A close look at a tumor’s or patient’s genetics can provide important, possibly lifesaving clues to avoiding and treating cancer. Therefore say scientists who outlined their analysis Tuesday in five presentations at the American Association for Cancer Research’s annual meeting, in Denver.”That is an interesting group of presentations,” John S. Witte, a professor in the Institute for Individual Genetics at the University of California, San Francisco, said throughout a midday press meeting. “All the studies impact on the potential to predict risk or recurrence or response to treatment,” he said. In the first study, experts led by Dr. Charles Mullighan, an assistant member at St. Jude Children’s Analysis Hospital, Memphis, discovered that children with acute lymphoblastic leukemia (ALL) who’ve mutations in the JAK tyrosine kinase gene generally possess poor outcomes, including an increased threat of recurrence of their cancer. The acquiring suggests the gene is actually a potential diagnostic tool and a new 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 were not previously known to occur in children with ALL, these were discovered in ten percent of these patients. The mutations were connected with a deletion of the genes IKZF1 and CDKN2A/B and poor final 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 individuals without these genetic alterations, the researchers found.
But there was good news, too. “Whenever we treated the cancer cellular material with a JAK inhibitor, the cellular material died,” Mullighan stated. “This suggests that these JAC mutations are a new therapeutic target in this subtype of leukemia.” Another study on leukemia discovered that a set of genetic variants increases the risk for persistent lymphocytic leukemia (CLL). The findings of the study add more parts 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.
About 15,000 Americans will establish CLL every year, and 4,000 will die, so it is one of the rarer cancers, Slager said during the teleconference. However, “should you have a member of family with chronic lymphocytic leukemia, your chances of obtaining the disease are eight instances greater than that of the general population,” she noted. An earlier analysis identified seven DNA sequencing aberrations called “one nucleotide polymorphisms” (SNPs) that might result in chronic lymphocytic leukemia. In the current study, researchers confirmed these findings in a separate sample of patients. They found the strongest genetic association for the disease was for a SNP on the 11q24 gene, where the risk was 50 percent higher. This was followed by a 39 percent improved risk with another SNP on the 6p25 gene.”Our results will hopefully understand the biology of the disease, which may help us predict the disease, and it could help all of us develop better remedies and prognostic markers,” Slager said. Results of another research presented at the meeting showed that genetic variants in what’s referred to as the microRNA digesting pathway may predict a woman’s risk for ovarian malignancy.”Ovarian cancer is the fifth leading cause of cancer in females in the usa, and one of the major risk elements is a family group history of ovarian cancer, indicating that a genetic component contributes to ovarian malignancy risk,” Dr. Xifeng Wu, a professor in the section of epidemiology at the University of Texas M. D. Anderson Cancer Middle in Houston, said through the teleconference. For the analysis, Wu’s and team evaluated 70 SNPs in eight microRNA pathway genes. We were holding extracted from 380 ovarian cancer cases, in addition to from 146 healthy females.
The researchers found 16 SNPs which were predictive of ovarian cancer risk. Sufferers who carried five or fewer of these SNPs had been at low risk for ovarian cancer. However, patients with six and seven SNPs got greater than a twofold improved risk, and the ones 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, along with other genetic and lifestyle risk factors, could be used to build up 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 section of urology at the University of Southern California, reported
selecting a DNA modification called a “methylation design,” that may medical diagnosis bladder cancer and identify patients at risk meant for recurrence of the condition.
“Bladder cancer may be the fifth many common cancer in guys and the sixth many common in females,” Liang said during the teleconference. “It is mainly within smokers.”DNA methylation is a process in which genes can be either silenced or activated in cancer. For the study, researchers measured DNA methylation in 12 patients who did not have bladder cancer, 52 patients with noninvasive bladder tumors and 39 individuals with invasive bladder tumors.
Comparing cancerous cells with normal bladder tissue, they found 158 “hypermethylated” loci and 366 “hypomethylated” locations. In addition, they found 21 locations that were hypermethylated in the normal-appearing bladder tissue in sufferers with bladder cancer.
These loci could be markers for identifying people at risk for bladder cancer, the researchers said. Furthermore, the scientists discovered that noninvasive tumors had a definite pattern of hypomethylation compared with invasive tumors. This selecting supports the idea that two types of bladder malignancy develop along different paths. Bladder cancer can easily recur, Liang noted. “It needs regular and invasive monitoring. We think these email address details are clinically useful and also have benefits for the individual, because we can identify these methylation changes in the patient’s urine,” he explained.
“So, we can use a noninvasive method to monitor the individual and may also have the ability to display screen for bladder malignancy in high-risk populations, like smokers,” he said. In a final report, experts led by Sunita Setlur, an instructor in pathology at Brigham and Women’s Hospital and Harvard Medical College, found no association between the gene variant UGT2B17 and the risk of prostate cancer. Although this gene had been linked to the risk for prostate cancer in two earlier research, this new research found no such association. For the study, researchers viewed 269 men of whom 156 had prostate cancer. The experts looked at the number of copies of the UGT2B7 gene and found that although deletion patterns for UGT2B17 and UGT2B28 genes had been between 3.4 percent and 19.9,
this did not boost the risk for prostate cancer.”We didn’t see any association between polymorphism of UGT2B17 and UGT2B28 with malignancy,” Setlur stated during Tuesday’s teleconference.