Clinicopathological features of younger (aged ≤ 50 years) lung adenocarcinoma patients harboring the EML4-ALK fusion gene

Takuro Kometani, Kenji Sugio, Atsushi Osoegawa, Takashi Seto, Yukito Ichinose

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background: The EML4-ALK fusion gene has recently been identified as a driver mutation in a subset of non-small cell lung cancers. In subsequent studies, EML4-ALK has been detected in a low percentage of patients, and was associated with a lack of EGFR or KRAS mutations, younger age, and adenocarcinoma with acinar histology. Cases with the EML4-ALK fusion gene were examined to clarify the clinicopathological characteristics of young adenocarcinoma patients. Methods: Between December 1998 and May 2009, 85 patients aged ≤ 50 with lung adenocarcinoma were treated at our hospital. We examined 49 samples from adenocarcinoma patients who underwent surgical resection, chemotherapy, and/or radiotherapy for the EML4-ALK gene. None of the patients received ALK inhibitors because these drugs had not been approved in Japan before 2012. EML4-ALK fusion genes were screened using multiplex reverse-transcription PCR assay, and were confirmed by direct sequencing. Results: The EML4-ALK fusion gene was detected in five tumors (10.2%). One patient had stage IB disease, one had stage IIIA, and three had stage IV. Histologically, there was one solid adenocarcinoma, two acinar adenocarcinomas, and two papillary adenocarcinomas. EML4-ALK fusion genes were mutually exclusive to EGFR and KRAS mutations. The five-year survival rate was 59.4% in patients without EML4-ALK fusion and was not reached in patients with EML4-ALK fusion. Conclusion: The EML4-ALK fusion gene may be a strong oncogene in younger patients with lung adenocarcinoma.

Original languageEnglish
Pages (from-to)563-570
Number of pages8
JournalThoracic Cancer
Volume9
Issue number5
DOIs
Publication statusPublished - May 2018
Externally publishedYes

Fingerprint

Gene Fusion
Adenocarcinoma
Mutation
Papillary Adenocarcinoma
Adenocarcinoma of lung
Oncogenes
Non-Small Cell Lung Carcinoma
Reverse Transcription
Histology
Japan
Radiotherapy
Survival Rate
Drug Therapy
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Oncology
  • Pulmonary and Respiratory Medicine

Cite this

Clinicopathological features of younger (aged ≤ 50 years) lung adenocarcinoma patients harboring the EML4-ALK fusion gene. / Kometani, Takuro; Sugio, Kenji; Osoegawa, Atsushi; Seto, Takashi; Ichinose, Yukito.

In: Thoracic Cancer, Vol. 9, No. 5, 05.2018, p. 563-570.

Research output: Contribution to journalArticle

Kometani, Takuro ; Sugio, Kenji ; Osoegawa, Atsushi ; Seto, Takashi ; Ichinose, Yukito. / Clinicopathological features of younger (aged ≤ 50 years) lung adenocarcinoma patients harboring the EML4-ALK fusion gene. In: Thoracic Cancer. 2018 ; Vol. 9, No. 5. pp. 563-570.
@article{29154b5108e840eb8adb5d6cbca56c5e,
title = "Clinicopathological features of younger (aged ≤ 50 years) lung adenocarcinoma patients harboring the EML4-ALK fusion gene",
abstract = "Background: The EML4-ALK fusion gene has recently been identified as a driver mutation in a subset of non-small cell lung cancers. In subsequent studies, EML4-ALK has been detected in a low percentage of patients, and was associated with a lack of EGFR or KRAS mutations, younger age, and adenocarcinoma with acinar histology. Cases with the EML4-ALK fusion gene were examined to clarify the clinicopathological characteristics of young adenocarcinoma patients. Methods: Between December 1998 and May 2009, 85 patients aged ≤ 50 with lung adenocarcinoma were treated at our hospital. We examined 49 samples from adenocarcinoma patients who underwent surgical resection, chemotherapy, and/or radiotherapy for the EML4-ALK gene. None of the patients received ALK inhibitors because these drugs had not been approved in Japan before 2012. EML4-ALK fusion genes were screened using multiplex reverse-transcription PCR assay, and were confirmed by direct sequencing. Results: The EML4-ALK fusion gene was detected in five tumors (10.2{\%}). One patient had stage IB disease, one had stage IIIA, and three had stage IV. Histologically, there was one solid adenocarcinoma, two acinar adenocarcinomas, and two papillary adenocarcinomas. EML4-ALK fusion genes were mutually exclusive to EGFR and KRAS mutations. The five-year survival rate was 59.4{\%} in patients without EML4-ALK fusion and was not reached in patients with EML4-ALK fusion. Conclusion: The EML4-ALK fusion gene may be a strong oncogene in younger patients with lung adenocarcinoma.",
author = "Takuro Kometani and Kenji Sugio and Atsushi Osoegawa and Takashi Seto and Yukito Ichinose",
year = "2018",
month = "5",
doi = "10.1111/1759-7714.12616",
language = "English",
volume = "9",
pages = "563--570",
journal = "Thoracic Cancer",
issn = "1759-7706",
publisher = "Blackwell Publishing Asia Pty Ltd",
number = "5",

}

TY - JOUR

T1 - Clinicopathological features of younger (aged ≤ 50 years) lung adenocarcinoma patients harboring the EML4-ALK fusion gene

AU - Kometani, Takuro

AU - Sugio, Kenji

AU - Osoegawa, Atsushi

AU - Seto, Takashi

AU - Ichinose, Yukito

PY - 2018/5

Y1 - 2018/5

N2 - Background: The EML4-ALK fusion gene has recently been identified as a driver mutation in a subset of non-small cell lung cancers. In subsequent studies, EML4-ALK has been detected in a low percentage of patients, and was associated with a lack of EGFR or KRAS mutations, younger age, and adenocarcinoma with acinar histology. Cases with the EML4-ALK fusion gene were examined to clarify the clinicopathological characteristics of young adenocarcinoma patients. Methods: Between December 1998 and May 2009, 85 patients aged ≤ 50 with lung adenocarcinoma were treated at our hospital. We examined 49 samples from adenocarcinoma patients who underwent surgical resection, chemotherapy, and/or radiotherapy for the EML4-ALK gene. None of the patients received ALK inhibitors because these drugs had not been approved in Japan before 2012. EML4-ALK fusion genes were screened using multiplex reverse-transcription PCR assay, and were confirmed by direct sequencing. Results: The EML4-ALK fusion gene was detected in five tumors (10.2%). One patient had stage IB disease, one had stage IIIA, and three had stage IV. Histologically, there was one solid adenocarcinoma, two acinar adenocarcinomas, and two papillary adenocarcinomas. EML4-ALK fusion genes were mutually exclusive to EGFR and KRAS mutations. The five-year survival rate was 59.4% in patients without EML4-ALK fusion and was not reached in patients with EML4-ALK fusion. Conclusion: The EML4-ALK fusion gene may be a strong oncogene in younger patients with lung adenocarcinoma.

AB - Background: The EML4-ALK fusion gene has recently been identified as a driver mutation in a subset of non-small cell lung cancers. In subsequent studies, EML4-ALK has been detected in a low percentage of patients, and was associated with a lack of EGFR or KRAS mutations, younger age, and adenocarcinoma with acinar histology. Cases with the EML4-ALK fusion gene were examined to clarify the clinicopathological characteristics of young adenocarcinoma patients. Methods: Between December 1998 and May 2009, 85 patients aged ≤ 50 with lung adenocarcinoma were treated at our hospital. We examined 49 samples from adenocarcinoma patients who underwent surgical resection, chemotherapy, and/or radiotherapy for the EML4-ALK gene. None of the patients received ALK inhibitors because these drugs had not been approved in Japan before 2012. EML4-ALK fusion genes were screened using multiplex reverse-transcription PCR assay, and were confirmed by direct sequencing. Results: The EML4-ALK fusion gene was detected in five tumors (10.2%). One patient had stage IB disease, one had stage IIIA, and three had stage IV. Histologically, there was one solid adenocarcinoma, two acinar adenocarcinomas, and two papillary adenocarcinomas. EML4-ALK fusion genes were mutually exclusive to EGFR and KRAS mutations. The five-year survival rate was 59.4% in patients without EML4-ALK fusion and was not reached in patients with EML4-ALK fusion. Conclusion: The EML4-ALK fusion gene may be a strong oncogene in younger patients with lung adenocarcinoma.

UR - http://www.scopus.com/inward/record.url?scp=85046082319&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85046082319&partnerID=8YFLogxK

U2 - 10.1111/1759-7714.12616

DO - 10.1111/1759-7714.12616

M3 - Article

C2 - 29517858

AN - SCOPUS:85046082319

VL - 9

SP - 563

EP - 570

JO - Thoracic Cancer

JF - Thoracic Cancer

SN - 1759-7706

IS - 5

ER -