<i>CD274</i> amplification was caused by genomic rearrangements not affecting the open reading frame, thus leading to massively increased <i>CD274</i> transcripts and high level expression of PD-L1.<b>Conclusions:</b> A subset (4/210, 1.9%) of human SCLC patient cases exhibits massive expression of PD-L1 caused by focal amplification of <i>CD274</i> Such tumors may be particularly susceptible to immune checkpoint blockade.<i></i>.
2019;12:eaau2922) shows that inhibition of the LSD1 demethylase can induce derepression of NOTCH receptor genes and subsequent activation of the NOTCH pathway, potently suppressing the growth of SCLC.
2019;12:eaau2922) shows that inhibition of the LSD1 demethylase can induce derepression of NOTCH receptor genes and subsequent activation of the NOTCH pathway, potently suppressing the growth of SCLC.
2019;https://doi.org/10.1158/2159-8290.CD-18-1020) demonstrated that DDR inhibition can activate the stimulator of interferon genes (STING) innate immune pathway, providing strong rationale for combining DDR inhibition and ICB to treat SCLC.
3p14.2 allele loss was very frequent in 32 lung cancer cell lines [100% of small cell lung cancer and 88% of non-small cell lung cancer (NSCLC)] and 108 primary NSCLC cancers (45%), with numerous breakpoints indicating involvement of several distinct regions in the FRA3B site.
6-(7-Nitro-2,1,3-benzoxadiazol-4-ylthio)hexanol, a specific glutathione S-transferase inhibitor, overcomes the multidrug resistance (MDR)-associated protein 1-mediated MDR in small cell lung cancer.
Small-cell lung cancer is characterized by molecular aberrancies such as overexpression of the antiapoptotic protein Bcl-2, which is regulated in part by the inhibitory IkappaB, a target of the ubiquitin-proteasome degradative pathway.
Small cell lung cancer exhibited increased expression of MRP5, activation of Wnt pathway inhibitors, and upregulation of p38 MAPK activating genes, while NSCLC showed downregulation of CDKN2A, and upregulation of MAPK9 and EGFR.
Small-cell lung cancer (SCLC) is an excellent candidate for early detection given there are no successful therapeutic options for late-stage disease, and it displays almost universal inactivation of TP53.
Small cell lung cancer (SCLC) transformation is one of the resistance mechanisms associated with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs).