Abstract
Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities.
| Original language | English |
|---|---|
| Pages (from-to) | 527-537 |
| Number of pages | 11 |
| Journal | General Thoracic and Cardiovascular Surgery |
| Volume | 59 |
| Issue number | 8 |
| DOIs | |
| Publication status | Published - Aug 2011 |
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Keywords
- Biology
- Lung cancer
- Molecular oncology
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Surgery
- Pulmonary and Respiratory Medicine
Cite this
Molecular oncology of lung cancer. / Toyooka, Shinichi; Mitsudomi, Tetsuya; Sou, Junichi; Aokage, Keiju; Yamane, Masaomi; Oto, Takahiro; Kiura, Katsuyuki; Miyoshi, Shinichiro.
In: General Thoracic and Cardiovascular Surgery, Vol. 59, No. 8, 08.2011, p. 527-537.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Molecular oncology of lung cancer
AU - Toyooka, Shinichi
AU - Mitsudomi, Tetsuya
AU - Sou, Junichi
AU - Aokage, Keiju
AU - Yamane, Masaomi
AU - Oto, Takahiro
AU - Kiura, Katsuyuki
AU - Miyoshi, Shinichiro
PY - 2011/8
Y1 - 2011/8
N2 - Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities.
AB - Progress in genetic engineering has made it possible to elucidate the molecular biological abnormalities in lung cancer. Mutations in KRAS and P53 genes, loss of specific alleles, and DNA methylation of the tumor suppressor genes were the major abnormalities investigated between 1980 and the 2000s. In 2004, mutations in the epidermal growth factor receptor (EGFR) gene that cause oncogene addiction were discovered in non-small-cell lung cancers (NSCLCs), especially in adenocarcinomas. Because they are strongly associated with sensitivity to EGFR-tyrosine kinase inhibitors (EGFR-TKIs), a great deal of knowledge has been acquired in regard to both EGFR and other genes in the EGFR family and their downstream genes. Moreover, in 2007 the existence of the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene was discovered in NSCLC; and the same as EGFR-TKIs, ALK inhibitors are being found to be highly effective in lung cancers that have this translocation. These discoveries graphically illustrate that molecular biological findings are directly linked to the development of clinical oncology and to improving the survival rates of lung cancer patients. Here, we review the remarkable progress in molecular biological knowledge acquired thus far in regard to lung cancer, especially NSCLC, and the future possibilities.
KW - Biology
KW - Lung cancer
KW - Molecular oncology
UR - http://www.scopus.com/inward/record.url?scp=80052769870&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=80052769870&partnerID=8YFLogxK
U2 - 10.1007/s11748-010-0743-3
DO - 10.1007/s11748-010-0743-3
M3 - Article
C2 - 21850578
AN - SCOPUS:80052769870
VL - 59
SP - 527
EP - 537
JO - General Thoracic and Cardiovascular Surgery
JF - General Thoracic and Cardiovascular Surgery
SN - 1863-6705
IS - 8
ER -