Procaspase- 3 Status in Benign Prostatic Hyperplasia and Carcinoma (A Correlative Retrospective Study)
Background: Benign prostatic hyperplasia and prostatic adenocarcinoma are two of the most common pathologic mass lesions. Both are encountered mainly in elderly males. The caspases family is a group of at least 15 known proteases that serve as initiator & effector molecules of the apoptosis path...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
College of Medicine University of Baghdad
2009-10-01
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| Series: | مجلة كلية الطب |
| Subjects: | |
| Online Access: | http://iqjmc.uobaghdad.edu.iq/index.php/19JFacMedBaghdad36/article/view/1134 |
| Summary: | Background: Benign prostatic hyperplasia and prostatic adenocarcinoma are two of the most common pathologic mass lesions. Both are encountered mainly in elderly males. The caspases family is a group of at least 15 known proteases that serve as initiator & effector molecules of the apoptosis pathway. Caspase-3, in particular, is thought to play a pathogenetic role in both prostatic hyperplasia and carcinoma. Finasteride is a medication that has routinely been given to patients with hyperplasia and carcinoma; its prostate size-reducing effect is thought to be mediated through caspases.
Patients and methods: fifty patients with prostatic mass lesions were included in this study (20 with hyperplasia & 30 with adenocarcinoma); all were on finasteride treatment. The carcinoma cases were graded according to Gleason scoring system. All cases were analyzed for procaspase-3 strength of staining.
Results: benign hyperplasia & well-differentiated carcinomas show high expression of procaspase-3, in contrast loss of expression of this marker was noted in moderately & poorly differentiated carcinomas.
Conclusion: there is a strong statistical correlation between caspase-3 expression and the degree of tumor differentiation. This may allow the utilization of this marker as a potential prognostic factor, especially in limited biopsy samples. |
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| ISSN: | 0041-9419 2410-8057 |