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  1. Article ; Online: Commentary on "Region 2 of 8q24 is associated with the risk of aggressive prostate cancer in Caribbean men of African descent from Guadeloupe (French West Indies)".

    Koochekpour, Shahriar

    Asian journal of andrology

    2015  Volume 17, Issue 1, Page(s) 160

    MeSH term(s) African Continental Ancestry Group/genetics ; Chromosomes, Human, Pair 8/genetics ; Genetic Predisposition to Disease/genetics ; Humans ; Male ; Prostatic Neoplasms/epidemiology ; Prostatic Neoplasms/genetics
    Language English
    Publishing date 2015-01
    Publishing country China
    Document type Comment ; Journal Article
    ZDB-ID 2075824-8
    ISSN 1745-7262 ; 1008-682X
    ISSN (online) 1745-7262
    ISSN 1008-682X
    DOI 10.4103/1008-682X.143305
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5739: Show issues Location:
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  2. Article ; Online: Biological and clinical significance of androgens and androgen receptor in prostate cancer.

    Koochekpour, Shahriar

    International journal of biological sciences

    2014  Volume 10, Issue 6, Page(s) 652–653

    MeSH term(s) Androgens/metabolism ; Humans ; Male ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism
    Chemical Substances AR protein, human ; Androgens ; Receptors, Androgen
    Language English
    Publishing date 2014-06-10
    Publishing country Australia
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2179208-2
    ISSN 1449-2288 ; 1449-2288
    ISSN (online) 1449-2288
    ISSN 1449-2288
    DOI 10.7150/ijbs.9576
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Commentary on "Region 2 of 8q24 is associated with the risk of aggressive prostate cancer in Caribbean men of African descent from Guadeloupe (French West Indies)"

    Shahriar Koochekpour

    Asian Journal of Andrology, Vol 17, Iss 1, Pp 160-

    2015  Volume 160

    Keywords Medicine ; R ; Diseases of the genitourinary system. Urology ; RC870-923
    Language English
    Publishing date 2015-02-01T00:00:00Z
    Publisher Wolters Kluwer Medknow Publications
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Glutamate, a metabolic biomarker of aggressiveness and a potential therapeutic target for prostate cancer.

    Koochekpour, Shahriar

    Asian journal of andrology

    2013  Volume 15, Issue 2, Page(s) 212–213

    Language English
    Publishing date 2013-01-14
    Publishing country China
    Document type Comment ; Journal Article
    ZDB-ID 2075824-8
    ISSN 1745-7262 ; 1008-682X
    ISSN (online) 1745-7262
    ISSN 1008-682X
    DOI 10.1038/aja.2012.145
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5739: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  5. Article ; Online: DNA methylome and the complexity of discovering prostate cancer biomarkers.

    Koochekpour, Shahriar

    Asian journal of andrology

    2011  Volume 13, Issue 5, Page(s) 661–662

    MeSH term(s) Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; CpG Islands ; DNA Methylation ; Humans ; Male ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism
    Chemical Substances Biomarkers, Tumor
    Language English
    Publishing date 2011-07-04
    Publishing country China
    Document type Journal Article
    ZDB-ID 2075824-8
    ISSN 1745-7262 ; 1008-682X
    ISSN (online) 1745-7262
    ISSN 1008-682X
    DOI 10.1038/aja.2011.90
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5739: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  6. Article ; Online: Comment on "Effect of transferred NK4 gene on proliferation, migration, invasion, and apoptosis of human prostate cancer DU145 cells" by Dan Yue et al. in Asian Journal of Andrology.

    Koochekpour, Shahriar

    Asian journal of andrology

    2010  Volume 12, Issue 3, Page(s) 444–446

    MeSH term(s) Adenocarcinoma/genetics ; Adenocarcinoma/secondary ; Adenocarcinoma/therapy ; Autocrine Communication/genetics ; Gene Expression Regulation, Neoplastic ; Genetic Therapy ; Hepatocyte Growth Factor/chemistry ; Hepatocyte Growth Factor/genetics ; Hepatocyte Growth Factor/physiology ; Humans ; Male ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Prostatic Neoplasms/therapy
    Chemical Substances HGF protein, human ; Hepatocyte Growth Factor (67256-21-7)
    Language English
    Publishing date 2010-04-19
    Publishing country China
    Document type Comment ; Journal Article
    ZDB-ID 2075824-8
    ISSN 1745-7262 ; 1008-682X
    ISSN (online) 1745-7262
    ISSN 1008-682X
    DOI 10.1038/aja.2010.26
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5739: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Androgen receptor splice variants and prostate cancer: From bench to bedside.

    Wadosky, Kristine M / Koochekpour, Shahriar

    Oncotarget

    2017  Volume 8, Issue 11, Page(s) 18550–18576

    Abstract: Therapeutic interventions for advanced prostate cancer (PCa) center on inhibiting androgen receptor (AR) and downstream signaling pathways. Resistance to androgen deprivation therapy and/or AR antagonists is inevitable and molecular mechanisms driving ... ...

    Abstract Therapeutic interventions for advanced prostate cancer (PCa) center on inhibiting androgen receptor (AR) and downstream signaling pathways. Resistance to androgen deprivation therapy and/or AR antagonists is inevitable and molecular mechanisms driving castration-resistant PCa (CR-PCa) primarily involve alterations in AR expression and activity. Detailed molecular biology work over the past decade, discussed at length in this review article, has revealed several AR transcripts that result from alternative splicing. These AR splice variants are increased in cell and mouse models of CR-PCa and in CR-PCa tumors. Several AR variants lack the ligand binding domain, but retain their ability to bind DNA and activate transcription-linking constitutive AR function and therapeutic failure. ARV7 is the only variant endogenously detected at the protein level and thus has undergone more thorough molecular characterization. Clinical trials in PCa are currently investigating ARV7 utility as a biomarker and new therapeutics that inhibit ARV7 . Overall, this review will illustrate the historical perspectives of AR splice variant discovery using fundamental molecular biology techniques and how it changed the clinical approach to both therapeutic decisions and strategy. The body of work investigating AR splice variants in PCa represents a true example of translational research from bench to bedside.
    MeSH term(s) Alternative Splicing ; Humans ; Male ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Protein Isoforms ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism
    Chemical Substances AR protein, human ; Protein Isoforms ; Receptors, Androgen
    Language English
    Publishing date 2017-01-08
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.14537
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Androgen receptor signaling and mutations in prostate cancer.

    Koochekpour, Shahriar

    Asian journal of andrology

    2010  Volume 12, Issue 5, Page(s) 639–657

    Abstract: Normal and neoplastic growth of the prostate gland are dependent on androgen receptor (AR) expression and function. Androgenic activation of the AR, in association with its coregulatory factors, is the classical pathway that leads to transcriptional ... ...

    Abstract Normal and neoplastic growth of the prostate gland are dependent on androgen receptor (AR) expression and function. Androgenic activation of the AR, in association with its coregulatory factors, is the classical pathway that leads to transcriptional activity of AR target genes. Alternatively, cytoplasmic signaling crosstalk of AR by growth factors, neurotrophic peptides, cytokines or nonandrogenic hormones may have important roles in prostate carcinogenesis and in metastatic or androgen-independent (AI) progression of the disease. In addition, cross-modulation by various nuclear transcription factors acting through basal transcriptional machinery could positively or negatively affect the AR or AR target genes expression and activity. Androgen ablation leads to an initial favorable response in a significant number of patients; however, almost invariably patients relapse with an aggressive form of the disease known as castration-resistant or hormone-refractory prostate cancer (PCa). Understanding critical molecular events that lead PCa cells to resist androgen-deprivation therapy is essential in developing successful treatments for hormone-refractory disease. In a significant number of hormone-refractory patients, the AR is overexpressed, mutated or genomically amplified. These genetic alterations maintain an active presence for a highly sensitive AR, which is responsive to androgens, antiandrogens or nonandrogenic hormones and collectively confer a selective growth advantage to PCa cells. This review provides a brief synopsis of the AR structure, AR coregulators, posttranslational modifications of AR, duality of AR function in prostate epithelial and stromal cells, AR-dependent signaling, genetic changes in the form of somatic and germline mutations and their known functional significance in PCa cells and tissues.
    MeSH term(s) African Continental Ancestry Group/genetics ; Animals ; European Continental Ancestry Group/genetics ; Gene Expression ; Humans ; Male ; Mutation ; Prostatic Neoplasms/ethnology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Transcription Factors ; Transcriptional Activation
    Chemical Substances Receptors, Androgen ; Transcription Factors
    Language English
    Publishing date 2010-08-16
    Publishing country China
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2075824-8
    ISSN 1745-7262 ; 1008-682X
    ISSN (online) 1745-7262
    ISSN 1008-682X
    DOI 10.1038/aja.2010.89
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5739: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  9. Article ; Online: Molecular mechanisms underlying resistance to androgen deprivation therapy in prostate cancer.

    Wadosky, Kristine M / Koochekpour, Shahriar

    Oncotarget

    2016  Volume 7, Issue 39, Page(s) 64447–64470

    Abstract: Prostate cancer (PCa) is the most widely diagnosed male cancer in the Western World and while low- and intermediate-risk PCa patients have a variety of treatment options, metastatic patients are limited to androgen deprivation therapy (ADT). This ... ...

    Abstract Prostate cancer (PCa) is the most widely diagnosed male cancer in the Western World and while low- and intermediate-risk PCa patients have a variety of treatment options, metastatic patients are limited to androgen deprivation therapy (ADT). This treatment paradigm has been in place for 75 years due to the unique role of androgens in promoting growth of prostatic epithelial cells via the transcription factor androgen receptor (AR) and downstream signaling pathways. Within 2 to 3 years of ADT, disease recurs-at which time, patients are considered to have castration-recurrent PCa (CR-PCa). A universal mechanism by which PCa becomes resistant to ADT has yet to be discovered. In this review article, we discuss underlying molecular mechanisms by which PCa evades ADT. Several major resistance pathways center on androgen signaling, including intratumoral and adrenal androgen production, AR-overexpression and amplification, expression of AR mutants, and constitutively-active AR splice variants. Other ADT resistance mechanisms, including activation of glucocorticoid receptor and impairment of DNA repair pathways are also discussed. New therapies have been approved for treatment of CR-PCa, but increase median survival by only 2-8 months. We discuss possible mechanisms of resistance to these new ADT agents. Finally, the practicality of the application of "precision oncology" to this continuing challenge of therapy resistance in metastatic or CR-PCa is examined. Empirical validation and clinical-based evidence are definitely needed to prove the superiority of "precision" treatment in providing a more targeted approach and curative therapies over the existing practices that are based on biological "cause-and-effect" relationship.
    MeSH term(s) Androgen Antagonists/adverse effects ; Androgen Antagonists/therapeutic use ; Animals ; Antineoplastic Agents, Hormonal/adverse effects ; Antineoplastic Agents, Hormonal/therapeutic use ; Drug Resistance, Neoplasm/genetics ; Humans ; Kallikreins/blood ; Male ; Mutation ; Neoplasm Staging ; Phosphorylation ; Prostate-Specific Antigen/blood ; Prostatic Neoplasms, Castration-Resistant/blood ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/pathology ; Receptors, Androgen/drug effects ; Receptors, Androgen/genetics ; Receptors, Androgen/metabolism ; Risk Factors ; Signal Transduction/drug effects ; Treatment Outcome
    Chemical Substances AR protein, human ; Androgen Antagonists ; Antineoplastic Agents, Hormonal ; Receptors, Androgen ; KLK3 protein, human (EC 3.4.21.-) ; Kallikreins (EC 3.4.21.-) ; Prostate-Specific Antigen (EC 3.4.21.77)
    Language English
    Publishing date 2016-08-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.10901
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Riluzole induces AR degradation via endoplasmic reticulum stress pathway in androgen-dependent and castration-resistant prostate cancer cells.

    Wadosky, Kristine M / Shourideh, Mojgan / Goodrich, David W / Koochekpour, Shahriar

    The Prostate

    2018  Volume 79, Issue 2, Page(s) 140–150

    Abstract: Background: Prostate cancer (PCa) is diagnosed at the highest rate of all non-cutaneous male cancers in the United States. The androgen-dependent (AD) transcription factor, androgen receptor (AR), drives PCa-but inhibiting AR or androgen biosynthesis ... ...

    Abstract Background: Prostate cancer (PCa) is diagnosed at the highest rate of all non-cutaneous male cancers in the United States. The androgen-dependent (AD) transcription factor, androgen receptor (AR), drives PCa-but inhibiting AR or androgen biosynthesis induces remission for only a short time. At which point, patients acquire more aggressive castration-resistant (CR) disease with re-activated AR-dependent signaling. To combat treatment resistance, down-regulating AR protein expression has been considered as a potential treatment strategy for CR-PCa.
    Methods: AD- and CR-PCa cell lines were treated with the well-tolerated FDA-approved oral medicine, riluzole. Expression of full-length or wild-type AR (AR-FL) and constitutively active AR-splice variant 7 (AR-V7) was assessed by immunoblotting. AR-FL/AR-V7 activity was measured using qRT-PCR of AR-target genes. Cytoplasmic [Ca
    Results: We demonstrate that riluzole downregulates AR-FL, mutant ARs, and AR-V7 proteins expression by protein degradation through ERS pathway and selective autophagy. Riluzole also significantly inhibited AR transcription activity by decreasing its target genes expression (PSA, TMPRSS2, and KLK2).
    Conclusions: We provide key mechanistic insights by which riluzole exerts its anti-tumorigenic effects and induces AR protein degradation via ERS pathways. Our findings support the potential utility of riluzole for treatment of PCa.
    MeSH term(s) Activating Transcription Factor 6/metabolism ; Androgens/metabolism ; Autophagy/drug effects ; Cell Line, Tumor ; Drug Interactions ; Endoplasmic Reticulum Stress/drug effects ; Endoribonucleases/antagonists & inhibitors ; Endoribonucleases/metabolism ; Humans ; Male ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Protein Serine-Threonine Kinases/antagonists & inhibitors ; Protein Serine-Threonine Kinases/metabolism ; Receptors, Androgen/biosynthesis ; Receptors, Androgen/metabolism ; Riluzole/pharmacology ; Sequestosome-1 Protein/metabolism ; Signal Transduction/drug effects ; Sulfonamides/pharmacology ; Thiophenes/pharmacology
    Chemical Substances AR protein, human ; ATF6 protein, human ; Activating Transcription Factor 6 ; Androgens ; Receptors, Androgen ; SQSTM1 protein, human ; STF 083010 ; Sequestosome-1 Protein ; Sulfonamides ; Thiophenes ; Riluzole (7LJ087RS6F) ; ERN1 protein, human (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-)
    Language English
    Publishing date 2018-10-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 604707-5
    ISSN 1097-0045 ; 0270-4137
    ISSN (online) 1097-0045
    ISSN 0270-4137
    DOI 10.1002/pros.23719
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1608: Show issues Location:
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