We found that the co-occurrence of early TP53 mutations in ALK+ NSCLC can lead to chromosomal instability: 24% of TP53-mutated patients showed amplifications of known cancer genes such as MYC (14%), CCND1 (10%), TERT (5%), BIRC2 (5%), ORAOV1 (5%), and YAP1 (5%).
The clinical development candidate CCT245737 is an orally active CHK1 inhibitor with preclinical activity in RAS mutant NSCLC and Eµ-MYC driven B-cell lymphoma.
Overexpression of epidermal growth factor receptor (EGF-R), K-ras gene mutations and c-myc gene amplification were studied in tumor and normal lung tissues from 100 patients with non-small cell lung cancer.
Remarkable advances in the understanding of NSCLC cancer biology have been made over the past decade, including the discovery of critical mutations in oncogenes (i.e., mutation of K-Ras and c-myc gene), as well as the loss of tumor-suppressor genes, such as TP53, 16INK4, or Rb.
This report has important clinical implications for the treatment of patients with neuroblastoma or other tumors that overexpress MYC(N) and harbor ALK mutations, such as non-small-cell lung cancer.
Moreover, pathway analysis and knockdown studies suggest a role for MYC transcriptional activity in the expression of these pathways in KRAS-mutant NSCLC cells.
These results suggest that low dose erlotinib-cisplatin combination exhibits its anti-tumor activity by targeting angiogenesis through the modulation of the c-MYC/HIF-1α/VEGF pathway in NSCLC with EGFR exon 19 deletions.
However, information concerning three oncogenes may soon prove to be helpful in the clinical arena: the myc genes in SCLC, and the ras genes and c-erbB-2 in NSCLC.
SCT signs indicated that swollen lymph nodes and spiculation, spinous process and deep lobulation signs often occurred in the chest of NSCLC patients, and pleural indentation appeared in the majority of patients; the chi-square test results showed that the positive rates of p53 and c-Myc proteins were not related to pathological types of NSCLC, but significantly correlated with tumor differentiation (p<0.05); the positive rates of p53 and c-Myc proteins were correlated with tumor diameter, spiculation and deep lobulation signs and lymph node metastasis (p<0.05), but not associated with spinous process, vacuole and pleural indentation signs (p>0.05).
NDRG1 promoted stem-like properties of LTICs in NSCLC including iPSC (induced pluripotent stem cell) factors (OCT4, SOX2, KLF4, and C-MYC), the spheres-forming ability and the tumorigenicity of NSCLC.
An enzyme-linked immunosorbent assay (ELISA) was developed in-house to examine plasma IgG antibodies for three linear peptide antigens derived from BIRC5a, BIRC5b, and MYC in 211 patients with NSCLC and 200 control subjects.
Expression of PD-L1 in NSCLC tissues was analyzed by immunostaining using a PD-L1 (22C3) PharmDx protocol using the Dako Automated Link 48 platform and expression of MYC was determined using anti-c-MYC (Y69) (ab320720).
Here, prostaglandin E2 (PGE2) exposure rapidly upregulates the expression of the MYC gene followed by the elevation of miR-17-92 levels, which in turn suppresses PTEN expression, thus enhancing apoptosis resistance in non-small cell lung cancer (NSCLC) cells.
We have employed multiplexed stable isotope-resolved metabolomics to track the metabolism of [<sup>13</sup>C<sub>6</sub>]glucose, D<sub>2</sub>-glycine, [<sup>13</sup>C<sub>2</sub>]glycine, and D<sub>3</sub>-serine into purine nucleotides in freshly resected cancerous and matched noncancerous lung tissues from nonsmall cell lung cancer (NSCLC) patients, and we compared the metabolism with established NSCLC PC9 and A549 cell lines <i>in vitro</i> Surprisingly, [<sup>13</sup>C<sub>6</sub>]glucose was the best carbon source for purine synthesis in human NSCLC tissues, in contrast to the noncancerous lung tissues from the same patient, which showed lower mitotic indices and MYC expression.
Sulforaphane inhibits cancer stem-like cell properties and cisplatin resistance through miR-214-mediated downregulation of c-MYC in non-small cell lung cancer.