Combined cytogenetic and molecular genetic analyses of fifty-nine untreated human prostate carcinomas

Zitzelsberger, Horst; Szűcs, Sándor; Robens, Elisabeth; Höfler, Heinz; Bauchinger, M.

doi:10.1016/0165-4608(96)00065-9

Cited by 21 publications

(7 citation statements)

References 35 publications

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“…In cytogenetic studies, deletion at 6q13-q23 has been detected in seven cases in three studies (Web b et al, 1996;Zitzelsberger et al, 1996;Teixeira et al, 2000), and this is the second most frequently deleted chromosome region (after 10q, which has 10 cases). One cancer showed an interstitial deletion of 6q15-q23.…”

Section: Introductionmentioning

confidence: 96%

Defining the region(s) of deletion at 6q16–q22 in human prostate cancer

Hyytinen

Saadut

Chen

et al. 2002

Genes Chromosomes & Cancer

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Deletion of the long arm of chromosome 6 (6q) frequently occurs in many neoplasms, including carcinomas of the prostate and breast and melanoma, suggesting the location of a tumor-suppressor gene or genes at 6q. At present, however, the region of deletion has not been well defined, and the target gene of deletion remains to be identified. In this study, we analyzed 44 primary prostate cancers with 16 polymorphic markers for loss of heterozygosity (LOH) by using PCR-based techniques. We also examined 23 cell lines/xenografts of prostate cancer with 38 markers for LOH by the method of homozygosity mapping of deletion. LOH at 6q16 - q22 was detected in 21 of 44 (48%) primary tumors and in 12 of 23 (52%) cell lines/xenografts. Two regions of LOH were defined. One was 7.5 cM at 6q16 - q21 between markers D6S1716 and D6S1580, and the other was 4.3 cM at 6q22 between D6S261 and D6S1702. Whereas no correlation was found between LOH at 6q16-q22 and patient age at diagnosis or Gleason score, tumors at higher stage appear to have more frequent LOH. These findings suggest that deletion of 6q16 - q22 is a frequent event in prostate cancer, and that the deletion originates from two distinct regions. These results should be useful in identifying the target gene(s) of deletion at 6q.

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Section: Introductionmentioning

confidence: 96%

Defining the region(s) of deletion at 6q16–q22 in human prostate cancer

Hyytinen

Saadut

Chen

et al. 2002

Genes Chromosomes & Cancer

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“…One of the most important genetic changes takes place on the long arm of chromosome 16. Although deletion of 16q22 has been detected in only a few cases by cytogenetic analysis [Webb et al, 1996; Zitzelsberger et al, 1996], the frequency is as high as 31% (105 of 339 cases) in CGH studies—with most cases involving 16q13‐23 [Dong, 2001]. In one study, deletion of 16q occurred in 11 (55%) of the 20 metastases examined [Cher et al, 1996].…”

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confidence: 99%

Dual roles of E‐cadherin in prostate cancer invasion

Chunthapong

Seftor

Khalkhali‐Ellis

et al. 2004

J of Cellular Biochemistry

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The role(s) of E-cadherin in tumor progression, invasion, and metastasis remains somewhat enigmatic. In order to investigate various aspects of E-cadherin biological activity, particularly in prostate cancer progression, our laboratory cloned unique subpopulations of the heterogeneous DU145 human prostatic carcinoma cell line and characterized their distinct biological functions. The data revealed that the highly invasive, fibroblastic-like subpopulation of DU145 cells (designated DU145-F) expressed less than 0.1-fold of E-cadherin protein when compared to the parental DU145 or the poorly invasive DU145 cells (designated DU145-E). Experimental disruption of E-cadherin function stimulated migration and invasion of DU145-E and other E-cadherin-positive prostate cancer cell lines, but did not affect the fibroblastic-like DU145-F subpopulation. Within the medium of parental DU145 cells, the presence of an 80 kDa E-cadherin fragment was detected. Subsequent functional analyses revealed the stimulatory effect of this fragment on the migratory and invasive capability of E-cadherin-positive cells. These results suggest that E-cadherin plays an important role in regulating the invasive potential of prostate cancer cells through an unique paracrine mechanism.

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“…CIN is frequently reported in prostate cancer specimens (Webb et al, 1996;Zitzelsberger et al, 1996;Deliveliotis et al, 2003) and is thought to be a major event during the transformation of normal prostate epithelium to prostate cancer (Phillips et al, 2001). In addition, significant number of prostate cancer specimens and established cell lines show tetraploidy or near tetraploidy (Webb et al, 1996;Bernardino et al, 1997;Haapala et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

MAD2ΔC induces aneuploidy and promotes anchorage-independent growth in human prostate epithelial cells

Cheung

et al. 2007

Oncogene

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The mitotic arrest deficient 2 (MAD2) is suggested to play a key role in a functional mitotic checkpoint because of its inhibitory effect on anaphase-promoting complex/cyclosome (APC/C) during mitosis. The binding of MAD2 to mitotic checkpoint regulators MAD1 and Cdc20 is thought to be crucial for its function and loss of which leads to functional inactivation of the MAD2 protein. However, little is known about the biological significance of this MAD2 mutant in human cells. In this study, we stably transfected a C-terminal-deleted MAD2 gene (MAD2DC) into a human prostate epithelial cell line, Hpr-1 and studied its effect on chromosomal instability, cell proliferation, mitotic checkpoint control and soft agar colony-forming ability. We found that MAD2DC was able to induce aneuploidy through promoting chromosomal duplication, which was a result of an impaired mitotic checkpoint and cytokinesis, suggesting a crucial role of MAD2-mediated mitotic checkpoint in chromosome stability in human cells. In addition, the MAD2DC-transfected cells displayed anchorage-independent growth in soft agar after challenged by 7,12-dimethylbenz[A]anthracene (DMBA), demonstrating a cancer-promoting effect of a defective mitotic checkpoint in human cells. Furthermore, the DMBA-induced transformation was accompanied by a complete loss of DNA damage-induced p53 response and activation of the MAPK pathway in MAD2DC cells. These results indicate that a defective mitotic checkpoint alone is not a direct cause of tumorigenesis, but it may predispose human cells to carcinogen-induced malignant transformation. The evidence presented here provides a link between MAD2 inactivation and malignant transformation of epithelial cells.

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Combined cytogenetic and molecular genetic analyses of fifty-nine untreated human prostate carcinomas

Cited by 21 publications

References 35 publications

Defining the region(s) of deletion at 6q16–q22 in human prostate cancer

Defining the region(s) of deletion at 6q16–q22 in human prostate cancer

Dual roles of E‐cadherin in prostate cancer invasion

MAD2ΔC induces aneuploidy and promotes anchorage-independent growth in human prostate epithelial cells

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