Loss of chromosome 16q in lobular carcinoma in situ

Citation
Je. Etzell et al., Loss of chromosome 16q in lobular carcinoma in situ, HUMAN PATH, 32(3), 2001, pp. 292-296
Citations number
31
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
HUMAN PATHOLOGY
ISSN journal
00468177 → ACNP
Volume
32
Issue
3
Year of publication
2001
Pages
292 - 296
Database
ISI
SICI code
0046-8177(200103)32:3<292:LOC1IL>2.0.ZU;2-1
Abstract
Lobular carcinoma in situ (LCIS) and infiltrating lobular carcinoma may rep resent different forms of the same disease based on their frequent clinical association and similar histologic features. Patients with LCIS are at inc reased risk of multicentric and bilateral disease. Thus, LCIS may represent both a precursor to infiltrating lobular carcinoma and a marker of risk fo r breast cancer. To identify genomic alterations in LCIS, comparative genom ic hybridization was performed on 17 cases without concurrent invasive carc inoma. Loss involving chromosome 16q was present in 88% of cases and was th e sole detected alteration in 29%. Gain involving Iq was second in frequenc y, occurring in 41% of tumors, and in all cases was associated with loss of 16q. Other recurrent changes were loss involving 17p (18%), 8p (12%), and 12q24 (12%). E-cadherin immunohistochemistry was performed on all LCIS case s to evaluate the correlation of loss involving 16q22, the site of the E-ca dherin gene, and altered protein expression. Most cases with 16q22 loss sho wed altered E-cadherin expression (12 of 13). These results in LCIS are sim ilar to changes reported in infiltrating lobular cancer, confirming a genet ic relationship between them, HUM PATHOL 32:292-296. Copyright (C) 2001 by W.B. Saunders Company.