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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.
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| Author(s) |
Aubele, M. M. Cummings, M. C. Mattis, A. E. Zitzelsberger, H. F. Walch, A. K. Kremer, M. Hofler, H. Werner, M
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| Title |
Accumulation of chromosomal imbalances from intraductal proliferative lesions to adjacent in situ and invasive ductal breast cancer
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| Journal name |
Diagnostic Molecular Pathology
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| Publication date |
2000
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| Volume number |
9
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| Issue number |
1
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| ISSN |
1052-9551
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| Start page |
14
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| End page |
19
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| Total pages |
6
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| Place of publication |
Philadelphia, U.S.A.
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| Publisher |
Williams & Wilkins
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| Collection year |
2000
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| Language |
eng
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| Subject |
C1 321020 Pathology 730108 Cancer and related disorders
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| 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.
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| Keyword(s) |
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
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