Click
here to close Hello! We notice that
you are using Internet Explorer, which is not supported by Echinobase
and may cause the site to display incorrectly. We suggest using a
current version of Chrome,
FireFox,
or Safari.
Thorac Cancer
2014 May 01;53:255-60. doi: 10.1111/1759-7714.12101.
Show Gene links
Show Anatomy links
Analysis of clinicopathological features of the echinoderm microtubule-associated protein-like-4-anaplastic lymphoma kinase fusion gene in Chinese patients with advanced non-small-cell lung cancer.
Liu YT
,
Shi YK
,
Hao XZ
,
Wang L
,
Li JL
,
Han XH
,
Li D
,
Zhou YJ
,
Tang L
.
Abstract
BACKGROUND: The echinoderm microtubule-associated protein-like-4-anaplastic lymphoma kinase (EML4-ALK) fusion gene defines a novel molecular subset of non-small-cell lung cancer (NSCLC). However, the clinicopathological features of patients with the EML4-ALK fusion gene have not been defined completely.
METHODS: Clinicopathological data of 200 Chinese patients with advanced NSCLC were analyzed retrospectively to explore their possible correlations with EML4-ALK fusions.
RESULTS: The EML4-ALK fusion gene was detected in 56 (28.0%) of the 200 NSCLC patients, and undetected in 22 (11.0%) patients because of an insufficient amount of pathological tissue. The median age of the patients with positive and negative EML4-ALK was 48 and 55 years, respectively. Patients with the EML4-ALK fusion gene were significantly younger (P< 0.001). The detection rate of the EML4-ALK fusion gene in patients who received primary tumor or metastatic lymph node resection was significantly higher than in patients who received fine-needle biopsy (P= 0.003). The detection rate of the EML4-ALK fusion gene in patients with a time lag from obtainment of the pathological tissue to EML4-ALK fusion gene detection ≤48 months was significantly higher than in patients >48 months (P= 0.020). The occurrence of the EML4-ALK fusion gene in patients with wild-type epidermal growth factor receptor (EGFR) was significantly higher than in patients with mutant-type EGFR (42.5% [37/87] vs. 6.3% [1/16], P= 0.005).
CONCLUSIONS: Younger age and wild-type EGFR were identified as clinicopathological characteristics of patients with advanced NSCLC who harbored the EML4-ALK fusion gene. The optimal time lag from the obtainment of the pathological tissue to the time of EML4-ALK fusion gene detection is ≤48 months.
Barreca,
Anaplastic lymphoma kinase in human cancer.
2011, Pubmed
Barreca,
Anaplastic lymphoma kinase in human cancer.
2011,
Pubmed
Camidge,
Optimizing the detection of lung cancer patients harboring anaplastic lymphoma kinase (ALK) gene rearrangements potentially suitable for ALK inhibitor treatment.
2010,
Pubmed
Dimou,
From the bench to bedside: biological and methodology considerations for the future of companion diagnostics in nonsmall cell lung cancer.
2011,
Pubmed
Gridelli,
Lung cancer in the elderly.
1997,
Pubmed
Inamura,
EML4-ALK fusion is linked to histological characteristics in a subset of lung cancers.
2008,
Pubmed
,
Echinobase
Koivunen,
EML4-ALK fusion gene and efficacy of an ALK kinase inhibitor in lung cancer.
2008,
Pubmed
McLeer-Florin,
Dual IHC and FISH testing for ALK gene rearrangement in lung adenocarcinomas in a routine practice: a French study.
2012,
Pubmed
Paik,
Screening of anaplastic lymphoma kinase rearrangement by immunohistochemistry in non-small cell lung cancer: correlation with fluorescence in situ hybridization.
2011,
Pubmed
Perner,
EML4-ALK fusion lung cancer: a rare acquired event.
2008,
Pubmed
Rikova,
Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer.
2007,
Pubmed
Rodig,
Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population.
2009,
Pubmed
Shaw,
Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK.
2009,
Pubmed
Shinmura,
EML4-ALK fusion transcripts, but no NPM-, TPM3-, CLTC-, ATIC-, or TFG-ALK fusion transcripts, in non-small cell lung carcinomas.
2008,
Pubmed
Soda,
Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer.
2007,
Pubmed
,
Echinobase
Takahashi,
Clinicopathologic features of non-small-cell lung cancer with EML4-ALK fusion gene.
2010,
Pubmed
,
Echinobase
Takeuchi,
Multiplex reverse transcription-PCR screening for EML4-ALK fusion transcripts.
2008,
Pubmed
Wong,
The EML4-ALK fusion gene is involved in various histologic types of lung cancers from nonsmokers with wild-type EGFR and KRAS.
2009,
Pubmed
,
Echinobase
Yi,
Correlation of IHC and FISH for ALK gene rearrangement in non-small cell lung carcinoma: IHC score algorithm for FISH.
2011,
Pubmed
Zhang,
Fusion of EML4 and ALK is associated with development of lung adenocarcinomas lacking EGFR and KRAS mutations and is correlated with ALK expression.
2010,
Pubmed