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  1. AU="Nora M Navone"
  2. AU="Jönsson, Klas"
  3. AU="de Steenwinkel, Jurriaan E M"
  4. AU="Yadav, Kabir"
  5. AU="Sasmaz, Mahmut Unsal"
  6. AU="Solá-Sánchez, Ernesto"
  7. AU="Cinquanta, Lucrezia"
  8. AU="Drivenes, Jakob Lillemoen"
  9. AU="Martín, José Ignacio Valero"
  10. AU=Mahmood Shah Sayed Mustafa
  11. AU=Sales-Peres Silvia Helena de Carvalho
  12. AU="Boyea, Beth Lincoln"
  13. AU=Martorell-Marugan Jordi
  14. AU="Serventi, Lisa"
  15. AU=O'Shea John J AU=O'Shea John J
  16. AU="Jiang, Dahai"
  17. AU="Sheng, Chu-Qiao"
  18. AU="Rodríguez, Fausto J."
  19. AU="Sadowski, Peter"
  20. AU="Noguera, Austin"
  21. AU="Daigneault, Tina"
  22. AU="Flores-Martínez, José Juan"
  23. AU="Gan, Yu-Ling"
  24. AU=Banno Asoka AU=Banno Asoka
  25. AU="Bertolin, Kalyne"
  26. AU="Rising, James A"
  27. AU="Jackson Voelkel"
  28. AU="Arias, Marisa"
  29. AU="Le, Uyen Nguyen Phuong"
  30. AU="Shim, Yun M"
  31. AU="Ngan, Hau Lan"
  32. AU="Shah, Fawad Ali"
  33. AU="Rodriguez Chinesta, J M"
  34. AU="Reddy, Avril"
  35. AU="Vachani, Anil"
  36. AU="Lofland, Gabriela"
  37. AU="Zou, Xiaoyan"
  38. AU="Norhafizah Bt Sahril"

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  1. Artikel ; Online: Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis

    Hyunho Han / Yan Wang / Josue Curto / Sreeharsha Gurrapu / Sara Laudato / Alekya Rumandla / Goutam Chakraborty / Xiaobo Wang / Hong Chen / Yan Jiang / Dhiraj Kumar / Emily G. Caggiano / Monica Capogiri / Boyu Zhang / Yan Ji / Sankar N. Maity / Min Hu / Shanshan Bai / Ana M. Aparicio /
    Eleni Efstathiou / Christopher J. Logothetis / Nicholas Navin / Nora M. Navone / Yu Chen / Filippo G. Giancotti

    Cell Reports, Vol 39, Iss 1, Pp 110595- (2022)

    2022  

    Abstract: Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate ... ...

    Abstract Summary: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition.
    Schlagwörter CP: Cancer ; Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2022-04-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel: A 3D in vitro model of patient-derived prostate cancer xenograft for controlled interrogation of in vivo tumor-stromal interactions

    Fong, Eliza L.S / Antonios G. Mikos / Daniel A. Harrington / Jun Yang / Mary C. Farach-Carson / Micaela Morgado / Nora M. Navone / Xinhai Wan

    Biomaterials. 2016 Jan., v. 77

    2016  

    Abstract: Patient-derived xenograft (PDX) models better represent human cancer than traditional cell lines. However, the complex in vivo environment makes it challenging to employ PDX models to investigate tumor-stromal interactions, such as those that mediate ... ...

    Abstract Patient-derived xenograft (PDX) models better represent human cancer than traditional cell lines. However, the complex in vivo environment makes it challenging to employ PDX models to investigate tumor-stromal interactions, such as those that mediate prostate cancer (PCa) bone metastasis. Thus, we engineered a defined three-dimensional (3D) hydrogel system capable of supporting the co-culture of PCa PDX cells and osteoblastic cells to recapitulate the PCa-osteoblast unit within the bone metastatic microenvironment in vitro. Our 3D model not only maintained cell viability but also preserved the typical osteogenic phenotype of PCa PDX cells. Additionally, co-culture cellularity was maintained over that of either cell type cultured alone, suggesting that the PCa-osteoblast cross-talk supports PCa progression in bone, as is hypothesized to occur in patients with prostatic bone metastasis. Strikingly, osteoblastic cells co-cultured with PCa PDX tumoroids organized around the tumoroids, closely mimicking the architecture of PCa metastases in bone. Finally, tumor-stromal signaling mediated by the fibroblast growth factor axis tightly paralleled that in the in vivo counterpart. Together, these findings indicate that this 3D PCa PDX model recapitulates important pathological properties of PCa bone metastasis, and validate the use of this model for controlled and systematic interrogation of complex in vivo tumor-stromal interactions.
    Schlagwörter cell viability ; coculture ; fibroblast growth factors ; humans ; hydrocolloids ; metastasis ; models ; patients ; phenotype ; prostatic neoplasms
    Sprache Englisch
    Erscheinungsverlauf 2016-01
    Umfang p. 164-172.
    Erscheinungsort Elsevier Ltd
    Dokumenttyp Artikel
    ZDB-ID 603079-8
    ISSN 0142-9612
    ISSN 0142-9612
    DOI 10.1016/j.biomaterials.2015.10.059
    Datenquelle NAL Katalog (AGRICOLA)

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  3. Artikel ; Online: Mechanistic Support for Combined MET and AR Blockade in Castration-Resistant Prostate Cancer

    Yuanyuan Qiao / Felix Y. Feng / Yugang Wang / Xuhong Cao / Sumin Han / Kari Wilder-Romans / Nora M. Navone / Christopher Logothetis / Russell S. Taichman / Evan T. Keller / Ganesh S. Palapattu / Ajjai S. Alva / David C. Smith / Scott A. Tomlins / Arul M. Chinnaiyan / Todd M. Morgan

    Neoplasia : An International Journal for Oncology Research, Vol 18, Iss 1, Pp 1-

    2016  Band 9

    Abstract: A recent phase III trial of the MET kinase inhibitor cabozantinib in men with castration-resistant prostate cancer (CRPC) failed to meet its primary survival end point; however, most men with CRPC have intact androgen receptor (AR) signaling. As previous ...

    Abstract A recent phase III trial of the MET kinase inhibitor cabozantinib in men with castration-resistant prostate cancer (CRPC) failed to meet its primary survival end point; however, most men with CRPC have intact androgen receptor (AR) signaling. As previous work supports negative regulation of MET by AR signaling, we hypothesized that intact AR signaling may have limited the efficacy of cabozantinib in some of these patients. To assess the role of AR signaling on MET inhibition, we first performed an in silico analysis of human CRPC tissue samples stratified by AR signaling status (+ or −), which identified MET expression as markedly increased in AR− samples. In vitro, AR signaling inhibition in AR+ CRPC models increased MET expression and resulted in susceptibility to ligand (HGF) activation. Likewise, MET inhibition was only effective in blocking cancer phenotypes in cells with MET overexpression. Using multiple AR+ CRPC in vitro and in vivo models, we showed that combined cabozantinib and enzalutamide (AR antagonist) treatment was more efficacious than either inhibitor alone. These data provide a compelling rationale to combine AR and MET inhibition in CRPC and may explain the negative results of the phase III cabozantinib study in CRPC. Similarly, the expression of MET in AR− disease, whether due to AR inhibition or loss of AR signaling, suggests potential utility for MET inhibition in select patients with AR therapy resistance and in AR− prostate cancer.
    Schlagwörter Medicine ; R ; Internal medicine ; RC31-1245 ; Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282
    Erscheinungsdatum 2016-01-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Androgen regulation of 5α-reductase isoenzymes in prostate cancer

    Jin Li / Zhiyong Ding / Zhengxin Wang / Jing-Fang Lu / Sankar N Maity / Nora M Navone / Christopher J Logothetis / Gordon B Mills / Jeri Kim

    PLoS ONE, Vol 6, Iss 12, p e

    implications for prostate cancer prevention.

    2011  Band 28840

    Abstract: The enzyme 5α-reductase, which converts testosterone to dihydrotestosterone (DHT), performs key functions in the androgen receptor (AR) signaling pathway. The three isoenzymes of 5α-reductase identified to date are encoded by different genes: SRD5A1, ... ...

    Abstract The enzyme 5α-reductase, which converts testosterone to dihydrotestosterone (DHT), performs key functions in the androgen receptor (AR) signaling pathway. The three isoenzymes of 5α-reductase identified to date are encoded by different genes: SRD5A1, SRD5A2, and SRD5A3. In this study, we investigated mechanisms underlying androgen regulation of 5α-reductase isoenzyme expression in human prostate cells. We found that androgen regulates the mRNA level of 5α-reductase isoenzymes in a cell type-specific manner, that such regulation occurs at the transcriptional level, and that AR is necessary for this regulation. In addition, our results suggest that AR is recruited to a negative androgen response element (nARE) on the promoter of SRD5A3 in vivo and directly binds to the nARE in vitro. The different expression levels of 5α-reductase isoenzymes may confer response or resistance to 5α-reductase inhibitors and thus may have importance in prostate cancer prevention.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2011-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Quantification of mineralized bone response to prostate cancer by noninvasive in vivo microCT and non-destructive ex vivo microCT and DXA in a mouse model.

    Murali Ravoori / Aneta J Czaplinska / Charles Sikes / Lin Han / Evan M Johnson / Wei Qiao / Chaan Ng / Dianna D Cody / William A Murphy / Kim-Anh Do / Nora M Navone / Vikas Kundra

    PLoS ONE, Vol 5, Iss 3, p e

    2010  Band 9854

    Abstract: To compare nondestructive in vivo and ex vivo micro-computed tomography (muCT) and ex vivo dual-energy-X-ray-absorptiometry (DXA) in characterizing mineralized cortical and trabecular bone response to prostate cancer involving the skeleton in a mouse ... ...

    Abstract To compare nondestructive in vivo and ex vivo micro-computed tomography (muCT) and ex vivo dual-energy-X-ray-absorptiometry (DXA) in characterizing mineralized cortical and trabecular bone response to prostate cancer involving the skeleton in a mouse model.In vivo microCT was performed before and 10 weeks after implantation of human prostate cancer cells (MDA-PCa-2b) or vehicle into SCID mouse femora. After resection, femora were imaged by nondestructive ex vivo specimen microCT at three voxel sizes (31 micro, 16 micro, 8 micro) and DXA, and then sectioned for histomorphometric analysis of mineralized bone. Bone mineral density (BMD), trabecular parameters (number, TbN; separation, TbSp; thickness, TbTh) and mineralized bone volume/total bone volume (BV/TV) were compared and correlated among imaging methods and histomorphometry. Statistical tests were considered significant if P<0.05. Ten weeks post inoculation, diaphyseal BMD increased in the femur with tumor compared to the opposite femur by all modalities (p<0.005, n = 11). Diaphyseal BMD by in vivo microCT correlated with ex vivo 31 and 16 microm microCT and histomorphometry BV/TV (r = 0.91-0.94, P<0.001, n = 11). DXA BMD correlated less with bone histomorphometry (r = 0.73, P<0.001, n = 11) and DXA did not distinguish trabeculae from cortex. By in vivo and ex vivo microCT, trabecular BMD decreased (P<0.05, n = 11) as opposed to the cortex. Unlike BMD, trabecular morphologic parameters were threshold-dependent and when using "fixed-optimal-thresholds," all except TbTh demonstrated trabecular loss with tumor and correlated with histomorphometry (r = 0.73-0.90, P<0.05, n = 11).Prostate cancer involving the skeleton can elicit a host bone response that differentially affects the cortex compared to trabeculae and that can be quantified noninvasively in vivo and nondestructively ex vivo.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2010-03-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel: PRUNE2 is a human prostate cancer suppressor regulated by the intronic long noncoding RNA PCA3

    Salameh, Ahmad / Alessandro K. Lee / Marina Cardó-Vila / Diana N. Nunes / Eleni Efstathiou / Fernanda I. Staquicini / Andrey S. Dobroff / Serena Marchióò / Nora M. Navone / Hitomi Hosoya / Richard C. Lauer / Sijin Wen / Carolina C. Salmeron / Anh Hoang / Irene Newsham / Leandro A. Lima / Dirce M. Carraro / Salvatore Oliviero / Mikhail G. Kolonin /
    Richard L. Sidman / Kim-Anh Do / Patricia Troncoso / Christopher J. Logothetis / Ricardo R. Brentani / George A. Calin / Webster K. Cavenee / Emmanuel Dias-Neto / Renata Pasqualini / Wadih Arap

    Proceedings of the National Academy of Sciences of the United States of America. 2015 July 7, v. 112, no. 27

    2015  

    Abstract: Prostate cancer antigen 3 ( PCA3 ) is the most specific prostate cancer biomarker but its function remains unknown. Here we identify PRUNE2 , a target protein-coding gene variant, which harbors the PCA3 locus, thereby classifying PCA3 as an antisense ... ...

    Abstract Prostate cancer antigen 3 ( PCA3 ) is the most specific prostate cancer biomarker but its function remains unknown. Here we identify PRUNE2 , a target protein-coding gene variant, which harbors the PCA3 locus, thereby classifying PCA3 as an antisense intronic long noncoding (lnc)RNA. We show that PCA3 controls PRUNE2 levels via a unique regulatory mechanism involving formation of a PRUNE2/PCA3 double-stranded RNA that undergoes adenosine deaminase acting on RNA (ADAR)-dependent adenosine-to-inosine RNA editing. PRUNE2 expression or silencing in prostate cancer cells decreased and increased cell proliferation, respectively. Moreover, PRUNE2 and PCA3 elicited opposite effects on tumor growth in immunodeficient tumor-bearing mice. Coregulation and RNA editing of PRUNE2 and PCA3 were confirmed in human prostate cancer specimens, supporting the medical relevance of our findings. These results establish PCA3 as a dominant-negative oncogene and PRUNE2 as an unrecognized tumor suppressor gene in human prostate cancer, and their regulatory axis represents a unique molecular target for diagnostic and therapeutic intervention.
    Schlagwörter RNA editing ; adenosine deaminase ; antigens ; biomarkers ; cell proliferation ; double-stranded RNA ; humans ; loci ; mice ; neoplasm cells ; non-coding RNA ; oncogenes ; prostatic neoplasms ; tumor suppressor genes ; PRUNE2 ; PCA3 ; long noncoding RNA ; ADAR ; prostate cancer
    Sprache Englisch
    Erscheinungsverlauf 2015-0707
    Umfang p. 8403-8408.
    Erscheinungsort National Academy of Sciences
    Dokumenttyp Artikel
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1507882112
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  7. Artikel: PRUNE2 is a human prostate cancer suppressor regulated by the intronic long noncoding RNA PCA3

    Salameh, Ahmad / Alessandro K. Lee / Marina Cardó-Vila / Diana N. Nunes / Eleni Efstathiou / Fernanda I. Staquicini / Andrey S. Dobroff / Serena Marchióò / Nora M. Navone / Hitomi Hosoya / Richard C. Lauer / Sijin Wen / Carolina C. Salmeron / Anh Hoang / Irene Newsham / Leandro A. Lima / Dirce M. Carraro / Salvatore Oliviero / Mikhail G. Kolonin /
    Richard L. Sidman / Kim-Anh Do / Patricia Troncoso / Christopher J. Logothetis / Ricardo R. Brentani / George A. Calin / Webster K. Cavenee / Emmanuel Dias-Neto / Renata Pasqualini / Wadih Arap

    Proceedings of the National Academy of Sciences of the United States of America

    Band v. 112,, Heft no. 2

    Abstract: Prostate cancer antigen 3 ( PCA3 ) is the most specific prostate cancer biomarker but its function remains unknown. Here we identify PRUNE2 , a target protein-coding gene variant, which harbors the PCA3 locus, thereby classifying PCA3 as an antisense ... ...

    Abstract Prostate cancer antigen 3 ( PCA3 ) is the most specific prostate cancer biomarker but its function remains unknown. Here we identify PRUNE2 , a target protein-coding gene variant, which harbors the PCA3 locus, thereby classifying PCA3 as an antisense intronic long noncoding (lnc)RNA. We show that PCA3 controls PRUNE2 levels via a unique regulatory mechanism involving formation of a PRUNE2/PCA3 double-stranded RNA that undergoes adenosine deaminase acting on RNA (ADAR)-dependent adenosine-to-inosine RNA editing. PRUNE2 expression or silencing in prostate cancer cells decreased and increased cell proliferation, respectively. Moreover, PRUNE2 and PCA3 elicited opposite effects on tumor growth in immunodeficient tumor-bearing mice. Coregulation and RNA editing of PRUNE2 and PCA3 were confirmed in human prostate cancer specimens, supporting the medical relevance of our findings. These results establish PCA3 as a dominant-negative oncogene and PRUNE2 as an unrecognized tumor suppressor gene in human prostate cancer, and their regulatory axis represents a unique molecular target for diagnostic and therapeutic intervention.
    Sprache Englisch
    Dokumenttyp Artikel
    ISSN 0027-8424
    Datenquelle AGRIS - International Information System for the Agricultural Sciences and Technology

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