Journal
JOURNAL OF CLINICAL PATHOLOGY
Volume 74, Issue 11, Pages 681-685Publisher
BMJ PUBLISHING GROUP
DOI: 10.1136/jclinpath-2021-207906
Keywords
genetics; neoplasms; pathology; molecular; molecular biology
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STK11 gene plays a crucial role in tumorigenesis, with mutations associated with Peutz-Jeghers syndrome, lung adenocarcinoma, and potentially affecting prognosis and response to immunotherapy in cancer patients. Further studies are needed to validate STK11 mutations as a routine clinical biomarker.
STK11 encodes for the protein liver kinase B1, a serine/threonine kinase which is involved in a number of physiological processes including regulation of cellular metabolism, cell polarity and the DNA damage response. It acts as a tumour suppressor via multiple mechanisms, most classically through AMP-activated protein kinase-mediated inhibition of the mammalian target of rapamycin signalling pathway. Germline loss-of-function mutations in STK11 give rise to Peutz-Jeghers syndrome, which is associated with hamartomatous polyps of the gastrointestinal tract, mucocutaneous pigmentation and a substantially increased lifetime risk of many cancers. In the sporadic setting, STK11 mutations are commonly seen in a subset of adenocarcinomas of the lung in addition to a number of other tumours occurring at various sites. Mutations in STK11 have been associated with worse prognoses across a range of malignancies and may be a predictor of poor response to immunotherapy in a subset of lung cancers, though further studies are needed before the presence of STK11 mutations can be implemented as a routine clinical biomarker.
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