Premium
Inactivation of the PTEN/MMAC1/TEP1 gene in human lung cancers
Author(s) -
Kohno Takashi,
Takahashi Mina,
Manda Ryokuhei,
Yokota Jun
Publication year - 1998
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199806)22:2<152::aid-gcc10>3.0.co;2-s
Subject(s) - pten , cancer research , frameshift mutation , biology , tumor suppressor gene , nonsense mutation , missense mutation , mutation , lung cancer , gene , carcinogenesis , pathology , genetics , medicine , pi3k/akt/mtor pathway , apoptosis
The PTEN/MMAC1/TEP1 gene has been isolated as a tumor suppressor gene that is altered in several types of human tumors including brain, breast, and prostate cancers. In the present study, we report PTEN/MMAC1/TEP1 alterations in human lung cancers. Intragenic homozygous deletions were detected in 6 (40%) of 15 small cell lung carcinoma (SCLC) cell lines and in 2 (8%) of 25 non–small cell lung carcinoma (NSCLC) cell lines. A nonsense mutation and a missense mutation were detected in 2 (8%) NSCLC cell lines. An intragenic homozygous deletion, a 1‐bp frameshift mutation, and a nonsense somatic mutation were also detected in three (6%) of 47 surgical specimens. All the lung tumors with PTEN/MMAC1/TEP1 mutations were homozygous for the mutant alleles. These findings suggest that PTEN/MMAC1/TEP1 plays a role as a tumor suppressor gene in the genesis and/or progression of human lung cancer. Genes Chromosomes Cancer 22:152–156, 1998. © 1998 Wiley‐Liss, Inc.