| First Author | Munkhbaatar E | Year | 2020 |
| Journal | Nat Commun | Volume | 11 |
| Issue | 1 | Pages | 4527 |
| PubMed ID | 32913197 | Mgi Jnum | J:297025 |
| Mgi Id | MGI:6468876 | Doi | 10.1038/s41467-020-18372-1 |
| Citation | Munkhbaatar E, et al. (2020) MCL-1 gains occur with high frequency in lung adenocarcinoma and can be targeted therapeutically. Nat Commun 11(1):4527 |
| abstractText | Evasion of programmed cell death represents a critical form of oncogene addiction in cancer cells. Understanding the molecular mechanisms underpinning cancer cell survival despite the oncogenic stress could provide a molecular basis for potential therapeutic interventions. Here we explore the role of pro-survival genes in cancer cell integrity during clonal evolution in non-small cell lung cancer (NSCLC). We identify gains of MCL-1 at high frequency in multiple independent NSCLC cohorts, occurring both clonally and subclonally. Clonal loss of functional TP53 is significantly associated with subclonal gains of MCL-1. In mice, tumour progression is delayed upon pharmacologic or genetic inhibition of MCL-1. These findings reveal that MCL-1 gains occur with high frequency in lung adenocarcinoma and can be targeted therapeutically. |
