle risk factors, could 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 study in the section of urology at the University of Southern California, reported
locating a DNA modification known as a “methylation pattern,” that may medical diagnosis bladder cancer and detect patients at risk meant for recurrence of the disease.
“Bladder cancer is the fifth the majority of common cancer in males and the sixth many common in females,” Liang said during the teleconference. “It is mainly found in smokers.”DNA methylation is an activity in which genes can be either silenced or activated in cancer. For the study, experts measured DNA methylation in 12 patients who didn’t have bladder cancer, 52 patients with non-invasive bladder tumors and 39 individuals with invasive bladder tumors.
Comparing cancerous cells with normal bladder tissue, they discovered 158 “hypermethylated” loci and 366 “hypomethylated” locations. In addition, they found 21 places that were hypermethylated in the normal-appearing bladder cells in individuals with bladder cancer.
These loci may be markers for identifying people at risk for bladder cancer, the researchers said. Furthermore, the scientists found that noninvasive tumors had a definite pattern of hypomethylation compared with invasive tumors. This locating supports the theory that two forms of bladder malignancy develop along different paths. Bladder cancer can simply recur, Liang noted. “It needs regular and invasive monitoring. We think these email address details are clinically useful and have benefits for the individual, because we can detect these methylation changes in the patient’s urine,” he explained.
“So, we are able to use a noninvasive method to monitor the patient and may also be able to display screen for bladder cancer in high-risk populations, like smokers,” he said. In a 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 your gene variant UGT2B17 and the chance of prostate cancer. Although this gene have been linked to the risk for prostate cancer in two earlier studies, this new study found no such association. For the study, researchers viewed 269 men of whom 156 had prostate cancer. The researchers looked at the number of copies of the UGT2B7 gene and discovered that although deletion patterns for UGT2B17 and UGT2B28 genes had been between 3.4 percent and 19.9,
this did not raise the risk for prostate cancer.”We did not see any association between polymorphism of UGT2B17 and UGT2B28 with cancer,” Setlur said during Tuesday’s teleconference.