LKB1 modulates lung cancer differentiation and metastasis

By Hongbin Ji, M. R. Ramsey, D. Hayes, C. Fan, Kate L. McNamara, P. Kozlowski, C. Torrice, Michael C. Wu, T. Shimamura, Samanthi A. Perera and 24 more. Nature, 2007

1,083 citations recorded by the source corpus.

Subfields: Cancer Research, Oncology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/c8b1cfceed9f6ff0e924c06896821fe5bebd7493

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Citations in the corpus

Co-occurring genomic alterations define major subsets of KRAS - mutant lung adenocarcinoma with distinct biology, immune profiles, and therapeutic vulnerabilities (2015, positive): “This finding is consistent with prior work in GEMMs of lung adenocarcinoma initiated by somatic activation of an endogenous KrasG12D allele, whereby concomitant genetic inactivation of either Stk11/Lkb1 or Trp53 sufficed to promote fully invasive and widely metastatic lung adenocarcinoma with shorte”
Autophagy in malignant transformation and cancer progression (2015, positive): “Moreover, somatic mutations in STK11 have been documented in a considerable percentage of squamous cell carcinomas and lung adenocarcinomas (Ji et al , 2007).”
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).”
AMPK in Health and Disease. (2009, background): “Since the constitutively active AMPK fragment 1 (1-312) is not activated by the PT1 compound, it is proposed that PT1 acts by reversing the autoinhibition of the AIS (313-335).”
Tumor suppressors and cell metabolism: a recipe for cancer growth. (2009, background): “2002), and complete loss of LKB1 results in resistance to senescence and the development of aggressive cancers (Ji et al. 2007; Contreras et al. 2008; Gurumurthy et al. 2008).”
LKB1 and AMPK control of mTOR signalling and growth (2009, background): “LKB1 mutations are found in NSCLC, which represent 85% of lung cancer, and mutation rate estimates vary between 20% and 40% depending on the study and the methodology employed for detecting LKB1 alterations (Ji et al. 2007, Hezel & Bardeesy 2008).”
Conditional mouse lung cancer models using adenoviral or lentiviral delivery of Cre recombinase (2009, background): “The activation of oncogenic K-ras along with loss of p16 Ink4a or Ink4a/Arf tumor suppressors, which are mutated in 20%–50% of human cases, have been describe”
Regulation of cancer cell metabolism (2011, background): “LKB1 is also frequently mutated in sporadic cases of non-small-cell lung cance”
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 ”
The LKB1-AMPK pathway: metabolism and growth control in tumor suppression (2009, background): “, in which at least 15–35% of cases have this lesio”
Metabolic heterogeneity in human lung tumors (2016, positive): “Oncogene expression is sufficient to reprogram some aspects of nutrient utilization, suggesting that cell-autonomous metabolism is driven in part by the oncogenotype (Gao et al., 2009; Ji et al., 2007; Son et al., 2013).”