PMID- 21718596
OWN - NLM
STAT- MEDLINE
DCOM- 20130320
LR  - 20211203
IS  - 1000-467X (Print)
IS  - 1944-446X (Electronic)
IS  - 1944-446X (Linking)
VI  - 30
IP  - 7
DP  - 2011 Jul
TI  - Correlation of genes associated with drug response to prognosis of large cell 
      lung carcinoma.
PG  - 497-504
LID - 10.5732/cjc.010.10503 [doi]
AB  - Platinum-based chemotherapy remains the main treatment of advanced lung cancer. 
      However, platinum resistance has become a major treatment obstacle. Novel 
      therapies, particularly tyrosine kinase inhibitors of the epidermal growth factor 
      receptor (EGFR-TKI) and agents that target vascular endothelial growth factor 
      (VEGF), have improved the treatment. Both chemotherapy and targeted therapy have 
      their molecular mechanisms. This study aimed to determine the mutation, 
      amplification, or expression status and interrelationships of the epidermal 
      growth factor receptor (EGFR), K-Ras proto-oncogene, excision repair 
      cross-complementation group 1 (ERCC1), and VEGF genes as well as their 
      correlations to prognosis of large cell lung carcinoma (LCLC) after EGFR-targeted 
      therapy, chemotherapy, and anti-VEGF therapy. EGFR and K-Ras mutations in 60 
      specimens of LCLC were detected by direct DNA sequencing. EGFR, ERCC1, and VEGF 
      protein expression was detected by immunohistochemistry (IHC). EGFR gene copy 
      number was detected by fluorescence in situ hybridization (FISH). One (1.7%) 
      patient had an EGFR L858M point mutation in exon 21, 3 (5.0%) had K-Ras 
      mutations, and 10 (19.6%) had EGFR amplification (FISH positive). Positive rates 
      of EGFR, ERCC1, and VEGF proteins were 38.3%, 56.7%, and 70.0%, respectively. 
      EGFR amplification was positively correlated to EGFR protein expression (r = 
      0.390, P = 0.005). The positive rate of VEGF protein was significantly higher in 
      patients with lymph node metastasis than in those without (84.6% vs. 58.8%, P = 
      0.046). No significant correlations were observed among the EGFR, K-Ras, ERCC1, 
      and VEGF genes. EGFR gene amplification and the low rate of EGFR mutation suggest 
      that patients with LCLC are likely to obtain little benefit from anti-EGFR 
      therapies.
FAU - Chen, Cheng
AU  - Chen C
AD  - Department of Medical Thoracic Oncology, Tianjin Medical University Cancer 
      Institute and Hospital, Tianjin 300060, P. R. China.
FAU - Jiang, Xiang-Li
AU  - Jiang XL
FAU - Zhang, Cui-Cui
AU  - Zhang CC
FAU - Li, Kai
AU  - Li K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Chin J Cancer
JT  - Chinese journal of cancer
JID - 101498232
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (MAS1 protein, human)
RN  - 0 (Proto-Oncogene Mas)
RN  - 0 (VEGFA protein, human)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - EC 2.7.10.1 (EGFR protein, human)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 3.1.- (ERCC1 protein, human)
RN  - EC 3.1.- (Endonucleases)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Carcinoma, Large Cell/drug therapy/*genetics/metabolism/pathology
MH  - DNA-Binding Proteins/*metabolism
MH  - Endonucleases/*metabolism
MH  - ErbB Receptors/*genetics/metabolism
MH  - Female
MH  - Gene Amplification
MH  - Genes, ras/*genetics
MH  - Humans
MH  - Lung Neoplasms/drug therapy/*genetics/metabolism/pathology
MH  - Lymphatic Metastasis
MH  - Male
MH  - Middle Aged
MH  - Mutation
MH  - Neoplasm Staging
MH  - Proto-Oncogene Mas
MH  - Survival Rate
MH  - Vascular Endothelial Growth Factor A/*metabolism
PMC - PMC4013425
EDAT- 2011/07/02 06:00
MHDA- 2013/03/21 06:00
PMCR- 2011/07/01
CRDT- 2011/07/02 06:00
PHST- 2011/07/02 06:00 [entrez]
PHST- 2011/07/02 06:00 [pubmed]
PHST- 2013/03/21 06:00 [medline]
PHST- 2011/07/01 00:00 [pmc-release]
AID - cjc.010.10503 [pii]
AID - cjc-30-07-497 [pii]
AID - 10.5732/cjc.010.10503 [doi]
PST - ppublish
SO  - Chin J Cancer. 2011 Jul;30(7):497-504. doi: 10.5732/cjc.010.10503.