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Article: Correlation of increased apoptosis and proliferation with development of prostatic intraepithelial neoplasia (PIN) in ventral prostate of the Noble rat

TitleCorrelation of increased apoptosis and proliferation with development of prostatic intraepithelial neoplasia (PIN) in ventral prostate of the Noble rat
Authors
Issue Date2000
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34304
Citation
Prostate, 2000, v. 44 n. 1, p. 31-39 How to Cite?
AbstractBACKGROUND. Imbalance between cell proliferation and cell apoptosis has been considered a key factor in carcinogenesis. Prostatic intraepithelial neoplasia (PIN) is the most likely precancereous lesion and represents the major target for chemoprevention of prostate cancer. The proliferative and apoptotic activities involved in the development of PIN remain to be elucidated. METHODS. Ventral prostates were removed from Noble rats that were treated with a combination of testosterone (T) and estradiol (E2) for certain periods of time, and processed for histopathological grading. To evaluate the relationship between cell proliferation and apoptosis, immunohistochemistry for proliferating cell nuclear antigen (PCNA), Ki-67, and in situ DNA nick labeling (TUNEL) for identifying apoptotic cells, were performed on paraffin sections from prostate samples with PIN lesions. The results were correlated with expression patterns of Bcl-2 and Bax, two proteins related to cell survival and cell apoptosis. RESULTS. Pathologically, low-grade PIN (LGPIN) and high-grade PIN (HGPIN) were observed in ducts or alveoli after 3 and 5 months of T + E2 treatment, respectively. Quantitative evaluation of Ki-67 showed an increased proliferative activity in HGPIN. In contrast to normal prostatic ducts and alveoli, which showed no positive staining for Ki-67 in the nuclei of luminal cells, 25% Ki-67-positive cells were detected in luminal cells of HGPIN. Only 7.5% Ki-67-positive cells were found belonging to the basal cell type. The Ki-67 index showed a higher growth rate from normal to HGPIN. The PCNA results showed a similar expression pattern to that of Ki-67 in normal prostate, LGPIN, and HGPIN. Apoptotic index (number of apoptotic cells/total number of cell counted) was significantly higher (P = 0.028) in HGPIN(3.23%) than in control prostate (1.19%). In contrast to control prostate, which showed no definite expression of Bcl-2, an intense positive expression of Bcl-2 in HGPIN was observed. Positive expression of Bax protein was observed in glandular epithelial cells of normal control prostate and HGPIN as well. CONCLUSIONS. Overexpression of Bcl-2 and higher Ki-67 or PCNA indices in HGPIN suggest that abnormal growth of premalignant lesions might result from an increase in cell proliferation. An increased apoptotic rate in HGPIN further implicates that active apoptosis may accelerate cell turnover in the development of premalignant lesions of the prostate. (C) 2000 Wileys-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/67961
ISSN
2015 Impact Factor: 3.778
2015 SCImago Journal Rankings: 1.477
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXie, Wen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorTsao, SWen_HK
dc.date.accessioned2010-09-06T05:59:51Z-
dc.date.available2010-09-06T05:59:51Z-
dc.date.issued2000en_HK
dc.identifier.citationProstate, 2000, v. 44 n. 1, p. 31-39en_HK
dc.identifier.issn0270-4137en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67961-
dc.description.abstractBACKGROUND. Imbalance between cell proliferation and cell apoptosis has been considered a key factor in carcinogenesis. Prostatic intraepithelial neoplasia (PIN) is the most likely precancereous lesion and represents the major target for chemoprevention of prostate cancer. The proliferative and apoptotic activities involved in the development of PIN remain to be elucidated. METHODS. Ventral prostates were removed from Noble rats that were treated with a combination of testosterone (T) and estradiol (E2) for certain periods of time, and processed for histopathological grading. To evaluate the relationship between cell proliferation and apoptosis, immunohistochemistry for proliferating cell nuclear antigen (PCNA), Ki-67, and in situ DNA nick labeling (TUNEL) for identifying apoptotic cells, were performed on paraffin sections from prostate samples with PIN lesions. The results were correlated with expression patterns of Bcl-2 and Bax, two proteins related to cell survival and cell apoptosis. RESULTS. Pathologically, low-grade PIN (LGPIN) and high-grade PIN (HGPIN) were observed in ducts or alveoli after 3 and 5 months of T + E2 treatment, respectively. Quantitative evaluation of Ki-67 showed an increased proliferative activity in HGPIN. In contrast to normal prostatic ducts and alveoli, which showed no positive staining for Ki-67 in the nuclei of luminal cells, 25% Ki-67-positive cells were detected in luminal cells of HGPIN. Only 7.5% Ki-67-positive cells were found belonging to the basal cell type. The Ki-67 index showed a higher growth rate from normal to HGPIN. The PCNA results showed a similar expression pattern to that of Ki-67 in normal prostate, LGPIN, and HGPIN. Apoptotic index (number of apoptotic cells/total number of cell counted) was significantly higher (P = 0.028) in HGPIN(3.23%) than in control prostate (1.19%). In contrast to control prostate, which showed no definite expression of Bcl-2, an intense positive expression of Bcl-2 in HGPIN was observed. Positive expression of Bax protein was observed in glandular epithelial cells of normal control prostate and HGPIN as well. CONCLUSIONS. Overexpression of Bcl-2 and higher Ki-67 or PCNA indices in HGPIN suggest that abnormal growth of premalignant lesions might result from an increase in cell proliferation. An increased apoptotic rate in HGPIN further implicates that active apoptosis may accelerate cell turnover in the development of premalignant lesions of the prostate. (C) 2000 Wileys-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34304en_HK
dc.relation.ispartofProstateen_HK
dc.rightsThe Prostate. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntibodies, Monoclonalen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshCell Divisionen_HK
dc.subject.meshGenes, bcl-2 - physiologyen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshIn Situ Nick-End Labelingen_HK
dc.subject.meshKi-67 Antigen - analysis - physiologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshProliferating Cell Nuclear Antigen - analysis - physiologyen_HK
dc.subject.meshProstate - pathologyen_HK
dc.subject.meshProstatic Intraepithelial Neoplasia - etiology - pathologyen_HK
dc.subject.meshProstatic Neoplasms - etiology - pathologyen_HK
dc.subject.meshProto-Oncogene Proteins - analysis - physiologyen_HK
dc.subject.meshProto-Oncogene Proteins c-bcl-2en_HK
dc.subject.meshRatsen_HK
dc.subject.meshbcl-2-Associated X Proteinen_HK
dc.titleCorrelation of increased apoptosis and proliferation with development of prostatic intraepithelial neoplasia (PIN) in ventral prostate of the Noble raten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-4137&volume=44&spage=31&epage=39&date=2000&atitle=Correlation+of+increased+apoptosis+and+proliferation+with+development+of+prostatic+intraepithelial+neoplasia+(PIN)+in+ventral+prostate+of+the+Noble+raten_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid10861755-
dc.identifier.scopuseid_2-s2.0-0034659763en_HK
dc.identifier.hkuros51906en_HK
dc.identifier.hkuros50191-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034659763&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume44en_HK
dc.identifier.issue1en_HK
dc.identifier.spage31en_HK
dc.identifier.epage39en_HK
dc.identifier.isiWOS:000087411900005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXie, W=21647230200en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK

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