Inactivation of LKB1/STK11 is a common event in adenocarcinomas of the lung.

By M. Sanchez-Cespedes, P. Parrella, Manel Esteller, S. Nomoto, B. Trink, J. Engles, W. Westra, J. Herman, D. Sidransky. Cancer Research, 2002

656 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/db418365c6db8399507b921f0e23b01d836cb2a4

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Citations in the corpus

Mapping the hallmarks of lung adenocarcinoma with massively parallel sequencing (2012, background): “Lung adenocarcinomas also often harbor loss-of-function mutations and deletions in tumor suppressor genes TP53, STK11, RB1, NF1, CDKN2A, SMARCA4, and KEAP1 (Ding et al., 2008; Kan et al., 2010; Sanchez-Cespedes et al., 2002).”
AMP-activated protein kinase: an energy sensor that regulates all aspects of cell function. (2011, background): “As expected for a tumor suppressor, the STK11 gene is also frequently mutated in spontaneous cancers, including ;30% of non-small-cell lung cancers (Sanchez-Cespedes et al. 2002; Ji et al. 2007) and 20% of cervical cancers, including the cervical cancer in the patient Henrietta Lacks that gave rise…”
AMP‐activated protein kinase – development of the energy sensor concept (2006, background): “Moreover, mutations in the LKB1 gene are also seen in some sporadic cancers, especially adenocarcinoma of the lung (Sanchez-Cespedes et al. 2002).”
AMPK phosphorylation of raptor mediates a metabolic checkpoint. (2008, background): “In addition, LKB1 mutations occur in a large percentage (30%– 40%) of sporadic non-small-cell lung cancers (NSCLC) (Sanchez-Cespedes et al., 2002; Ji et al., 2007).”
OncodriveFML: a general framework to identify coding and non-coding regions with cancer driver mutations (2016, background): “…a tumor suppressor in the control of the activity of AMP-activated protein kinase (AMPK) family members, thereby playing a role in various processes such as cell metabolism, cell polarity, apoptosis, and DNA damage response, often bearing inactivating mutations in in lung adenocarcinomas [29, 30].”
LKB1 and AMPK control of mTOR signalling and growth (2009, background): “(1) Tumours in Peutz-Jeghers patients or sporadic NSCLC lacking LKB1 may be sensitive to mTORC1 inhibitors including rapamycin analogues or mTOR kinase inhibitors.”