Karyotypic abnormalities in fibroadenomas of the breast

Petersson, Catarina; Pandis, Nikos; Rizou, Helene; Mertens, Fredrik; Dietrich, Claudia U.; Adeyinka, Adewale; Idvall, Ingrid; Bondeson, Lennart; Georgiou, G.; Ingvar, Christian; Heim, Sverre; Mitelman, Felix

doi:10.1002/(sici)1097-0215(19970127)70:3<282::aid-ijc6>3.0.co;2-t

Cited by 27 publications

(6 citation statements)

References 15 publications

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“…Under GTG banding, 66 to 88% of the cells in all the fibroadenomas analyzed in the present study presented normal karyotypes (46,XX). Only four (cases 1-4) of the 12 fibroadenomas in our sample exhibited clonal chromosomal alterations (Table 1), which is consistent with the 18 to 30% frequency of cases presenting chromosomal abnormalities in previous studies of this kind (7)(8)(9)(10)(11). Clonal numerical alterations involved chromosomes 8, 18, 19, and 21.…”

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confidence: 90%

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Cytogenetic description of breast fibroadenomas: alterations related solely to proliferation?

Burbano

Lima

Khayat

et al. 2001

Braz J Med Biol Res

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Twelve breast fibroadenomas were analyzed cytogenetically and only four were found to have clonal alterations. The presence of chromosomal alterations in fibroadenomas must be the consequence of the proliferating process and must not be related to the etiology of this type of lesion. In contrast, the few fibroadenomas that exhibit chromosomal alterations are likely to be those presenting a risk of neoplastic transformation. Clonal numerical alterations involved chromosomes 8, 18, 19, and 21. Of the chromosomal alterations found in the present study, only monosomy of chromosomes 19 and 21 has been reported in breast fibroadenomas. The loss of chromosome 21 was the most frequent alteration found in our sample. The study of benign proliferations and their comparison with chromosome alterations in their malignant counterparts ought to result in a better understanding of the genes acting on cell proliferation alone, and of the genes that cause these cells to exhibit varied behaviors such as recurrences, spontaneous regression and fast growth.

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confidence: 90%

“…Few cytogenetic studies of fibroadenomas are available (4)(5)(6)(7)(8)(9)(10) and the data remain inconclusive. With the exception of Petersson et al (7) and Tibiletti et al (10), the number of samples analyzed in each of these studies did not exceed 10 cases.…”

mentioning

confidence: 99%

Cytogenetic description of breast fibroadenomas: alterations related solely to proliferation?

Burbano

Lima

Khayat

et al. 2001

Braz J Med Biol Res

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“…Cytogenetic analysis of tumor specimens grown for short periods of time in culture has provided evidence for the presence of apparently unrelated clones in half of the tumors analyzed Pandis et al, 1993;Teixeira et al, 1994;. Clonal chromosome aberrations have also been reported in benign lesions including fibroadenoma, atypical hyperplasia, and intraductal papilloma (Dietrich et al, 1995;Kasami et al, 1997;Petersson et al, 1997;Rosenberg et al, 1996) as well as in benign epithelium in patients from breast cancer families (Petersson et al, 1996) or at no increased risk of breast cancer (Larson et al, 1998). Our results, in agreement with these studies, support the idea that formation of genetically divergent clones can occur in benign breast epithelium showing no morphologic abnormalities.…”

Section: Discussionmentioning

confidence: 99%

Genetic Heterogeneity in Ductal Carcinoma of the Breast

Lichy

Dalbègue

Zavar

et al. 2000

Laboratory Investigation

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SUMMARY:Genetic heterogeneity in breast cancer has been observed both by cytogenetic and loss of heterozygosity (LOH) analyses; however, the frequency with which genetically heterogeneous clones arise is unknown. In this study, a panel of 115 breast carcinomas was analyzed to determine the extent of clonal divergence in tumor foci at progressive stages of tumor evolution. Intraductal, infiltrating, and metastatic tumor components were microdissected from each tumor and tested for LOH at 20 microsatellite markers on seven chromosomal arms. Of these cases, 24 (21%) demonstrated genetically divergent clones during tumor progression. Clonal divergence, inferred from discordant LOH patterns, was observed most commonly between intraductal and infiltrating tumor (18 cases), but was also demonstrated between infiltrating and metastatic tumor (11 cases). Discordant LOH was observed with markers on one chromosomal arm in 16 cases, on two in 7 cases, and on four in 1 case, and was observed most commonly with markers on 17p, 17q, and 16q. More detailed microdissection of four cases provided evidence for a specific chronology of genetic alterations occurring during the progression of each tumor. The results indicate that the different tumor components observed microscopically in breast cancer specimens often represent genetically divergent clones. (Lab Invest 2000, 80:291-301).E lucidation of the sequence of genetic events responsible for progression of breast cancer from in situ to infiltrating and metastatic carcinoma is an important goal of efforts to understand the biological basis of this common malignancy. Progression is believed to occur through the accumulation of genetic changes via a process of clonal evolution and clonal selection (Brenner and Aldaz, 1997;Nowell, 1976). Surgically resected breast carcinoma specimens provide a unique resource for analyzing the genetic changes that occur during progression, because specimens typically contain foci of tumor in various stages of progression, including in situ carcinoma, invasive tumor, and lymph node metastases. Morphologically normal epithelial constituents of the breast are usually represented in such specimens, and foci of benign proliferative epithelial lesions may also be present.Detailed studies of colon cancer have shown that adenomatous epithelium adjacent to carcinoma typically has some but not all of the genetic lesions present in the fully developed malignancy, consistent with direct progression from adenoma to carcinoma (Boland et al, 1995;Fearon and Vogelstein, 1990;Vogelstein et al, 1988). By analogy, it might be expected that a similar analysis of breast tumors in different stages of progression would likewise show the accumulation of genetic changes with progression. However, genetic analysis of breast cancer specimens has suggested that the individual foci of tumor identifiable by microscopic examination may not show the precursor-product relationship often observed in colon cancer. Cytogenetic studies in particular have revealed sufficient genetic...

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“…Reciprocal translocations t(8;12)(q24;p12), t(12;14)(p11;q11) and t(12;21)(p12;q22) have been reported in breast diseases (Rohen et al, 1993; see for reviews Petersson et al, 1997;Cavalli et al, 2001; http://cgap.nci.nih.gov/Chromosomes/RecurrentAberrations). The 12p13, 12q12 and 12q24 regions have the highest frequencies of breaks (Teixeira et al, 2002).…”

Section: Comparison Of Our Results With Literature Datamentioning

confidence: 99%

Multicolour-banding fluorescence in situ hybridisation (mbanding-FISH) to identify recurrent chromosomal alterations in breast tumour cell lines

Letessier

Murati

et al. 2005

Br J Cancer

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Recurrent chromosome breakpoints in tumour cells may point to cancer genes, but not many have been molecularly characterised. We have used multicolour-banding fluorescence in situ hybridisation (mbanding-FISH) on breast tumour cell lines to identify regions of chromosome break created by inversions, duplications, insertions and translocations on chromosomes 1, 5, 8, 12 and 17. We delineate a total of 136 regions of break, some of them occurring with high frequency. We further describe two examples of dualcolour FISH characterisation of breakpoints, which target the 1p36 and 5p11 -12 regions. Both breaks involve genes whose function is unknown to date. The mbanding-FISH strategy constitutes an efficient first step in the search for potential cancer genes.

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Karyotypic abnormalities in fibroadenomas of the breast

Cited by 27 publications

References 15 publications

Cytogenetic description of breast fibroadenomas: alterations related solely to proliferation?

Cytogenetic description of breast fibroadenomas: alterations related solely to proliferation?

Genetic Heterogeneity in Ductal Carcinoma of the Breast

Multicolour-banding fluorescence in situ hybridisation (mbanding-FISH) to identify recurrent chromosomal alterations in breast tumour cell lines

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