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Article ; Online: Identifying Research Priorities in Adult Day Centers to Support Evidence-Based Care of Vulnerable Older Adults.

Sadarangani, Tina / Zagorski, William / Parker, Lauren / Missaelides, Lydia

Progress in community health partnerships : research, education, and action

2021 Volume 15, Issue 1, Page(s) 127–131

Abstract: Adult day centers (ADCs) are essential community resources that allow frail older adults to remain in their communities. Research demonstrates that ADC staff have the capacity to leverage their culturally and socially congruent relationships with clients ...

Abstract	Adult day centers (ADCs) are essential community resources that allow frail older adults to remain in their communities. Research demonstrates that ADC staff have the capacity to leverage their culturally and socially congruent relationships with clients and caregivers, to deliver evidence-based interventions that improve health outcomes. Yet, they remain a largely overlooked neighborhood resource for older adults with complex health care needs. The National Adult Day Services Association (NADSA) created a multistakeholder work group to identify priority areas for research to enhance the quality of services offered in ADCs and the delivery of evidence-based practices to clients. This perspective piece, which presents the workgroup's findings in the form of key research priorities, is intended as practical guide for researchers seeking to align their research questions with the needs of ADCs and those they serve. In addition to identifying areas of further exploration, we discuss current studies being undertaken within the ADC setting.
MeSH term(s)	Aged ; Caregivers ; Community-Based Participatory Research ; Evidence-Based Medicine ; Humans ; Research Personnel
Language	English
Publishing date	2021-03-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2275483-0
ISSN	1557-055X ; 1557-0541
ISSN (online)	1557-055X
ISSN	1557-0541
DOI	10.1353/cpr.2021.0012
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Article ; Online: A National Survey of Data Currently being Collected by Adult Day Service Centers Across the United States.

Sadarangani, Tina / Anderson, Keith / Vora, Paayal / Missaelides, Lydia / Zagorski, William

Journal of applied gerontology : the official journal of the Southern Gerontological Society

2021 Volume 41, Issue 3, Page(s) 729–735

Abstract: An understanding of adult day service centers' (ADC) impacts on clients' health and well-being has been hampered by a lack of large-scale data. Standardizing data collection is critical to strengthening ADC programs, demonstrating their effectiveness, ... ...

Abstract	An understanding of adult day service centers' (ADC) impacts on clients' health and well-being has been hampered by a lack of large-scale data. Standardizing data collection is critical to strengthening ADC programs, demonstrating their effectiveness, and enabling them to leverage additional funding streams beyond Medicaid. We distributed an electronic survey on current data collection efforts to ADCs nationally to determine categories of data ADCs are collecting related to clients' health. In our sample (
MeSH term(s)	Activities of Daily Living ; Caregivers ; Humans ; Medicaid ; Outcome Assessment, Health Care ; Surveys and Questionnaires ; United States
Language	English
Publishing date	2021-05-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	155897-3
ISSN	1552-4523 ; 0733-4648
ISSN (online)	1552-4523
ISSN	0733-4648
DOI	10.1177/07334648211013974
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Article ; Online: Retraction for Braden et al., "Distinct Action of the Retinoblastoma Pathway on the DNA Replication Machinery Defines Specific Roles for Cyclin-Dependent Kinase Complexes in Prereplication Complex Assembly and S-Phase Progression".

Braden, Wesley A / Lenihan, Jon M / Lan, Zhengdao / Luce, K Scott / Zagorski, William / Bosco, Emily / Reed, Michael F / Cook, Jeanette G / Knudsen, Erik S

Molecular and cellular biology

2020 Volume 40, Issue 17

Language	English
Publishing date	2020-08-14
Publishing country	United States
Document type	Journal Article ; Retraction of Publication
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.00319-20
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Zs.A 1666: Show issues

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Article: Retinoblastoma deficiency increases chemosensitivity in lung cancer.

Zagorski, William A / Knudsen, Erik S / Reed, Michael F

Cancer research

2007 Volume 67, Issue 17, Page(s) 8264–8273

Abstract: The retinoblastoma (RB) tumor suppressor is mutated or functionally inactivated in the majority of human malignancies, and p16(INK4a)-cyclin D1-cyclin-dependent kinase 4-RB pathway aberrations are present in nearly all cases of non-small cell lung cancer ...

Abstract	The retinoblastoma (RB) tumor suppressor is mutated or functionally inactivated in the majority of human malignancies, and p16(INK4a)-cyclin D1-cyclin-dependent kinase 4-RB pathway aberrations are present in nearly all cases of non-small cell lung cancer (NSCLC). Here, the distinct role of RB loss in tumorigenic proliferation and sensitivity to chemotherapeutics was determined in NSCLC cells. Attenuation of RB led to a proliferative advantage in vitro and aggressive tumorigenic growth in xenograft models. Clinically, such aggressive disease is treated with genotoxic and cytotoxic chemotherapeutic agents. In vitro analysis showed that RB deficiency resulted in bypass of the checkpoint response to multiple chemotherapeutic challenges concomitant with an elevated apoptotic response. Correspondingly, RB deficiency in xenograft models led to increased chemosensitivity. However, this response was transient, and a durable response was dependent on prolonged chemotherapeutic administration. Together, these findings show that although RB deficiency enhances sensitivity to chemotherapeutic challenge, efficient and sustainable response is highly dependent on the specific therapeutic regimen, in addition to the molecular environment.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Cell Proliferation ; Drug Resistance, Neoplasm/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Mice ; Mice, Nude ; Retinoblastoma Protein/genetics ; Treatment Outcome ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; Retinoblastoma Protein
Language	English
Publishing date	2007-09-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-06-4753
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Article: RB activity alters checkpoint response and chemosensitivity in lung cancer lines.

Reed, Michael F / Zagorski, William A / Knudsen, Erik S

The Journal of surgical research

2007 Volume 142, Issue 2, Page(s) 364–372

Abstract: Background: The retinoblastoma tumor suppressor (RB) is a key regulator of cell cycle progression and is functionally inactivated in the majority of human non-small cell lung cancers (NSCLC). The specific influence of RB on therapeutic response in NSCLC ...

Abstract	Background: The retinoblastoma tumor suppressor (RB) is a key regulator of cell cycle progression and is functionally inactivated in the majority of human non-small cell lung cancers (NSCLC). The specific influence of RB on therapeutic response in NSCLC remains elusive. Materials and methods: We investigated the consequence of reintroduction of RB on checkpoint response and chemosensitivity in NSCLC cell lines. RB introduction into RB-proficient (NCI-H1299) and -deficient (H1734, H2172) NSCLC cells was achieved by adenoviral infection. RB/E2F target gene expression was determined by immunoblot analysis. Cell cycle response and viability after chemotherapeutic exposure were assessed by flow cytometry and MTT viability assay. Results: RB reconstitution in RB-deficient lines restored regulation of topoIIalpha, thymidylate synthase, and cyclin A. Similarly, RB overexpression in RB-proficient cells caused further regulation of some RB/E2F target genes including thymidylate synthase and topoIIalpha. In addition, RB overexpression resulted in restoration of the G1 arrest mechanism. Exposure of RB-proficient cells to cisplatin, etoposide, or 5-fluorouracil elicited arrest in various phases of the cell cycle while lines deficient for RB exhibited different checkpoint responses. However, introduction of RB restored ability to arrest following chemotherapeutic exposure. Chemotherapeutic challenge resulted in varying effects on cellular viability independent of RB status, yet restoration of RB activity conferred partial chemoresistance. Conclusions: These results demonstrate that RB reconstitution into RB-deficient NSCLC lines establishes regulation of certain RB/E2F target genes and restores G1 arrest mechanisms. Furthermore, introduction of RB enhances the G1 checkpoint response to chemotherapeutics and decreases chemosensitivity. Knowledge of RB-dependent chemosensitivity may ultimately contribute to individualized therapy based on molecular characterization of tumors.
MeSH term(s)	Adenoviridae/genetics ; Antineoplastic Agents/pharmacology ; Cell Line, Transformed ; Cell Line, Tumor ; Cell Survival/physiology ; Drug Resistance, Neoplasm/physiology ; E2F Transcription Factors/metabolism ; G1 Phase/physiology ; Gene Expression Regulation, Neoplastic ; Genes, cdc/physiology ; Genetic Vectors ; Humans ; Kidney/cytology ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/physiopathology ; Retinoblastoma Protein/genetics ; Retinoblastoma Protein/metabolism
Chemical Substances	Antineoplastic Agents ; E2F Transcription Factors ; Retinoblastoma Protein
Language	English
Publishing date	2007-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80170-7
ISSN	1095-8673 ; 0022-4804
ISSN (online)	1095-8673
ISSN	0022-4804
DOI	10.1016/j.jss.2007.03.038
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Article ; Online: The carboxy-terminal tail of human cytomegalovirus (HCMV) US28 regulates both chemokine-independent and chemokine-dependent signaling in HCMV-infected cells.

Stropes, Melissa P / Schneider, Olivia D / Zagorski, William A / Miller, Jeanette L C / Miller, William E

Journal of virology

2009 Volume 83, Issue 19, Page(s) 10016–10027

Abstract: The human cytomegalovirus (HCMV)-encoded G-protein-coupled receptor (GPCR) US28 is a potent activator of a number of signaling pathways in HCMV-infected cells. The intracellular carboxy-terminal domain of US28 contains residues critical for the ... ...

Abstract	The human cytomegalovirus (HCMV)-encoded G-protein-coupled receptor (GPCR) US28 is a potent activator of a number of signaling pathways in HCMV-infected cells. The intracellular carboxy-terminal domain of US28 contains residues critical for the regulation of US28 signaling in heterologous expression systems; however, the role that this domain plays during HCMV infection remains unknown. For this study, we constructed an HCMV recombinant virus encoding a carboxy-terminal domain truncation mutant of US28, FLAG-US28/1-314, to investigate the role that this domain plays in US28 signaling. We demonstrate that US28/1-314 exhibits a more potent phospholipase C-beta (PLC-beta) signal than does wild-type US28, indicating that the carboxy-terminal domain plays an important role in regulating agonist-independent signaling in infected cells. Moreover, HMCV-infected cells expressing the US28/1-314 mutant exhibit a prolonged calcium signal in response to CCL5, indicating that the US28 carboxy-terminal domain also regulates agonist-dependent signaling. Finally, while the chemokine CX3CL1 behaves as an inverse agonist or inhibitor of constitutive US28 signaling to PLC-beta, we demonstrate that CX3CL1 functions as an agonist with regard to US28-stimulated calcium release. This study is the first to demonstrate that the carboxy terminus of US28 controls US28 signaling in the context of HCMV infection and indicates that chemokines such as CX3CL1 can decrease constitutive US28 signals and yet simultaneously promote nonconstitutive US28 signals.
MeSH term(s)	Amino Acid Sequence ; Cell Separation ; Chemokine CX3CL1/metabolism ; Chromosomes, Artificial, Bacterial/metabolism ; Cytomegalovirus/metabolism ; Fibroblasts/virology ; Flow Cytometry ; Humans ; Inositol Phosphates/chemistry ; Models, Biological ; Molecular Sequence Data ; Mutation ; Protein Structure, Tertiary ; Receptors, Chemokine/metabolism ; Signal Transduction ; Viral Proteins/metabolism
Chemical Substances	CX3CL1 protein, human ; Chemokine CX3CL1 ; Inositol Phosphates ; Receptors, Chemokine ; US28 receptor, Cytomegalovirus ; Viral Proteins
Language	English
Publishing date	2009-07-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.00354-09
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Article ; Online: US28 is a potent activator of phospholipase C during HCMV infection of clinically relevant target cells.

Miller, William E / Zagorski, William A / Brenneman, Joanna D / Avery, Diana / Miller, Jeanette L C / O'Connor, Christine M

PloS one

2012 Volume 7, Issue 11, Page(s) e50524

Abstract: Members of the cytomegalovirus family each encode two or more genes with significant homology to G-protein coupled receptors (GPCRs). In rodent models of pathogenesis, these viral encoded GPCRs play functionally significant roles, as their deletion ... ...

Abstract	Members of the cytomegalovirus family each encode two or more genes with significant homology to G-protein coupled receptors (GPCRs). In rodent models of pathogenesis, these viral encoded GPCRs play functionally significant roles, as their deletion results in crippled viruses that cannot traffic properly and/or replicate in virally important target cells. Of the four HCMV encoded GPCRs, US28 has garnered the most attention due to the fact that it exhibits both agonist-independent and agonist-dependent signaling activity and has been demonstrated to promote cellular migration and proliferation. Thus, it appears that the CMV GPCRs play important roles in viral replication in vivo as well as promote the development of virus-associated pathology. In the current study we have utilized a series of HCMV/US28 recombinants to investigate the expression profile and signaling activities of US28 in a number of cell types relevant to HCMV infection including smooth muscle cells, endothelial cells and cells derived from glioblastoma multiforme (GBM) tumors. The results indicate that US28 is expressed and exhibits constitutive agonist-independent signaling activity through PLC-β in all cell types tested. Moreover, while CCL5/RANTES and CX3CL1/Fractalkine both promote US28-dependent Ca(++) release in smooth muscle cells, this agonist-dependent effect appears to be cell-specific as we fail to detect US28 driven Ca(++) release in the GBM cells. We have also investigated the effects of US28 on signaling via endogenous GPCRs including those in the LPA receptor family. Our data indicate that US28 can enhance signaling via endogenous LPA receptors. Taken together, our results indicate that US28 induces a variety of signaling events in all cell types tested suggesting that US28 signaling likely plays a significant role during HCMV infection and dissemination in vivo.
MeSH term(s)	Calcium/metabolism ; Cell Line ; Cell Line, Tumor ; Chemokine CCL5/pharmacology ; Chemokine CX3CL1/pharmacology ; Cytomegalovirus/enzymology ; Cytomegalovirus/pathogenicity ; Cytomegalovirus Infections/enzymology ; Cytomegalovirus Infections/metabolism ; Humans ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Receptors, Chemokine/metabolism ; Type C Phospholipases/metabolism ; Viral Proteins/metabolism
Chemical Substances	Chemokine CCL5 ; Chemokine CX3CL1 ; Receptors, Chemokine ; US28 receptor, Cytomegalovirus ; Viral Proteins ; Type C Phospholipases (EC 3.1.4.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2012-11-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0050524
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Article: RB loss promotes aberrant ploidy by deregulating levels and activity of DNA replication factors.

Srinivasan, Seetha V / Mayhew, Christopher N / Schwemberger, Sandy / Zagorski, William / Knudsen, Erik S

The Journal of biological chemistry

2007 Volume 282, Issue 33, Page(s) 23867–23877

Abstract: The retinoblastoma tumor suppressor (RB) is functionally inactivated in many human cancers. Classically, RB functions to repress E2F-mediated transcription and inhibit cell cycle progression. Consequently, RB ablation leads to loss of cell cycle control ... ...

Abstract	The retinoblastoma tumor suppressor (RB) is functionally inactivated in many human cancers. Classically, RB functions to repress E2F-mediated transcription and inhibit cell cycle progression. Consequently, RB ablation leads to loss of cell cycle control and aberrant expression of E2F target genes. Emerging evidence indicates a role for RB in maintenance of genomic stability. Here, mouse adult fibroblasts were utilized to demonstrate that aberrant DNA content in RB-deficient cells occurs concomitantly with an increase in levels and chromatin association of DNA replication factors. Furthermore, following exposure to nocodazole, RB-proficient cells arrest with 4 n DNA content, whereas RB-deficient cells bypass the mitotic block, continue DNA synthesis, and accumulate cells with higher ploidy and micronuclei. Under this condition, RB-deficient cells also retain high levels of tethered replication factors, MCM7 and PCNA, indicating that DNA replication occurs in these cells under nonpermissive conditions. Exogenous expression of replication factors Cdc6 or Cdt1 in RB-proficient cells does not recapitulate the RB-deficient cell phenotype. However, ectopic E2F expression in RB-proficient cells elevated ploidy and bypassed the response to nocodazole-induced cessation of DNA replication in a manner analogous to RB loss. Collectively, these results demonstrate that deregulated S phase control is a key mechanism by which RB-deficient cells acquire elevated ploidy.
MeSH term(s)	Animals ; Cell Cycle Proteins/genetics ; Cells, Cultured ; Chromatin/metabolism ; DNA Replication ; DNA-Binding Proteins/genetics ; E2F Transcription Factors/genetics ; Fibroblasts/cytology ; Gene Expression Regulation ; Mice ; Minichromosome Maintenance Complex Component 7 ; Nuclear Proteins/genetics ; Ploidies ; Proliferating Cell Nuclear Antigen/genetics ; Retinoblastoma Protein/deficiency ; S Phase
Chemical Substances	CDC6 protein, human ; CDT1 protein, human ; Cell Cycle Proteins ; Chromatin ; DNA-Binding Proteins ; E2F Transcription Factors ; Nuclear Proteins ; Proliferating Cell Nuclear Antigen ; Retinoblastoma Protein ; MCM7 protein, human (EC 3.6.4.12) ; Minichromosome Maintenance Complex Component 7 (EC 3.6.4.12)
Language	English
Publishing date	2007-06-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M700542200
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Article ; Online: Inhibition of retinoblastoma tumor suppressor activity by RNA interference in lung cancer lines.

Reed, Michael F / Zagorski, William A / Howington, John A / Zilfou, Jack T / Knudsen, Erik S

The Annals of thoracic surgery

2006 Volume 82, Issue 1, Page(s) 249–253

Abstract: Background: Inactivation of retinoblastoma (RB) tumor suppressor function occurs frequently in lung cancer. Short-hairpin RNA can be constructed to target specific sequences and efficiently knock down protein expression. We developed a short-hairpin RNA ...

Abstract	Background: Inactivation of retinoblastoma (RB) tumor suppressor function occurs frequently in lung cancer. Short-hairpin RNA can be constructed to target specific sequences and efficiently knock down protein expression. We developed a short-hairpin RNA approach to specifically target Rb in lung cancer cells to determine the influence of RB knockdown on proliferation. Methods: NCI-H520 human lung cancer cells (wild-type Rb) were transfected with pMSCVpuro-Rb3C, a plasmid containing a short-hairpin sequence targeted to human Rb. Transfectants harboring the construct were selected with puromycin. Loss of RB expression in selected cell populations was determined by immunoblotting. Proliferating cells were counted to establish growth rates. Retinoblastoma-proficient and RB-deficient tumor growth was monitored in nude mice. Results: Transfection with pMSCVpuro-Rb3C dramatically diminished RB expression and led to aberrant expression of RB-regulated genes. Cells harboring pMSCVpuro-Rb3C grew at an increased rate compared with control cells: 480.6 +/- 37.7 versus 159.4 +/- 36.2 (relative cell count at 12 days). Tumor growth in nude mice also increased with RB knockdown compared with control mice: 135.2 +/- 73.6 mm3 versus 40.0 +/- 17.0 mm3 (tumor volume at 10 days). Conclusions: Inhibition of RB expression is efficiently achieved in lung cancer cells with short-hairpin RNA. Genetic targets of RB are deregulated with RB knockdown. Retinoblastoma depletion increases growth in vitro and in murine xenografts. These studies indicate that even in the context of an established tumor cell line, RB limits tumorigenic proliferation. Additionally, this model will serve as an ideal system to evaluate the role of RB activity on therapeutic response.
MeSH term(s)	Animals ; Antigens, Neoplasm/biosynthesis ; Antigens, Neoplasm/genetics ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/pathology ; Cell Cycle Proteins/biosynthesis ; Cell Cycle Proteins/genetics ; Cell Division/drug effects ; Cell Line, Tumor/cytology ; Cell Line, Tumor/drug effects ; Cell Line, Tumor/transplantation ; DNA Topoisomerases, Type II/biosynthesis ; DNA Topoisomerases, Type II/genetics ; DNA-Binding Proteins/biosynthesis ; DNA-Binding Proteins/genetics ; Down-Regulation/drug effects ; Female ; Gene Expression Profiling ; Genes, Retinoblastoma ; Genes, cdc ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics ; Neoplasm Transplantation ; Oligonucleotide Array Sequence Analysis ; RNA Interference ; RNA, Small Interfering/pharmacology ; Retinoblastoma Protein/antagonists & inhibitors ; Retinoblastoma Protein/genetics ; Thymidylate Synthase/biosynthesis ; Thymidylate Synthase/genetics ; Transfection
Chemical Substances	Antigens, Neoplasm ; Cell Cycle Proteins ; DNA-Binding Proteins ; Neoplasm Proteins ; RNA, Small Interfering ; Retinoblastoma Protein ; Thymidylate Synthase (EC 2.1.1.45) ; DNA Topoisomerases, Type II (EC 5.99.1.3)
Language	English
Publishing date	2006-07
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	211007-6
ISSN	1552-6259 ; 0003-4975
ISSN (online)	1552-6259
ISSN	0003-4975
DOI	10.1016/j.athoracsur.2006.02.033
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Article: Mitogenic action of the androgen receptor sensitizes prostate cancer cells to taxane-based cytotoxic insult.

Hess-Wilson, Janet K / Daly, Hannah K / Zagorski, William A / Montville, Christopher P / Knudsen, Karen E

Cancer research

2006 Volume 66, Issue 24, Page(s) 11998–12008

Abstract: Prostate cancer cells are dependent on androgen for growth and survival; as such, inhibition of androgen receptor (AR) activity is the first line of intervention for disseminated disease. Recently, specific cytotoxic agents have been shown to extend ... ...

Abstract	Prostate cancer cells are dependent on androgen for growth and survival; as such, inhibition of androgen receptor (AR) activity is the first line of intervention for disseminated disease. Recently, specific cytotoxic agents have been shown to extend survival times in patients with advanced disease. Given the established ability of androgen to modify cell survival in prostate cancer cells, it is imperative to determine the effect of the hormonal environment on cytotoxic response. Here, we show that the response of prostate cancer cells to taxane-induced cell death is significantly enhanced by androgen stimulation in AR-positive, androgen-dependent prostate cancer cells. Similar results were observed on androgen-independent AR activation. By contrast, AR-positive yet androgen-independent or AR-negative cells were refractory to androgen influence on taxane function. The ability of androgen to potentiate taxane activity was dependent on its mitogenic capacity and was separable from overall AR activity, as coadministration of AR antagonists, G(1) cyclin-dependent kinase inhibitors, or high-dose (growth inhibitory) androgen nullified the proapoptotic function of androgen. Observed induction of cell death was attributed to caspase-dependent apoptosis and correlated with p53 activation. Combined, these data indicate that the cytotoxic effects of taxanes are substantially influenced by the hormonal environment and/or status of AR activity in prostate cancer cells and provide the foundation for refinement and optimization of cytotoxic intervention in prostate cancer.
MeSH term(s)	Androgens/physiology ; Bridged-Ring Compounds/therapeutic use ; Cell Division/drug effects ; Cell Line, Tumor ; Cell Survival/drug effects ; DNA Primers ; Humans ; Male ; Micronucleus Tests ; Prostate-Specific Antigen/genetics ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/pathology ; RNA, Neoplasm/genetics ; Receptors, Androgen/physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Taxoids/therapeutic use
Chemical Substances	Androgens ; Bridged-Ring Compounds ; DNA Primers ; RNA, Neoplasm ; Receptors, Androgen ; Taxoids ; taxane (1605-68-1) ; Prostate-Specific Antigen (EC 3.4.21.77)
Language	English
Publishing date	2006-12-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-06-2249
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