Proliferative Tumor Doubling Times of Prostatic Carcinoma

Prostate cancer (PCa) has a variable biology ranging from latent cancer to extremely aggressive tumors. Proliferative activities of cancers may indicate their biological potential. A flow cytometric assay to calculate maximum proliferative doubling times (Tmax) of PCa in radical prostatectomy specim...

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Main Authors: Priya N. Werahera, L. Michael Glode, Francisco G. La Rosa, M. Scott Lucia, E. David Crawford, Kenneth Easterday, Holly T. Sullivan, Rameshwar S. Sidhu, Elizabeth Genova, Tammy Hedlund
Format: Article
Language:English
Published: Wiley 2011-01-01
Series:Prostate Cancer
Online Access:http://dx.doi.org/10.1155/2011/301850
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author Priya N. Werahera
L. Michael Glode
Francisco G. La Rosa
M. Scott Lucia
E. David Crawford
Kenneth Easterday
Holly T. Sullivan
Rameshwar S. Sidhu
Elizabeth Genova
Tammy Hedlund
author_facet Priya N. Werahera
L. Michael Glode
Francisco G. La Rosa
M. Scott Lucia
E. David Crawford
Kenneth Easterday
Holly T. Sullivan
Rameshwar S. Sidhu
Elizabeth Genova
Tammy Hedlund
author_sort Priya N. Werahera
collection DOAJ
description Prostate cancer (PCa) has a variable biology ranging from latent cancer to extremely aggressive tumors. Proliferative activities of cancers may indicate their biological potential. A flow cytometric assay to calculate maximum proliferative doubling times (Tmax) of PCa in radical prostatectomy specimens after preoperative in vivo bromodeoxyuridine (BrdU) infusion is presented. Only 4/17 specimens had tumors large enough for flow cytometric analysis. The Tmax of tumors was similar and ranged from 0.6 to 3.6 months. Tumors had calculated doubling times 2- to 25-fold faster than their matched normal tissue. Variations in labeling index and Tmax were observed within a tumor as well as between different Gleason grades. The observed PSA doubling times (PSA-DT) ranged from 18.4 to 32.0 months, considerably slower than the corresponding Tmax of tumors involved. While lack of data for apoptotic rates is a limitation, apparent biological differences between latent versus aggressive PCa may be attributable to variations in apoptotic rates of these tumors rather than their cell proliferative rates.
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series Prostate Cancer
spelling doaj-art-769fe663bfa9453b9f46ffc22a74aef52025-08-20T02:07:14ZengWileyProstate Cancer2090-31112090-312X2011-01-01201110.1155/2011/301850301850Proliferative Tumor Doubling Times of Prostatic CarcinomaPriya N. Werahera0L. Michael Glode1Francisco G. La Rosa2M. Scott Lucia3E. David Crawford4Kenneth Easterday5Holly T. Sullivan6Rameshwar S. Sidhu7Elizabeth Genova8Tammy Hedlund9Department of Pathology, University of Colorado Anschutz Medical Campus, P.O. Box 6511, Aurora, CO 80045, USAMedical Oncology, University of Colorado Anschutz Medical Campus, CO 80045, USADepartment of Pathology, University of Colorado Anschutz Medical Campus, P.O. Box 6511, Aurora, CO 80045, USADepartment of Pathology, University of Colorado Anschutz Medical Campus, P.O. Box 6511, Aurora, CO 80045, USARadiation Oncology, University of Colorado Anschutz Medical Campus, CO 80045, USAPharmacy Department, University of Colorado Anschutz Medical Campus, CO 80045, USADepartment of Pathology, University of Colorado Anschutz Medical Campus, P.O. Box 6511, Aurora, CO 80045, USADepartment of Pathology, University of Colorado Anschutz Medical Campus, P.O. Box 6511, Aurora, CO 80045, USADepartment of Pathology, University of Colorado Anschutz Medical Campus, P.O. Box 6511, Aurora, CO 80045, USADepartment of Pathology, University of Colorado Anschutz Medical Campus, P.O. Box 6511, Aurora, CO 80045, USAProstate cancer (PCa) has a variable biology ranging from latent cancer to extremely aggressive tumors. Proliferative activities of cancers may indicate their biological potential. A flow cytometric assay to calculate maximum proliferative doubling times (Tmax) of PCa in radical prostatectomy specimens after preoperative in vivo bromodeoxyuridine (BrdU) infusion is presented. Only 4/17 specimens had tumors large enough for flow cytometric analysis. The Tmax of tumors was similar and ranged from 0.6 to 3.6 months. Tumors had calculated doubling times 2- to 25-fold faster than their matched normal tissue. Variations in labeling index and Tmax were observed within a tumor as well as between different Gleason grades. The observed PSA doubling times (PSA-DT) ranged from 18.4 to 32.0 months, considerably slower than the corresponding Tmax of tumors involved. While lack of data for apoptotic rates is a limitation, apparent biological differences between latent versus aggressive PCa may be attributable to variations in apoptotic rates of these tumors rather than their cell proliferative rates.http://dx.doi.org/10.1155/2011/301850
spellingShingle Priya N. Werahera
L. Michael Glode
Francisco G. La Rosa
M. Scott Lucia
E. David Crawford
Kenneth Easterday
Holly T. Sullivan
Rameshwar S. Sidhu
Elizabeth Genova
Tammy Hedlund
Proliferative Tumor Doubling Times of Prostatic Carcinoma
Prostate Cancer
title Proliferative Tumor Doubling Times of Prostatic Carcinoma
title_full Proliferative Tumor Doubling Times of Prostatic Carcinoma
title_fullStr Proliferative Tumor Doubling Times of Prostatic Carcinoma
title_full_unstemmed Proliferative Tumor Doubling Times of Prostatic Carcinoma
title_short Proliferative Tumor Doubling Times of Prostatic Carcinoma
title_sort proliferative tumor doubling times of prostatic carcinoma
url http://dx.doi.org/10.1155/2011/301850
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