Cancer’s Secrets Were Revealed By Gene Studies
A close look at a tumor’s or patient’s genetics can offer important, potentially lifesaving clues to preventing and treating cancer. Therefore say scientists who outlined their research 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 BAY AREA, said throughout a midday press meeting. “All of the studies impact on the potential to predict risk or recurrence or response to treatment,” he stated. In the first study, experts led by Dr. Charles Mullighan, an assistant member at St. Jude Children’s Study Hospital, Memphis, discovered that children with severe lymphoblastic leukemia (ALL) who’ve mutations in the JAK tyrosine kinase gene generally have poor outcomes, including a higher risk of recurrence of their malignancy. The acquiring suggests the gene is actually a potential diagnostic tool and a new therapeutic target. Despite improvements in treatment, some children with All of the 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, they were discovered in 10 percent of these patients. The mutations were connected with a deletion of the genes IKZF1 and CDKN2A/B and poor outcome. And, over four years, 71 percent of the children with JAK and IKZF1 alterations experienced a relapse of their disease, compared with just 23 percent for individuals without these genetic alterations, the researchers found.
But there was good news, too. “When we treated the malignancy cells with a JAK inhibitor, the cells died,” Mullighan stated. “This shows that these JAC mutations are a new therapeutic target in this subtype of leukemia.” Another study on leukemia found that a couple of genetic variants escalates the risk for chronic lymphocytic leukemia (CLL). The findings of the study add more pieces to the puzzle and may lead to better avoidance and prognosis of the condition, 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 each year, and 4,000 will die, so that it is among the rarer cancers, Slager said during the teleconference. However, “should you have a member of family with chronic lymphocytic leukemia, your likelihood of obtaining the disease are eight occasions higher than that of the general population,” she noted. A youthful analysis recognized seven DNA sequencing aberrations known as “single nucleotide polymorphisms” (SNPs) that may result in chronic lymphocytic leukemia. In the current study, researchers confirmed these results in another sample of patients. They discovered the strongest genetic association for the disease was for a SNP on the 11q24 gene, where in fact the risk was 50 percent higher. This is followed by a 39 percent improved risk with another SNP on the 6p25 gene.”Our results will hopefully understand the biology of the condition, which may help us predict the condition, and it could help us develop better treatments and prognostic markers,” Slager said. Outcomes of another study presented at the conference demonstrated that genetic variants in what’s referred to as the microRNA processing pathway may predict a woman’s risk for ovarian cancer.”Ovarian cancer may be the fifth leading cause of cancer in females in the usa, and among the major risk elements is a family history of ovarian cancer, 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 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 malignancy cases, as well as from 146 healthy ladies.
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 acquired greater than a twofold increased risk, and the ones with eight or more acquired over a fivefold increased risk. In addition, 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 develop an ovarian cancer risk-prediction model, Wu said. In a fourth study, researchers led by Dr. Gangning Liang, a co-employee professor of study in the section of urology at the University of Southern California, reported
finding a DNA modification known as a “methylation pattern,” that may medical diagnosis bladder cancer and detect patients at risk intended for recurrence of the condition.
“Bladder cancer is the fifth many common cancer in men and the sixth the majority of common in ladies,” Liang said during the teleconference. “It is mainly within smokers.”DNA methylation is an activity in which genes can 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 non-invasive bladder tumors and 39 patients with invasive bladder tumors.
Comparing cancerous tissue 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 cells in sufferers with bladder cancer.
These loci may be markers for identifying people at risk for bladder cancer, the researchers said. In addition, the scientists discovered that noninvasive tumors had a distinct pattern of hypomethylation weighed against invasive tumors. This locating supports the theory that two kinds of bladder cancer develop along different paths. Bladder cancer can easily recur, Liang noted. “It requires regular and invasive monitoring. We believe these results are clinically useful and also have benefits for the individual, because we can detect these methylation adjustments in the patient’s urine,” he explained.
“So, we can use a noninvasive solution to monitor the patient and may also have the ability to display 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 simply no association between your gene variant UGT2B17 and the chance of prostate cancer. Although this gene had been linked to the risk for prostate malignancy in two earlier studies, this new study found no this kind of association. For the analysis, researchers looked at 269 males of whom 156 got 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 increase the risk for prostate cancer.”We didn’t see any association between polymorphism of UGT2B17 and UGT2B28 with cancer,” Setlur said during Tuesday’s teleconference.