Pattern of chromosome 16q loss differs between an atypical proliferative lesion and an intraductal or invasive ductal carcinoma occurring subsequently in the same are of the breast

Citation
H. Tsuda et al., Pattern of chromosome 16q loss differs between an atypical proliferative lesion and an intraductal or invasive ductal carcinoma occurring subsequently in the same are of the breast, MOD PATHOL, 14(5), 2001, pp. 382-388
Citations number
28
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
MODERN PATHOLOGY
ISSN journal
0893-3952 → ACNP
Volume
14
Issue
5
Year of publication
2001
Pages
382 - 388
Database
ISI
SICI code
0893-3952(200105)14:5<382:POC1LD>2.0.ZU;2-E
Abstract
Atypical proliferative lesions of the breast, such as atypical ductal hyper plasia and atypical papilloma, are considered to be precursors of breast ca rcinomas and have frequently been shown to have loss of heterozygosity (LOH ) on chromosome 16q at the DNA level. We evaluated whether an atypical prol iferative lesion and a carcinoma that subsequently occurred in the same are a of the ipsilateral breast were of identical clonal origin in seven patien ts. Using DNA isolated from microdissected archival tissue of epithelial co mponents of both the biopsy specimen of the atypical proliferative lesion a nd the mastectomy specimen of the carcinoma, the pattern of LOH on 16q was compared between these two lesions using polymerase chain reaction -microsa tellite LOH analysis. As a control, LOH on 16q was examined in 13 cases of usual ductal hyperplasia, 10 usual papillomas, and 6 atypical ductal hyperp lasias. In the seven cases, LOH on 16q was detected in three of the six aty pical proliferative lesions and in five of the seven carcinomas, but the al lele with LOH or a deleted region always differed between the two. LOH was detected in both atypical proliferative lesions and carcinomas in one case, only in the atypical proliferative lesion in two cases, and only in carcin omas in three cases. In the controls, LOH on 16q was absent in usual ductal hyperplasias or usual papillomas but was detected in two of six atypical d uctal hyperplasias. Although atypical proliferative lesions were frequently confirmed to be of clonal nature with LOH on 16q, these lesions and carcin omas were considered to be clones, probably originated from a held with the se clones.