Open AccessRAPID COMMUNICATION
Author(s) -
Suzuki Kazufumi,
Daigo Yataro,
Fukuda Seisuke,
Tokino Takashi,
Isomura Minoru,
Isono Kaichi,
Wainwright Brandon,
Nakamura Yusuke
Publication year - 1997
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1997.tb00370.x
Subject(s) - loss of heterozygosity , esophagus , carcinogenesis , biology , tumor suppressor gene , pathology , cancer research , exon , epidermoid carcinoma , lung cancer , cell , gene , carcinoma , allele , genetics , medicine , anatomy
The high frequency of loss of heterozygosity that has been observed on the distal region of the long arm of chromosome 9 in squamous cell carcinomas of esophagus, lung, uterus, and head and neck indicates the presence of a tumor suppressor gene(s) in this region. To investigate the possible role of the PTC gene on chromosome 9q22.3, that was identified as the cause of nevoid basal cell carcinoma syndrome, during carcinogenesis in esophagus and lung, we examined 20 esophageal squamous cell carcinomas and 10 squamous cell carcinomas of the lung for mutations in any coding exon of PTC. Using single‐strand conformation polymorphism and direct sequencing, we detected no mutations other than two non‐deleterious polymorphisms. Our results suggest that inactivation of some tumor suppressor gene(s) on 9q other than PTC contributes to the development of squamous cell carcinomas in these tissues.