Differential expression of Met/hepatocyte growth factor receptor in subtypes of non-small cell lung cancers

Tsao, Ming‐Sound; Liu, Geoffrey; Chen, Jim-Ray; Pappas, Jane J.; Ho, J. C.; To, Christine; Viallet, Jean; Park, Morag; Zhu, Hong

doi:10.1016/s0169-5002(98)00007-5

Cited by 107 publications

(79 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…27 Cases were scored into 0 (absent or only focal weak), 1 (weak to moderate in ≤ 40% of tumor cells), 2 (weak to moderate in ≥ 40% of tumor cells), and 3 (strong in ≥ 10% of tumor cells); and then classified into negative (score 0 or 1) and positive (score 2 or 3) for EGFR and MET expression. ERBB2 expression was scored from 0 to 3+ according to the FDAapproved guidelines for the HercepTest and cases with scores of 2+ or 3+ were considered positive for expression.…”

Section: Patients and Samplesmentioning

confidence: 99%

Clinicopathologic analysis of programmed cell death-1 and programmed cell death-ligand 1 and 2 expressions in pulmonary adenocarcinoma: comparison with histology and driver oncogenic alteration status

et al. 2015

View full text Add to dashboard Cite

Immunotherapies targeting the programmed cell death-1/programmed cell death-ligand 1 pathway have emerged as promising therapeutic strategies for lung cancer. However, the expression pattern and prognostic implications of programmed cell death-ligand 1 and 2 and programmed cell death-1 in comparison with the histology and genetic alterations in pulmonary adenocarcinomas remains unclear and thus were addressed here. Programmed cell death-ligand 1 and 2 expression in tumor cells and the quantities of programmed cell death-1 + and CD8 + tumor-infiltrating lymphocytes were immunohistochemically evaluated in 497 resected pulmonary adenocarcinomas and analyzed according to clinicopathological and genetic statuses. Programmed cell death-ligand 1 and 2 expression were observed in 59% and 64% of pulmonary adenocarcinomas, respectively, and showed a strong positive correlation with each other (Po 0.001). Programmed cell death-ligand 1 expression was higher in nodal metastasis cases (P = 0.006), smokers (P = 0.056), poorly differentiated tumors and histologic subtypes of solid and micropapillary patterns (Po0.001). There was no significant difference in programmed cell death-ligand 1 and 2 expression according to EGFR mutation status. However, programmed cell death-ligand 1 expression was correlated with ALK translocation (P = 0.054) and expression of EGFR and MET (Po 0.001). Meanwhile, programmed cell death-ligand 2 expression was correlated with ALK translocation (P = 0.052), and expression of MET (Po 0.001) and ERBB2 (P = 0.013). The numbers of CD8 + and programmed cell death-1 + lymphocytes were higher in smokers (P = 0.012 and 0.016) and MET-expressing adenocarcinomas (Po 0.001). Patients expressing programmed cell death-ligand 1 and/or high ratios of programmed cell death-1 + /CD8 + lymphocytes showed shorter disease-free survival (P = 0.001). Our study demonstrated that programmed cell death-ligand 1 and 2 expression varied with histology, EGFR, ALK, MET, and ERBB2 statuses, and activation of the programmed cell death-1/programmed cell death-ligand 1 pathway may be a poor prognostic factor in pulmonary adenocarcinomas.

show abstract

Section: Patients and Samplesmentioning

confidence: 99%

Clinicopathologic analysis of programmed cell death-1 and programmed cell death-ligand 1 and 2 expressions in pulmonary adenocarcinoma: comparison with histology and driver oncogenic alteration status

et al. 2015

View full text Add to dashboard Cite

show abstract

“…MET is commonly overexpressed in NSCLC (Tsao et al, 1998;Ma et al, 2005) and may be a poor prognostic marker (Cheng et al, 2005;Rossi et al, 2005). It has been speculated that MET amplification accounts for approximately 10-20% of acquired resistance to gefitinib and erlotinib (Engelman and Ja¨nne, 2008).…”

Section: Met Amplificationmentioning

confidence: 99%

Overview of molecular testing in non-small-cell lung cancer: mutational analysis, gene copy number, protein expression and other biomarkers of EGFR for the prediction of response to tyrosine kinase inhibitors

2009

View full text Add to dashboard Cite

“…Total cellular RNA was isolated from the frozen tissues, as previously described (Tsao et al, 1998) and purified by the RNeasy Mini kit (Qiagen Inc., Mississauga, ON, Canada). The quality of the RNA preparations was confirmed by the Agilent Bioanalyzer (Agilent Technologies, Palo Alto, CA, USA).…”

Section: Reverse Transcription -Qpcrmentioning

confidence: 99%

Amplification of telomerase (hTERT) gene is a poor prognostic marker in non-small-cell lung cancer

et al. 2006

View full text Add to dashboard Cite

Telomerase reactivation is a hallmark of human carcinogenesis. Increased telomerase activity may result from gene amplification and/or overexpression. This study evaluates the prognostic value of hTERT gene amplification and mRNA overexpression in 144 resectable non-small-cell lung cancer (NSCLC) specimens. The hTERT gene copy number was assessed by quantitative polymerase chain reaction (qPCR) on laser-capture microdissected tumour cells of 81 tumours, and by fluorescence in situ hybridisation (FISH) on a subset of 59 tumours. hTERT mRNA level was determined by reverse transcription (RT) -qPCR in 130 tumours. In total, 57% of (46 out of 81) primary NSCLC specimens demonstrated hTERT amplification, which was significantly more common (Po0.001) in adenocarcinoma (30 out of 40) than in squamous cell carcinoma (13 out of 37). The hTERT mRNA overexpression was noted in 74% (94 out of 130) of tumours; it was more frequent in squamous cell than in adenocarcinoma (87 vs 68%, P ¼ 0.03). Overexpression was significantly associated with amplification (P ¼ 0.03), especially in adenocarcinoma. The hTERT gene amplification was prognostic for shorter recurrence-free survival (hazard ratio ¼ 2.16, P ¼ 0.03). These data indicate that gene amplification is an important mechanism for hTERT overexpression in lung adenocarcinoma and is an independent poor prognostic marker for disease-free survival in NSCLC.

show abstract

Differential expression of Met/hepatocyte growth factor receptor in subtypes of non-small cell lung cancers

Cited by 107 publications

References 26 publications

Clinicopathologic analysis of programmed cell death-1 and programmed cell death-ligand 1 and 2 expressions in pulmonary adenocarcinoma: comparison with histology and driver oncogenic alteration status

Clinicopathologic analysis of programmed cell death-1 and programmed cell death-ligand 1 and 2 expressions in pulmonary adenocarcinoma: comparison with histology and driver oncogenic alteration status

Overview of molecular testing in non-small-cell lung cancer: mutational analysis, gene copy number, protein expression and other biomarkers of EGFR for the prediction of response to tyrosine kinase inhibitors

Amplification of telomerase (hTERT) gene is a poor prognostic marker in non-small-cell lung cancer

Contact Info

Product

Resources

About