New Gene Target Discovered for Aggressive Lung Cancer
Small-cell lung cancer is a rare and fast-growing disease. Characterised by the formation of malignant (cancer) cells in the tissues of the lung, it can be fatal if left untreated. The aggressive form of lung cancer typically affects chronic smokers.
Whilst early disease detection can significantly improve survival rates, treatment options have remained relatively unchanged over the years. Chemotherapy is currently the primary treatment option for patients suffering from small-cell lung cancer. However, a large population will develop chemo-resistance, impacting treatment efficacy and leading to cancer reoccurrence.
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However, all that may change following the latest discovery in biomarkers diagnostics. Scientists at Northwestern Medicine have identified a new gene responsible for activating an aggressive subtype of small-cell lung cancer. The P subtype is known for having no current effective treatment and was the focus of the study published by the Science Advances journal earlier this month.
Scientists at Northwestern Medicine have named the newly discovered gene target, POU2AF2, after the novel functions documented in the study. They propose that the gene is essential for the tumour P subtype to thrive. Using genome-wide CRISPR screening, the team deleted POU2AF2 in small-cell lung cancer cells in vitro and in mice. Results showed that the cancer cells could not survive without the specific gene’s presence.
Scientists at Northwestern Medicine have named the newly discovered gene, POU2AF2, after the novel functions documented in the study.
“Although small-cell lung cancer consists of approximately 13% of all lung cancer cases, it has one of the lowest 5-year survival rates and a very poor prognosis,” the paper claims. The Northwestern Medicine team now believe that their findings can potentially serve as a biomarker to identify the P subtype of small-cell lung cancer at its earliest stage.
The discovery of the new gene target will likewise improve treatment options and help unlock improved diagnostic possibilities.
Authors of the paper include Aileen Patricia Szczepanski, Natsumi Tsuboyama, Jun Watanabe and Rintaro Hashizume, Zibo Zhao, and Lu Wang. The study was supported by the NIH Maximizing Investigators’ Research Award (MIRA) R35 grant, the Research scholar grant from the American Cancer Society, and the Lynn Sage cancer research grant.
Szczepanski, A.P., et al. (2022) POU2AF2/C11orf53 functions as a coactivator of POU2F3 by maintaining chromatin accessibility and enhancer activity. Science Advances. doi.org/10.1126/sciadv.abq2403.
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