Molecular biology of lung cancer
Cooper, WA; Lam, DC; O'Toole, SA; Minna, JD
HERO ID
2218106
Reference Type
Journal Article
Subtype
Review
Year
2013
Language
English
PMID
| HERO ID | 2218106 |
|---|---|
| Material Type | Review |
| In Press | No |
| Year | 2013 |
| Title | Molecular biology of lung cancer |
| Authors | Cooper, WA; Lam, DC; O'Toole, SA; Minna, JD |
| Journal | Journal of Thoracic Disease |
| Volume | 5 |
| Issue | Suppl 5 |
| Page Numbers | S479-S490 |
| Abstract | Lung cancers are characterised by abundant genetic diversity with relatively few recurrent mutations occurring at high frequency. However, the genetic alterations often affect a common group of oncogenic signalling pathways. There have been vast improvements in our understanding of the molecular biology that underpins lung cancer in recent years and this has led to a revolution in the diagnosis and treatment of lung adenocarcinomas (ADC) based on the genotype of an individual's tumour. New technologies are identifying key and potentially targetable genetic aberrations not only in adenocarcinoma but also in squamous cell carcinoma (SCC) of the lung. Lung cancer mutations have been identified in v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS), epidermal growth factor receptor (EGFR), BRAF and the parallel phosphatidylinositol 3-kinase (PI3K) pathway oncogenes and more recently in MEK and HER2 while structural rearrangements in ALK, ROS1 and possibly rearranged during transfection (RET) provide new therapeutic targets. Amplification is another mechanism of activation of oncogenes such as MET in adenocarcinoma, fibroblastgrowth factor receptor 1 (FGFR1) and discoidin domain receptor 2 (DDR2) in SCC. Intriguingly, many of these genetic alternations are associated with smoking status and with particular racial and gender differences, which may provide insight into the mechanisms of carcinogenesis and role of host factors in lung cancer development and progression. The role of tumour suppressor genes is increasingly recognised with aberrations reported in TP53, PTEN, RB1, LKB11 and p16/CDKN2A. Identification of biologically significant genetic alterations in lung cancer that lead to activation of oncogenes and inactivation of tumour suppressor genes has the potential to provide further therapeutic opportunities. It is hoped that these discoveries may make a major contribution to improving outcome for patients with this poor prognosis disease. |
| Doi | 10.3978/j.issn.2072-1439.2013.08.03 |
| Pmid | 24163741 |
| Is Certified Translation | No |
| Dupe Override | No |
| Comments | Journal: Journal of thoracic disease ISSN: 2072-1439 |
| Is Public | Yes |
| Language Text | English |