The prognostic value of p53 and DNA ploidy following radical prostatectomy

Deliveliotis, Ch.; Skolarikos, Andreas; Karayannis, A.; Tzelepis, Vasileios; Trakas, N.; Alargof, E.; Protogerou, Vassilis

doi:10.1007/s00345-003-0345-0

Cited by 17 publications

(11 citation statements)

References 18 publications

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“…These findings are consistent with previous reports that DNA ploidy adds useful prognostic information for some cancer patients (19,32,42,43). The number of S-Phase cancer cells was reported as an independent predictor of prostate cancer outcome (26).…”

Section: Resultssupporting

confidence: 82%

“…The MIB-1 staining index has been associated with PCa patient survival (27,28,33,41). DNA ploidy adds useful prognostic information for some PCa patients (19,32,(42)(43)(44). Our objective was to determine localization patterns of three distinct groups of biomarkers (cathepsin B, cell proliferation: MIB-1 and DNA ploidy) in the prostate needle biopsy sections in the hope of establishing localization similarities (or differences) in biopsy and RP specimens.…”

Section: Discussionmentioning

confidence: 99%

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Prediction of Aggressive Human Prostate Cancer by Cathepsin B

Sinha¹

2008

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE 01-03-2008 REPORT TYPE 5e. TASK NUMBEREmail: sinha001@tc.umn.edu 5f. WORK UNIT NUMBER PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERUniversity of Minnesota Minneapolis, MN 55455-2070 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES14. ABSTRACT I received approval of the DOD-HSRRB in April, 2005 and began the study shortly after receiving approval. We are enclosing copies of published and accepted papers in the Anticancer Research. These papers address parts of both Specific Aims outlined in the project. I submitted an abstract of our accepted paper, "Cathepsin B Expression Indicates that Prostate Cancer is Similar in African-American and Caucasian Men" to the Department of Defense Prostate cancer research program meeting: Innovative Minds in Prostate Cancer Today (IMPACT). Our abstract was selected and accepted for presentation on September 5-6 meetings in Atlanta, GA. This is significant achievement for our work that started in April 2005. Our paper, "Heterogeneity of Cathepsin B and Stefin A Expression in Gleason Pattern 3+3 (score 6) Prostate Cancer Needle Biopsies" was published in Anticancer Research 27: 1407-1414, 2007. We showed that small foci of Gleason pattern 3+3 (histological score 6) tumors in needle biopsies have heterogeneous cathepsin B and stefin A immunostaining. We have shown that score 6 tumors are heterogeneous and some of the tumors had micrometastases. We have suggested that stratification of these tumors by cathepsin B and stefin A in relation to clinical data may assist in identification of aggressive cancer and treatment selection. SUBJECT TERMS Introduction:Cathepsin B (CB) is required for degradation of basement membrane and extracellular matrix proteins, including prostate cancer (PC) cell invasion to the subjacent stroma and extracellular matrix proteins followed by met...

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Section: Resultssupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Prediction of Aggressive Human Prostate Cancer by Cathepsin B

Sinha¹

2008

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“…Studies evaluating DNA ploidy in prostate cancer have come to varying conclusions. Some studies on 45-850 (mean 139) cancers have suggested a relevant prognostic impact of ploidy (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20), while other studies on 33-447 (mean 122) cancers have failed to find significant associations (7,(20)(21)(22)(23)(24). Deletions affecting various chromosomal loci are a hallmark of prostate cancer.…”

Section: Introductionmentioning

confidence: 99%

The Combination of DNA Ploidy Status and PTEN/6q15 Deletions Provides Strong and Independent Prognostic Information in Prostate Cancer

Lennartz

Minner

Brasch

et al. 2016

Clinical Cancer Research

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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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The prognostic value of p53 and DNA ploidy following radical prostatectomy

Cited by 17 publications

References 18 publications

Prediction of Aggressive Human Prostate Cancer by Cathepsin B

Prediction of Aggressive Human Prostate Cancer by Cathepsin B

The Combination of DNA Ploidy Status and PTEN/6q15 Deletions Provides Strong and Independent Prognostic Information in Prostate Cancer

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

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