Karyotypic variation between independently cultured strains of the cell line MCF-7 identified by multicolour fluorescence in situ hybridization

Bahia, H.; Ashman, J. N. E.; Cawkwell, Lynn; Lind, Michael; Monson, J. R. T.; Drew, Phil; Greenman, John

doi:10.3892/ijo.20.3.489

Cited by 33 publications

(36 citation statements)

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“…Our observation that p53 is regulating HIC1 in MCF7 cells is in contrast to an earlier report describing that HIC1 is neither expressed in untreated MCF7 cells nor induced by p53 (Wales et al, 1995). These differences may be explained by the documented phenotypic variability of MCF7 cell clones grown in different laboratories (Bahia et al, 2002).…”

Section: Discussioncontrasting

confidence: 56%

Identification of the p53 family-responsive element in the promoter region of the tumor suppressor gene hypermethylated in cancer 1

et al. 2005

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The tumor suppressor gene hypermethylated in cancer 1 (HIC1), located on human chromosome 17p13.3, is frequently silenced in cancer by epigenetic mechanisms. Hypermethylated in cancer 1 belongs to the bric a`brac/ poxviruses and zinc-finger family of transcription factors and acts by repressing target gene expression. It has been shown that enforced p53 expression leads to increased HIC1 mRNA, and recent data suggest that p53 and Hic1 cooperate in tumorigenesis. In order to elucidate the regulation of HIC1 expression, we have analysed the HIC1 promoter region for p53-dependent induction of gene expression. Using progressively truncated luciferase reporter gene constructs, we have identified a p53-responsive element (PRE) 500 bp upstream of the TATA-box containing promoter P0 of HIC1, which is sequence specifically bound by p53 in vitro as assessed by electrophoretic mobility shift assays. We demonstrate that this HIC1 p53-responsive element (HIC1.PRE) is necessary and sufficient to mediate induction of transcription by p53. This result is supported by the observation that abolishing endogenous wild-type p53 function prevents HIC1 mRNA induction in response to UV-induced DNA damage. Other members of the p53 family, notably TAp73b and DNp63a, can also act through this HIC1.PRE to induce transcription of HIC1, and finally, hypermethylation of the HIC1 promoter attenuates inducibility by p53.

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Section: Discussioncontrasting

confidence: 56%

Identification of the p53 family-responsive element in the promoter region of the tumor suppressor gene hypermethylated in cancer 1

et al. 2005

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“…M-FISH was performed as described previously Bahia et al, 2002) using the SpectraVysiont Assay system (Abbott Laboratories, Maidenhead, UK). SpectraVysion consists of a 52-probe mix of WCPs labelled with different combinations of five fluorochromes (SpectrumGold, SpectrumRed, SpectrumGreen, SpectrumAqua and SpectrumFarRed).…”

Section: M-fishmentioning

confidence: 99%

Chromosomal analysis of non-small-cell lung cancer by multicolour fluorescent in situ hybridisation

et al. 2004

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The cytogenetic abnormalities in non-small-cell lung cancer remain elusive due primarily to the difficulty in obtaining metaphase spreads from solid tumours. We have used the molecular cytogenetic techniques of multicolour fluorescent in situ hybridisation (M-FISH) and comparative genomic hybridisation (CGH) to analyse four primary non-small-cell lung cancer samples and two established cell lines (COR-L23 and COR-L105) in order to identify common chromosomal aberrations. CGH revealed regions on 5p, 3q, 8q, 11q, 2q, 12p and 12q to be commonly over-represented and regions on 9p, 3p, 6q, 17p, 22q, 8p, 10p, 10q and 19p to be commonly under-represented. M-FISH revealed numerous complex chromosomal rearrangements. Translocations between chromosomes 5 and 14, 5 and 11 and 1 and 6 were observed in three of the six samples, with a further 14 translocations being observed in two samples each. Loss of the Y chromosome and gains of chromosomes 20 and 5p were also frequent. Chromosomes 4, 5, 8, 11, 12 and 19 were most frequently involved in interchromosomal translocations. Further investigation of the recurrent aberrations will be necessary to identify the specific breakpoints involved and any role they may have in the aetiology, diagnosis and prognosis of non-small-cell lung cancer.

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“…10,11 Before hybridization, metaphase preparations were enzymatically pretreated to remove cytoplasmic proteins and RNA molecules and to enhance the penetration of the probe. Exact pretreatment conditions varied between metaphase preparations depending on the volume of residual cytoplasm.…”

Section: M-fishmentioning

confidence: 99%

“…9 Multicolour-fluorescent in situ hybridization (M-FISH) is a recently developed technique designed to complement classical cytogenetic banding analysis. 10,11 Metaphase chromosomes prepared from fresh tumours subjected to short term culture are 'painted' with a combination of whole chromosome paints that allow each chromosome to be visualised in a unique colour (colour karyotyping). This technique, along with the technically similar spectral karyotyping (SKY), has greatly facilitated the identification of chromosome material involved in chromosomal rearrangements even in sup-optimal chromosome preparations.…”

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confidence: 99%

Chromosomal alterations in small cell lung cancer revealed by multicolour fluorescence in situ hybridization

Ashman

Brigham

Cowen

et al. 2002

Intl Journal of Cancer

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Small cell lung cancer (SCLC) is a major cause of cancer related morbidity and mortality. Karyotypic studies have revealed numerous chromosomal aberrations in most SCLC however, classical G-banding analysis is unable to fully characterise complex marker chromosomes. Recent developments in molecular cytogenetics now allow accurate identification of the chromosomal components of complicated rearrangements. We have applied the technique of multicolour fluorescence in situ hybridization (M-FISH) in combination with comparative genomic hybridization (CGH) to the analysis of 5 SCLC cell lines and 1 primary tumour specimen to characterise the chromosomal abnormalities. CGH analysis identified many similarities between specimens, with frequent DNA copy number decreases on chromosomes 3p, 5q, 10, 16q, 17p and frequent gains on 3q, 1p, 1q and 14q. In contrast, M-FISH analysis revealed a large number of structural abnormalities, with each specimen demonstrating an individual pattern of chromosomal translocations. Forty different translocations were identified with the vast majority (39) being unbalanced. Chromosome 5 was the most frequently rearranged chromosome (9 translocations) followed by chromosomes 2, 10 and 16 (6 translocations each). Further investigation of these frequently involved chromosomes is warranted to establish whether consistent break points are involved in these translocations, causing dysregulation of specific genes that are crucial for tumour progression and secondly to identify the affected genes.

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Karyotypic variation between independently cultured strains of the cell line MCF-7 identified by multicolour fluorescence in situ hybridization

Cited by 33 publications

References 0 publications

Identification of the p53 family-responsive element in the promoter region of the tumor suppressor gene hypermethylated in cancer 1

Identification of the p53 family-responsive element in the promoter region of the tumor suppressor gene hypermethylated in cancer 1

Chromosomal analysis of non-small-cell lung cancer by multicolour fluorescent in situ hybridisation

Chromosomal alterations in small cell lung cancer revealed by multicolour fluorescence in situ hybridization

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