Chromosomal aneuploidy in proliferative breast disease

Micale, Mark A.; Visscher, Daniel W.; Gulino, Sara E.; Wolman, Sandra R.

doi:10.1016/0046-8177(94)90167-8

Cited by 84 publications

(40 citation statements)

References 22 publications

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“…Unlike Micale et al (1994) and Visscher et al (1996), but more in keeping with the findings of Verdoodt et al (1994), we demonstrated increased chromosome 1 copy number in hyperplasia as well as in in situ and invasive malignancy. Due to truncation of nuclei in paraffin sections, signal number under-representation was consistently present, however, also assessing normal tissue within each section allowed comparisons between the different entities to be made.…”

Section: Discussionsupporting

confidence: 87%

“…LOH was also demonstrated in 0-13% of up to 23 cases of hyperplasia, including loci at 17q, 17p and 16q (Lakhani et al, 1996). Micale et al (1994) investigated chromosomal aneusomy in both proliferative and malignant lesions of the breast, using pericentromeric probes for FISH analysis on paraffin sections. Loss of chromosome 1 was not identified in any case and gain was not identified in any of the proliferative lesions but only in cases of DCIS and invasive carcinoma.…”

Section: Discussionmentioning

confidence: 99%

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Increasing chromosome 1 copy number parallels histological progression in breast carcinogenesis

Cummings

Aubele²,

Mattis

et al. 2000

Br J Cancer

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Summary Chromosome 1 copy number in the benign breast lesions hyperplasia and atypical duct hyperplasia (ADH) was investigated using fluorescence in situ hybridization on paraffin sections. Progression of chromosome 1 changes occurring in parallel with histological progression from normal through hyperplasia and ADH to ductal carcinoma in situ (DCIS) and invasive carcinoma was also assessed, both overall and within individual patients. The mean signal number for normal cells was 1.14, while that for hyperplasia was 1.56 and ADH was 1.5, while values for DCIS of 1.95 and invasive duct carcinoma of 1.79, were higher (P < 0.001). Six of the seven cases also showed a significant trend towards an increasing proportion of cells with greater than 2 signals per nucleus occurring with histological progression (P < 0.001). These results support the concept that benign proliferative breast disease is a biological precursor of in-situ and invasive ductal carcinoma, the early histological changes possibly indicating a field effect with further genetic changes required for the development of a malignant phenotype.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Increasing chromosome 1 copy number parallels histological progression in breast carcinogenesis

Cummings

Aubele²,

Mattis

et al. 2000

Br J Cancer

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“…Fluorescence in situ hybridization, by which many cells can be screened, independent of their capacity to proliferate in vitro, has become a complementary tool in cancer cytogenetics for the detection of numerical aberrations in interphase nuclei and for the classification of marker chromosomes (Kiechle-Schwarz et al, 1991;Le Beau, 1993;Micale et al, 1994;Muller et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Detection of circulating tumour cells in patients with breast or ovarian cancer by molecular cytogenetics

et al. 1999

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The detection and elimination of minimal disseminated disease in patients with solid tumours is one of the main current topics in clinical oncology (Pantel, 1996).A variety of assays of widely varying sensitivity have been utilized for the detection of circulating tumour cells such as light microscopy, cytogenetic analyses, fluorescence in situ hybridization (FISH), Southern blot analysis, immunocytochemistry, polymerase chain reaction (PCR) and flow cytometry (Kvalheim, 1996;Pantel, 1996;Vrendenburgh et al, 1996;Schoenfeld et al, 1997;Traystman et al, 1997).Because of the fact that breast and ovarian cancers do not appear to have tumour-specific chromosomal aberrations, tumour cell detection by molecular methods is based on the amplification of tissue-specific transcripts Bostick et al, 1998). In immunocytochemical assays, epithelial specific antibodies have been used to detect isolated tumour cells in bone marrow (BM) and blood (Cote et al, 1991(Cote et al, , 1995(Cote et al, , 1996Diel et al, 1996;Franklin et al, 1996).In an effort to obtain greater sensitivity, several investigators have developed techniques for the enrichment of tumour cells before their identification by immunocytochemistry, PCR or FISH (Hardingham et al, 1993(Hardingham et al, , 1995Berois et al, 1997;Eaton et al, 1997;Hildebrandt et al, 1997;Naume et al, 1997;Martin et al, 1998).Therefore, the aim of our study was to analyse the presence and frequency of circulating tumour cells in the peripheral blood of patients with breast or ovarian cancer by using a combination of magnetic activated cell sorting (MACS) and interphase FISH. MATERIALS AND METHODS PatientsIn this study we included 48 adult patients with a median age of 60.6 ± 13.3 years (range 30-86). Thirty-five had the diagnosis of breast cancer, 12 ovarian cancer and one uterine sarcoma. Twentyfive patients had primary disease (6/25 without involvement of axillary lymph nodes, 8/25 with solid metastases, 11/25 with lymph node metastases) and 23 had relapsed (20/23 with solid metastases). PB-samples were obtained following informed consent at the time of diagnosis, during or after therapy. MACSsorted tumour cells were analysed by interphase FISH, using α-satellite probes specific for the centromeric regions of chromosomes 7, 12, 17 and the region 17 q11.2-q12 (HER-2/neu). Controls were PB-samples from five normal volunteers to determine the background for each probe. Magnetic cell separationMononuclear cells were isolated from fresh blood by FicollHypaque gradient separation. After washing in PBS per 5 mm EDTA, 300 µl PBS buffer per 10 8 cells, 20 µl of CK-8 microbeads (Miltenyi Biotec GmbH, Bergisch Gladbach, Germany) were added. After gentle mixing and incubation for 15 min at 4°C, the cells were washed once in 5 ml buffer per 10 8 cells. The buffer was completely removed, and the cells were resuspended again in 400 µl buffer. The cell suspension was then applied to a prefilled Summary Detection of micrometastases in patients with solid tumours may aid the establishment of prognosi...

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“…The human gene for S100A4 occurs in a cluster of S100 genes on chromosome 1 (Engelkamp et al, 1993), a region of the human genome which is often ampli®ed in breast cancer (Devilee et al, 1991;Dutrillaux et al, 1990;Gendler et al, 1990;Merlo et al, 1989;Micale et al, 1994;Pandis et al, 1992), and elevated levels of S100A4 mRNA have been associated with malignant, relative to benign, breast tumours (Lloyd et al, submitted). However, it is not yet known whether the human S100A4 gene has the same metastasis-inducing properties as its rodent counterparts , when it is overexpressed in non-metastatic epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

et al. 1998

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The rodent S100-related calcium-binding protein, S100A4 induces metastasis in non-metastatic rat and mouse benign mammary cells and co-operates with benign-tumour-inducing changes in two transgenic mouse models, to yield metastatic mammary tumours. Cotransfection of the human gene for S100A4 with pSV2neo into the benign rat mammary cell line, Rama 37, yielded cells which expressed a low level of the endogenous S100A4 mRNA, and either high or undetectable levels of human S100A4 mRNA. The cells which expressed a high level of human S100A4 mRNA induced metastasis in the benign rat mammary cell line Rama 37 in an in vivo assay, whereas the cells which expressed an undetectable level of human S100A4 did not induce any detectable metastases. The primary tumours arising from the S100A4-expressing cells contained high levels of immunocytochemically-detected S100A4 and this high level of S100A4 and the metastatic potential were maintained when cells from a metastasis were re-injected into syngeneic rats. The results show that the human S100A4 possesses metastasis-inducing capabilities.

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Chromosomal aneuploidy in proliferative breast disease

Cited by 84 publications

References 22 publications

Increasing chromosome 1 copy number parallels histological progression in breast carcinogenesis

Increasing chromosome 1 copy number parallels histological progression in breast carcinogenesis

Detection of circulating tumour cells in patients with breast or ovarian cancer by molecular cytogenetics

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

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