Resistance to Apoptosis and Up Regulation of Bcl-2 In Benign Prostatic Hyperplasia After Androgen Deprivation

Cardillo, Marina; Berchem, Guy; Tarkington, Mary Anne; Krajewski, Stanisław; Krajewski, Maryla; Reed, John C.; Tehan, Timothy; Ortega, Louis G.; Lage, Janice M.; Gelmann, Edward P.

doi:10.1097/00005392-199707000-00073

Cited by 46 publications

(26 citation statements)

References 27 publications

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“…However, benign prostatic epithelium that has been subjected to various stresses such as radiation therapy or androgen ablation demonstrate strong expression of Bcl-2 in the surviving cells, which probably functions to block apoptosis induced through the p53 pathway. 8,9 Our prior study of Bcl-2 expression in benign and malignant prostatic tissues subjected to androgen ablation demonstrated a 30% incidence of Bcl-2 overexpression in the secretory cell layer, which may contribute to cell survival and to gland enlargement. 10 Kyprianou has investigated the role of Bcl-2 in benign prostatic hyperplasia, and reported expression of the antiapoptotic Bcl-2 protein concurrently with decreased apoptosis in BPH compared to normal prostatic epithelium.…”

Section: Discussionmentioning

confidence: 99%

Abnormalities of apoptotic and cell cycle regulatory proteins in distinct histopathologic components of benign prostatic hyperplasia

Gandour‐Edwards

Mack

DeVere-White

et al. 2004

Prostate Cancer Prostatic Dis

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Introduction: Benign prostatic hyperplasia (BPH) is a slowly progressive abnormal glandular enlargement with heterogeneous morphology. Disruption of apoptotic pathways has been suggested as an important regulatory mechanism in this common and significantly morbid disease. Methods: Prostatic tissue from 20 patients with BPH and no prior or subsequent prostatic carcinoma was obtained by transurethral prostatectomy (TURP) at the University of California Davis. Apoptotic regulatory proteins: BCL2, BAX and p27 were analyzed by immunohistochemistry and evaluated for expression in four distinct histologic patterns: hyperplastic epithelium, nodules, dilated glands and atrophic/inflammatory glands. Results: Particularly striking was the decreased expression of BAX and an abnormal BCL2 : BAX ratio within all nodules relative to expression in other epithelial patterns. p27 expression was decreased in 35% of the hyperplastic epithelial areas and 10% of the nodules. Discussion: Overall, abnormal expression of BCL2, BAX and/or p27 was identified in the hyperplastic epithelium of 19 (90%) of specimens and all 12 (100%) of the hyperplastic nodules. The high frequency of abnormalities in apoptosis regulatory genes, suggests that alteration of apoptotic pathways is important for the development of this condition.

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Section: Discussionmentioning

confidence: 99%

Abnormalities of apoptotic and cell cycle regulatory proteins in distinct histopathologic components of benign prostatic hyperplasia

Gandour‐Edwards

Mack

DeVere-White

et al. 2004

Prostate Cancer Prostatic Dis

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“…The treatment of BPH with ®nasteride has been shown to produce marked changes in the levels of these growth factors, the postulated mechanism including down-regulation of both the growth factor receptors and the hormones themselves [13,14]. Variation in the levels of bcl-2, as well as the rest of the bcl family of gene protein products, has also led to speculation about the role of varying apoptotic rates on the effects of ®nasteride [20].…”

Section: Discussionmentioning

confidence: 99%

Microvessel density in prostatic hyperplasia

Foley

Bailey

2000

BJU International

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Objectives To examine the prostates from patients with haematuria associated with benign prostatic hyperplasia (BPH) to determine their microvascular anatomy and thus assess histopathological differences in patients with significant haematuria. Patients and methods Prospectively, 11 patients with BPH and haematuria (mean age 70 years) and 19 control patients with BPH alone (mean age 72 years) were identified. Neither group had received hormone manipulation or had been catheterized. The sub‐urothelial compartment of the prostatic urethra in subsequent specimens from transurethral resection was examined using factor VIII/CD‐34 immuno‐histochemistry. The microvessel density (MVD) was calculated by counting vascular cross‐sectional profiles within a 0.81‐mm2 grid. The pathologist studying the specimens was unaware of the patients’ symptoms. Results The median (range) MVD in the haematuria group was 64 (28–137) and in the controls was 27 (14–39) (P < 0.001). Conclusion The MVD was significantly greater in the patients with haematuria, suggesting that suburo‐thelial microvessel proliferation may play an important role in mediating haematuria associated with BPH. This is the first time that a difference has been shown at the cellular level in patients with haematuria and could form an important foundation for subsequent research.

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“…This finding is consistent with the observation that in many prostate cancer tissue specimens, Bcl-2 staining is negative despite a high Gleason grade and stage. 6 The finding that Bcl-2 protein expression was lost in the androgen-unresponsive LNCaP cells suggest a number of possibilities, one of which is that Bcl-2 may Figure 10 Both androgen-responsive and androgen-unresponsive cells are sensitive to paclitaxel. Cells were treated with 500 nM paclitaxel and control cells with vehicle alone (0.1% ethanol).…”

Section: Discussionmentioning

confidence: 99%

Regulation of Bcl-2 during androgen-unresponsive progression of prostate cancer

Rothermund

Kondrikov

Lin

et al. 2002

Prostate Cancer Prostatic Dis

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Resistance to Apoptosis and Up Regulation of Bcl-2 In Benign Prostatic Hyperplasia After Androgen Deprivation

Abstract: BPH demonstrated increased staining for Bcl-2 after androgen deprivation that may render hyperplastic epithelium relatively resistant to apoptosis induced acutely by androgen withdrawal.

Cited by 46 publications

References 27 publications

Abnormalities of apoptotic and cell cycle regulatory proteins in distinct histopathologic components of benign prostatic hyperplasia

Abnormalities of apoptotic and cell cycle regulatory proteins in distinct histopathologic components of benign prostatic hyperplasia

Microvessel density in prostatic hyperplasia

Regulation of Bcl-2 during androgen-unresponsive progression of prostate cancer

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