Isochromosome 8q formation is associated with 8p loss of heterozygosity in a prostate cancer cell line

Virgin, Jeffrey B.; Hurley, Patrick; Nahhas, Fatimah A.; Bebchuk, Karen G.; Mohamed, Anwar N.; Sakr, Wael; Bright, Robert K.; Cher, Michael L.

doi:10.1002/(sici)1097-0045(19990915)41:1<49::aid-pros7>3.0.co;2-8

Cited by 24 publications

(12 citation statements)

References 26 publications

(26 reference statements)

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“…The formation of isochromosome 8q [i(8q)] in this prostate cancer cell line has previously been reported. 11 However, our results suggest that i(8q) is present in the benign prostate cell line and chromosome 8 is then lost in the cancer cell line, explaining the observed loss of 8p in the cancer cell line. Many known and putative tumour suppressor genes occur on 8p.…”

Section: Discussionmentioning

confidence: 58%

Genome-wide screening for genetic changes in a matched pair of benign and prostate cancer cell lines using array CGH

Brookman-Amissah

Duchesnes

Williamson

et al. 2005

Prostate Cancer Prostatic Dis

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Copy number alterations in a matched pair of benign epithelial and prostate cancer cell lines derived from the same patient were assessed using array-based comparative genomic hybridisation (aCGH). The cancer cell line showed a gain of chromosome 7, deletion of chromosome 8, gains (including high level) and losses on chromosome 11, loss of 18p and gain of 20q. Deletions on chromosome 8 were confirmed with microsatellite markers. The aCGH results were compared to gene expression data obtained using DNA microarrays and suggested the involvement of caspases and ICEBERG on 11q and E2F1 on chromosome 20q.

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Section: Discussionmentioning

confidence: 58%

Genome-wide screening for genetic changes in a matched pair of benign and prostate cancer cell lines using array CGH

Brookman-Amissah

Duchesnes

Williamson

et al. 2005

Prostate Cancer Prostatic Dis

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“…Subsequent reports have shown that hD52 is overexpressed in cancers of the lung (8,9), prostate (3,10,11), colon (12), and ovary (13), as well as in B cell malignancies (14). The hD52 gene has been localized to human chromosome 8q21 (2), a region frequently gained in breast and prostate carcinomas (15)(16)(17)(18). It has been reported that hD52 represents a target for gene amplification in human breast cancer (19), where hD52 was the first chromosome 8q21 target gene proposed in any cancer type.…”

Section: Introductionmentioning

confidence: 53%

Induction of Tumorigenesis and Metastasis by the Murine Orthologue of Tumor Protein D52

Lewis

Payton

Whitford

et al. 2007

Molecular Cancer Research

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Expression studies have consistently identified tumor protein D52 (TPD52) overexpression in tumor cells. Murine TPD52 (mD52) shares 86% identity with the human orthologue. To study a possible role for TPD52 in transformation, 3T3 fibroblasts were transfected with the full-length cDNA for mD52. Expression of mD52 was confirmed by reverse transcription-PCR (RT-PCR), real-time PCR, and Western blot analysis compared with 3T3 and vector-transfected 3T3 (3T3.V), and the resultant cell line was designated 3T3.mD52. At 4 weeks, 3T3.mD52 gained a 2-fold increase in growth rate, lost contact inhibition, and exhibited a marked phenotype change. Further characterization revealed an acquired ability for anchorage-independent cell growth. To determine whether 3T3.mD52 had become tumorigenic, naïve, healthy, immunocompetent syngeneic mice were inoculated subcutaneously with varying cell doses. Tumors measuring >1 cm 2 were detected 60 days postinoculation with 3T3.mD52, and a 50% subcutaneous tumor incidence was obtained with as few as 5 Â 10 5 3T3.mD52 cells. Remarkably, when lungs from 3T3.mD52 tumor-bearing mice were analyzed, numerous tumor nodules were observed, ranging from nodules less than 10 to nodules too numerous to count (inoculation with 1 Â 10 5 and 5 Â 10 6 cells, respectively). Further support for the metastatic capacity of 3T3.mD52 was the demonstration that transforming growth factor (TGF)-BR1 (receptor) expression decreased and TGF-B1 secretion increased in 3T3.mD52 compared with 3T3 controls. cDNA microarray analysis showed a gene expression pattern that further supported mD52-induced transformation and metastasis. Together, these data suggest that mD52 expression in 3T3 cells initiated cellular transformation, tumorigenesis, and progression to metastasis. (Mol Cancer Res 2007;5(2):133 -44)

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“…In addition, a comparative genomic hybridization study of small cell cancer of the lung revealed loss of the 4q11 -q23 region in 86% of cases (Petersen et al, 1997) and the same technique has revealed the loss of chromosome 4q in breast (Tanner et al, 1998) colon (Arribas et al, 1999) and prostate (Virgin et al, 1999) carcinoma. Moreover, a hemizygous 8 cM germline deletion spanning our region was also shown to be associated with hepatic cancer (Terada et al, 2001).…”

Section: Allele Lost Allele Retained Not Informative Not Informativementioning

confidence: 97%

Functional evidence for a squamous cell carcinoma mortality gene(s) on human chromosome 4

et al. 2002

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Isochromosome 8q formation is associated with 8p loss of heterozygosity in a prostate cancer cell line

Cited by 24 publications

References 26 publications

Genome-wide screening for genetic changes in a matched pair of benign and prostate cancer cell lines using array CGH

Genome-wide screening for genetic changes in a matched pair of benign and prostate cancer cell lines using array CGH

Induction of Tumorigenesis and Metastasis by the Murine Orthologue of Tumor Protein D52

Functional evidence for a squamous cell carcinoma mortality gene(s) on human chromosome 4

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