Accumulation of chromosomal imbalances from intraductal proliferative lesions to adjacent in situ and invasive ductal breast cancer

Aubele, M. M., Cummings, M. C., Mattis, A. E., Zitzelsberger, H. F., Walch, A. K., Kremer, M., Hofler, H. and Werner, M (2000) Accumulation of chromosomal imbalances from intraductal proliferative lesions to adjacent in situ and invasive ductal breast cancer. Diagnostic Molecular Pathology, 9 1: 14-19.


Author Aubele, M. M.
Cummings, M. C.
Mattis, A. E.
Zitzelsberger, H. F.
Walch, A. K.
Kremer, M.
Hofler, H.
Werner, M
Title Accumulation of chromosomal imbalances from intraductal proliferative lesions to adjacent in situ and invasive ductal breast cancer
Journal name Diagnostic Molecular Pathology   Check publisher's open access policy
Publication date 2000
Sub-type Article
DOI 10.1097/00019606-200003000-00003
Volume number 9
Issue number 1
ISSN 1052-9551
Start page 14
End page 19
Total pages 6
Place of publication Philadelphia, U.S.A.
Publisher Williams & Wilkins
Collection year 2000
Language eng
Subject C1
321020 Pathology
730108 Cancer and related disorders
Abstract Carcinoma of the breast is thought to evolve through a sequential progression from normal to proliferative epithelium and eventually into carcinoma. Here lumpectomy specimens from five patients were studied, selected for the presence of ductal hyperplasia without atypia, atypical ductal hyperplasia. ductal carcinoma in situ, and invasive ductal carcinoma. Laser microdissection of tissue allowed precise sampling and direct correlation of phenotypic and genotypic changes. Analyses of the samples revealed an increasing mean number of chromosomal changes occurring with increasing histologic severity, and for the first time chromosomal abnormalities were demonstrated in ductal hyperplasia without atypia. Chromosomal changes found in each of the four histologic entities included gains on 10q, 12q, 16p, and 20q and loss on 13q. In ductal hyperplasia without atypia, gain on 20q as well as loss on 13q was detected with high frequency (four of five samples). Alterations identified in more than 50% of atypical ductal hyperplasia samples included gains on 3p, 8q, 15q, and 22q and loss on 16q. In ductal carcinoma in situ, gain of DNA on Iq and 17q and loss on 4q were additionally found, and in invasive ductal carcinoma, further gains on 6p, 10q, 11q13, and 17p were identified. The chromosomal alterations occurring in the different histopathologic lesions strongly suggest that these regions harbor tumor suppressor genes or oncogenes significant for the development of ductal carcinoma of the breast.
Keyword Biochemistry & Molecular Biology
Biotechnology & Applied Microbiology
Pathology
Breast Cancer
Development And Progression
Comparative Genomic Hybridization
Laser Microdissection
Degenerate Oligonucleotide Primed Polymerase Chain Reaction
Carcinoma-in-situ
Term Follow-up
Oligonucleotide-primed Pcr
Increased Copy Number
Genetic Alterations
Dna Amplification
Solid Tumors
Cytogenetic Analysis
Hyperplasia
Q-Index Code C1

Document type: Journal Article
Sub-type: Article
Collection: School of Chemistry and Molecular Biosciences
 
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