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Statins improve outcomes in high-risk prostate cancer patients treated with definitive radiation therapy

February 19, 2016

"We also evaluated a JAK inhibitor in 10 mouse APL tumors and all of them responded, even those without a mutation in the gene," Wartman says. "This suggests that JAK1 is part of a crucial cancer pathway for this disease. Interestingly, JAK inhibitors are already in clinical trials for a number of cancers."

For Wartman, the research is personal. During his fourth year of medical school at Washington University, he was diagnosed with ALL. Chemotherapy put his cancer into remission, but five years later, it returned. Wartman then was treated with a stem cell transplant from his younger brother. He has now been cancer-free for two and a half years.

"This work is really important for me but also for so many other cancer patients and cancer survivors who want to know why they got cancer in the first place," Wartman says. "We think studies like this can help answer that question."

The researchers also found a large deletion in the Kdm6a (also known as Utx) gene in the mouse tumor genome. A similar deletion was found in another three of 14 mouse APL genomes they studied and in one human AML sample. Deletions in the same gene also have been associated with human cancers, including kidney and esophageal tumors and multiple myeloma, another blood cancer.

Ley says the new research also highlights the value of mouse models of cancer to find important mutations in patients.

"There's been an ongoing debate for 15 years about whether mouse models of cancer are relevant to cancer that develops in people," he explains. "By sequencing this genome, I think the answer is clear: this mouse model is remarkably similar to the human disease. This gives us a new way to use whole-genome sequencing to rapidly identify the most relevant mutations in human cancers."

Looking ahead, the researchers say they will complement their efforts to sequence human cancer genomes with their mouse genome counterparts, when good mouse models are available.

"We expect this to expedite our ability to determine whether mutations in patients are important for disease progression," Wilson says. "If we find the same mutations in human cancers and in a mouse model of the disease, then we know they are likely to be relevant, even if we've only seen the mutations in a small fraction of patients."

SOURCE Washington University School of Medicine