Researchers at the Johns Hopkins Kimmel Cancer Center have found that a gene associated with colorectal cancer, MUTYH, may also play a role in the development of other solid tumors. Their study, published in JCO Precision Oncology, analyzed over 350,000 patient biopsy samples and found that a single mutated copy of MUTYH may lead to a small increased risk of other cancer types.
The researchers, led by Channing Paller and Emmanuel Antonarakis, applied an advanced algorithm to analyze the genetic data of 354,366 solid tumor biopsies stored in the Foundation Medicine database. They found that individuals with a single, mutated copy of MUTYH had a genetic signature of additional genetic mutations and a defective base excision repair (BER) pathway. This genetic signature was associated with a modest increase in susceptibility to a subset of solid tumors, including adrenal gland cancers and pancreatic islet cell tumors.
The study suggests that MUTYH variants might be involved in a broader range of cancers than previously known, and the next question is whether this finding has therapeutic implications. If the BER pathway can be targeted for possible drug sensitivities, doctors might be able to add a new therapeutic approach to their arsenal of tools against solid cancers.