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Restoring PTPN12 function may prevent tumorigenesis in triple-negative breast cancer
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PTNPN12 tyrosine phosphatase, a tumor suppressing gene present in normal cells, was inactive in 60% of women with triple-negative breast cancer, said Stephen Elledge, PhD, this afternoon in a press conference. Restoring functionality may provide a new option for women who have few treatments for this disease.
“We found that when we take away this particular gene, there are multiple oncogenes that get turned on to drive tumorigenesis in these cells,” said Elledge, professor of genetics at Harvard Medical School and Brigham and Women’s Hospital. “We believe some of these cancers may be treatable with current drugs because this process unleashes oncogenes for which we already have drugs. These drugs already exist. We don’t have to put them through the pipeline; we just have to learn to use them better.”
He discussed the research during a press conference at the Era of Hope conference in Orlando, Fla. The conference aims to advance breast cancer research by bringing together scientists, clinicians and breast cancer advocates to discuss research funded by the Department of Defense Breast Cancer Research Program.
Elledge said multiple genetic alterations are needed to turn human mammary epithelial cells into various stages of cancer. To find the phenotype changes associated with tumorigenesis, researchers collected cells with a number of lesions and introduced various genetic changes, then looked for anchorage independent growth.
They determined that PTPN12 suppressed the growth and transformation of mammary epithelial cells. Restoring PTPN12 function in triple-negative breast cancer cells may block tumor formation and prevent metastasis.
The same effect is present in cells with inhibition of PTPN12-regulated tyrosine kinases. Elledge suggests triple-negative breast cancer cells are dependent on proto-oncogenic tyrosine kinases constrained by PTPN12.
“If we know which of these tyrosine kinases are activated, we do know some of them and we’ll figure out more, we can use drugs in combination to turn them off,” he said. “We already have drugs for many of these kinases and that’s what’s exciting about this. As we carry this work forward, we will be looking for other genes like PTPN12 that restrain normal tyrosine kinase signaling.” – by Jason Harris
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