Increased EZH2 expression in prostate cancer is associated with metastatic recurrence following external beam radiotherapy
Background Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy metastatic disease recurrence, and may promote radioresistance. Methods EZH2 expression was investigated using immunohistochemistry in diagno...
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| Vydané v: | The Prostate Ročník 79; číslo 10; s. 1079 - 1089 |
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| Hlavní autori: | , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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United States
Wiley Subscription Services, Inc
01.07.2019
John Wiley and Sons Inc |
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| ISSN: | 0270-4137, 1097-0045, 1097-0045 |
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| Abstract | Background
Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy metastatic disease recurrence, and may promote radioresistance.
Methods
EZH2 expression was investigated using immunohistochemistry in diagnostic prostate biopsies of 113 prostate cancer patients treated with radiotherapy with curative intent. Associations between EZH2 expression in malignant and benign tissue in prostate biopsy cores and outcomes were investigated using univariate and multivariate Cox regression analyses. LNCaP and PC3 cell radiosensitivity was investigated using colony formation and γH2AX assays following UNC1999 chemical probe‐mediated EZH2 inhibition.
Results
While there was no significant association between EZH2 expression and biochemical recurrence following radiotherapy, univariate analysis revealed that prostate cancer cytoplasmic and total EZH2 expression were significantly associated with metastasis development postradiotherapy (P = 0.034 and P = 0.003, respectively). On multivariate analysis, the prostate cancer total EZH2 expression score remained statistically significant (P = 0.003), while cytoplasmic EZH2 expression did not reach statistical significance (P = 0.053). No association was observed between normal adjacent prostate EZH2 expression and biochemical recurrence or metastasis. LNCaP and PC3 cell treatment with UNC1999 reduced histone H3 lysine 27 tri‐methylation levels. Irradiation of LNCaP or PC3 cells with a single 2 Gy fraction with UNC1999‐mediated EZH2 inhibition resulted in a statistically significant, though modest, reduction in cell colony number for both cell lines. Increased γH2AX foci were observed 24 hours after ionizing irradiation in LNCaP cells, but not in PC3, following UNC1999‐mediated EZH2 inhibition vs controls.
Conclusions
Taken together, these results reveal that high pretreatment EZH2 expression in prostate cancer in diagnostic biopsies is associated with an increased risk of postradiotherapy metastatic disease recurrence, but EZH2 function may only at most play a modest role in promoting prostate cancer cell radioresistance. |
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| AbstractList | Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy metastatic disease recurrence, and may promote radioresistance.
EZH2 expression was investigated using immunohistochemistry in diagnostic prostate biopsies of 113 prostate cancer patients treated with radiotherapy with curative intent. Associations between EZH2 expression in malignant and benign tissue in prostate biopsy cores and outcomes were investigated using univariate and multivariate Cox regression analyses. LNCaP and PC3 cell radiosensitivity was investigated using colony formation and γH2AX assays following UNC1999 chemical probe-mediated EZH2 inhibition.
While there was no significant association between EZH2 expression and biochemical recurrence following radiotherapy, univariate analysis revealed that prostate cancer cytoplasmic and total EZH2 expression were significantly associated with metastasis development postradiotherapy (P = 0.034 and P = 0.003, respectively). On multivariate analysis, the prostate cancer total EZH2 expression score remained statistically significant (P = 0.003), while cytoplasmic EZH2 expression did not reach statistical significance (P = 0.053). No association was observed between normal adjacent prostate EZH2 expression and biochemical recurrence or metastasis. LNCaP and PC3 cell treatment with UNC1999 reduced histone H3 lysine 27 tri-methylation levels. Irradiation of LNCaP or PC3 cells with a single 2 Gy fraction with UNC1999-mediated EZH2 inhibition resulted in a statistically significant, though modest, reduction in cell colony number for both cell lines. Increased γH2AX foci were observed 24 hours after ionizing irradiation in LNCaP cells, but not in PC3, following UNC1999-mediated EZH2 inhibition vs controls.
Taken together, these results reveal that high pretreatment EZH2 expression in prostate cancer in diagnostic biopsies is associated with an increased risk of postradiotherapy metastatic disease recurrence, but EZH2 function may only at most play a modest role in promoting prostate cancer cell radioresistance. BackgroundEnhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy metastatic disease recurrence, and may promote radioresistance.MethodsEZH2 expression was investigated using immunohistochemistry in diagnostic prostate biopsies of 113 prostate cancer patients treated with radiotherapy with curative intent. Associations between EZH2 expression in malignant and benign tissue in prostate biopsy cores and outcomes were investigated using univariate and multivariate Cox regression analyses. LNCaP and PC3 cell radiosensitivity was investigated using colony formation and γH2AX assays following UNC1999 chemical probe‐mediated EZH2 inhibition.ResultsWhile there was no significant association between EZH2 expression and biochemical recurrence following radiotherapy, univariate analysis revealed that prostate cancer cytoplasmic and total EZH2 expression were significantly associated with metastasis development postradiotherapy (P = 0.034 and P = 0.003, respectively). On multivariate analysis, the prostate cancer total EZH2 expression score remained statistically significant (P = 0.003), while cytoplasmic EZH2 expression did not reach statistical significance (P = 0.053). No association was observed between normal adjacent prostate EZH2 expression and biochemical recurrence or metastasis. LNCaP and PC3 cell treatment with UNC1999 reduced histone H3 lysine 27 tri‐methylation levels. Irradiation of LNCaP or PC3 cells with a single 2 Gy fraction with UNC1999‐mediated EZH2 inhibition resulted in a statistically significant, though modest, reduction in cell colony number for both cell lines. Increased γH2AX foci were observed 24 hours after ionizing irradiation in LNCaP cells, but not in PC3, following UNC1999‐mediated EZH2 inhibition vs controls.ConclusionsTaken together, these results reveal that high pretreatment EZH2 expression in prostate cancer in diagnostic biopsies is associated with an increased risk of postradiotherapy metastatic disease recurrence, but EZH2 function may only at most play a modest role in promoting prostate cancer cell radioresistance. Background: Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy metastatic disease recurrence, and may promote radioresistance. Methods: EZH2 expression was investigated using immunohistochemistry in diagnostic prostate biopsies of 113 prostate cancer patients treated with radiotherapy with curative intent. Associations between EZH2 expression in malignant and benign tissue in prostate biopsy cores and outcomes were investigated using univariate and multivariate Cox regression analyses. LNCaP and PC3 cell radiosensitivity was investigated using colony formation and γH2AX assays following UNC1999 chemical probe-mediated EZH2 inhibition. Results: While there was no significant association between EZH2 expression and biochemical recurrence following radiotherapy, univariate analysis revealed that prostate cancer cytoplasmic and total EZH2 expression were significantly associated with metastasis development postradiotherapy (P = 0.034 and P = 0.003, respectively). On multivariate analysis, the prostate cancer total EZH2 expression score remained statistically significant (P = 0.003), while cytoplasmic EZH2 expression did not reach statistical significance (P = 0.053). No association was observed between normal adjacent prostate EZH2 expression and biochemical recurrence or metastasis. LNCaP and PC3 cell treatment with UNC1999 reduced histone H3 lysine 27 tri-methylation levels. Irradiation of LNCaP or PC3 cells with a single 2 Gy fraction with UNC1999-mediated EZH2 inhibition resulted in a statistically significant, though modest, reduction in cell colony number for both cell lines. Increased γH2AX foci were observed 24 hours after ionizing irradiation in LNCaP cells, but not in PC3, following UNC1999-mediated EZH2 inhibition vs controls. Conclusions: Taken together, these results reveal that high pretreatment EZH2 expression in prostate cancer in diagnostic biopsies is associated with an increased risk of postradiotherapymetastatic disease recurrence, but EZH2 function may only at most play a modest role in promoting prostate cancer cell radioresistance. Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy metastatic disease recurrence, and may promote radioresistance.BACKGROUNDEnhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy metastatic disease recurrence, and may promote radioresistance.EZH2 expression was investigated using immunohistochemistry in diagnostic prostate biopsies of 113 prostate cancer patients treated with radiotherapy with curative intent. Associations between EZH2 expression in malignant and benign tissue in prostate biopsy cores and outcomes were investigated using univariate and multivariate Cox regression analyses. LNCaP and PC3 cell radiosensitivity was investigated using colony formation and γH2AX assays following UNC1999 chemical probe-mediated EZH2 inhibition.METHODSEZH2 expression was investigated using immunohistochemistry in diagnostic prostate biopsies of 113 prostate cancer patients treated with radiotherapy with curative intent. Associations between EZH2 expression in malignant and benign tissue in prostate biopsy cores and outcomes were investigated using univariate and multivariate Cox regression analyses. LNCaP and PC3 cell radiosensitivity was investigated using colony formation and γH2AX assays following UNC1999 chemical probe-mediated EZH2 inhibition.While there was no significant association between EZH2 expression and biochemical recurrence following radiotherapy, univariate analysis revealed that prostate cancer cytoplasmic and total EZH2 expression were significantly associated with metastasis development postradiotherapy (P = 0.034 and P = 0.003, respectively). On multivariate analysis, the prostate cancer total EZH2 expression score remained statistically significant (P = 0.003), while cytoplasmic EZH2 expression did not reach statistical significance (P = 0.053). No association was observed between normal adjacent prostate EZH2 expression and biochemical recurrence or metastasis. LNCaP and PC3 cell treatment with UNC1999 reduced histone H3 lysine 27 tri-methylation levels. Irradiation of LNCaP or PC3 cells with a single 2 Gy fraction with UNC1999-mediated EZH2 inhibition resulted in a statistically significant, though modest, reduction in cell colony number for both cell lines. Increased γH2AX foci were observed 24 hours after ionizing irradiation in LNCaP cells, but not in PC3, following UNC1999-mediated EZH2 inhibition vs controls.RESULTSWhile there was no significant association between EZH2 expression and biochemical recurrence following radiotherapy, univariate analysis revealed that prostate cancer cytoplasmic and total EZH2 expression were significantly associated with metastasis development postradiotherapy (P = 0.034 and P = 0.003, respectively). On multivariate analysis, the prostate cancer total EZH2 expression score remained statistically significant (P = 0.003), while cytoplasmic EZH2 expression did not reach statistical significance (P = 0.053). No association was observed between normal adjacent prostate EZH2 expression and biochemical recurrence or metastasis. LNCaP and PC3 cell treatment with UNC1999 reduced histone H3 lysine 27 tri-methylation levels. Irradiation of LNCaP or PC3 cells with a single 2 Gy fraction with UNC1999-mediated EZH2 inhibition resulted in a statistically significant, though modest, reduction in cell colony number for both cell lines. Increased γH2AX foci were observed 24 hours after ionizing irradiation in LNCaP cells, but not in PC3, following UNC1999-mediated EZH2 inhibition vs controls.Taken together, these results reveal that high pretreatment EZH2 expression in prostate cancer in diagnostic biopsies is associated with an increased risk of postradiotherapy metastatic disease recurrence, but EZH2 function may only at most play a modest role in promoting prostate cancer cell radioresistance.CONCLUSIONSTaken together, these results reveal that high pretreatment EZH2 expression in prostate cancer in diagnostic biopsies is associated with an increased risk of postradiotherapy metastatic disease recurrence, but EZH2 function may only at most play a modest role in promoting prostate cancer cell radioresistance. Background Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy metastatic disease recurrence, and may promote radioresistance. Methods EZH2 expression was investigated using immunohistochemistry in diagnostic prostate biopsies of 113 prostate cancer patients treated with radiotherapy with curative intent. Associations between EZH2 expression in malignant and benign tissue in prostate biopsy cores and outcomes were investigated using univariate and multivariate Cox regression analyses. LNCaP and PC3 cell radiosensitivity was investigated using colony formation and γH2AX assays following UNC1999 chemical probe‐mediated EZH2 inhibition. Results While there was no significant association between EZH2 expression and biochemical recurrence following radiotherapy, univariate analysis revealed that prostate cancer cytoplasmic and total EZH2 expression were significantly associated with metastasis development postradiotherapy (P = 0.034 and P = 0.003, respectively). On multivariate analysis, the prostate cancer total EZH2 expression score remained statistically significant (P = 0.003), while cytoplasmic EZH2 expression did not reach statistical significance (P = 0.053). No association was observed between normal adjacent prostate EZH2 expression and biochemical recurrence or metastasis. LNCaP and PC3 cell treatment with UNC1999 reduced histone H3 lysine 27 tri‐methylation levels. Irradiation of LNCaP or PC3 cells with a single 2 Gy fraction with UNC1999‐mediated EZH2 inhibition resulted in a statistically significant, though modest, reduction in cell colony number for both cell lines. Increased γH2AX foci were observed 24 hours after ionizing irradiation in LNCaP cells, but not in PC3, following UNC1999‐mediated EZH2 inhibition vs controls. Conclusions Taken together, these results reveal that high pretreatment EZH2 expression in prostate cancer in diagnostic biopsies is associated with an increased risk of postradiotherapy metastatic disease recurrence, but EZH2 function may only at most play a modest role in promoting prostate cancer cell radioresistance. Background Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy metastatic disease recurrence, and may promote radioresistance. Methods EZH2 expression was investigated using immunohistochemistry in diagnostic prostate biopsies of 113 prostate cancer patients treated with radiotherapy with curative intent. Associations between EZH2 expression in malignant and benign tissue in prostate biopsy cores and outcomes were investigated using univariate and multivariate Cox regression analyses. LNCaP and PC3 cell radiosensitivity was investigated using colony formation and gamma H2AX assays following UNC1999 chemical probe-mediated EZH2 inhibition. Results While there was no significant association between EZH2 expression and biochemical recurrence following radiotherapy, univariate analysis revealed that prostate cancer cytoplasmic and total EZH2 expression were significantly associated with metastasis development postradiotherapy (P = 0.034 and P = 0.003, respectively). On multivariate analysis, the prostate cancer total EZH2 expression score remained statistically significant (P = 0.003), while cytoplasmic EZH2 expression did not reach statistical significance (P = 0.053). No association was observed between normal adjacent prostate EZH2 expression and biochemical recurrence or metastasis. LNCaP and PC3 cell treatment with UNC1999 reduced histone H3 lysine 27 tri-methylation levels. Irradiation of LNCaP or PC3 cells with a single 2 Gy fraction with UNC1999-mediated EZH2 inhibition resulted in a statistically significant, though modest, reduction in cell colony number for both cell lines. Increased gamma H2AX foci were observed 24 hours after ionizing irradiation in LNCaP cells, but not in PC3, following UNC1999-mediated EZH2 inhibition vs controls. Conclusions Taken together, these results reveal that high pretreatment EZH2 expression in prostate cancer in diagnostic biopsies is associated with an increased risk of postradiotherapy metastatic disease recurrence, but EZH2 function may only at most play a modest role in promoting prostate cancer cell radioresistance. |
| Author | Hamdy, Freddie C. Prevo, Remko Sjoberg, Daniel D. Lilja, Hans Lamb, Alastair D. Bryant, Richard J. Cunliffe, Vincent T. Bountra, Chas Wu, Xiaoning Higgins, Geoffrey S. Scott, Helen Rieunier, Guillaume Verrill, Clare L. Carlsson, Sigrid V. Cerundolo, Lucia Macaulay, Valentine |
| AuthorAffiliation | 6 Department of Laboratory Medicine, Surgery (Urology), and Medicine (GU‐Oncology) Memorial Sloan Kettering Cancer Center New York New York 10 Department of Biomedical Science University of Sheffield Sheffield United Kingdom 7 Department of Translational Medicine Lund University Malmö Sweden 4 Urology Service at the Department of Surgery Memorial Sloan Kettering Cancer Center New York New York 9 Oxford NIHR Biomedical Research Centre University of Oxford Oxford United Kingdom 2 Nuffield Department of Surgical Sciences University of Oxford Oxford United Kingdom 3 Department of Epidemiology & Biostatistics Memorial Sloan Kettering Cancer Center New York New York 5 Department of Urology Institute of Clinical Sciences, Sahlgrenska Academy at Gothenburg University Gothenburg Sweden 8 Department of Oncology University of Oxford Oxford United Kingdom 11 Nuffield Department of Medicine, Structural Genomics Consortium University of Oxford Oxford United Kingdom 1 Department of Oncology, CRUK/MRC Oxford In |
| AuthorAffiliation_xml | – name: 1 Department of Oncology, CRUK/MRC Oxford Institute for Radiation Oncology University of Oxford Oxford United Kingdom – name: 9 Oxford NIHR Biomedical Research Centre University of Oxford Oxford United Kingdom – name: 2 Nuffield Department of Surgical Sciences University of Oxford Oxford United Kingdom – name: 8 Department of Oncology University of Oxford Oxford United Kingdom – name: 10 Department of Biomedical Science University of Sheffield Sheffield United Kingdom – name: 4 Urology Service at the Department of Surgery Memorial Sloan Kettering Cancer Center New York New York – name: 7 Department of Translational Medicine Lund University Malmö Sweden – name: 3 Department of Epidemiology & Biostatistics Memorial Sloan Kettering Cancer Center New York New York – name: 6 Department of Laboratory Medicine, Surgery (Urology), and Medicine (GU‐Oncology) Memorial Sloan Kettering Cancer Center New York New York – name: 11 Nuffield Department of Medicine, Structural Genomics Consortium University of Oxford Oxford United Kingdom – name: 5 Department of Urology Institute of Clinical Sciences, Sahlgrenska Academy at Gothenburg University Gothenburg Sweden |
| Author_xml | – sequence: 1 givenname: Xiaoning surname: Wu fullname: Wu, Xiaoning organization: University of Oxford – sequence: 2 givenname: Helen surname: Scott fullname: Scott, Helen organization: University of Oxford – sequence: 3 givenname: Sigrid V. surname: Carlsson fullname: Carlsson, Sigrid V. organization: Institute of Clinical Sciences, Sahlgrenska Academy at Gothenburg University – sequence: 4 givenname: Daniel D. surname: Sjoberg fullname: Sjoberg, Daniel D. organization: Memorial Sloan Kettering Cancer Center – sequence: 5 givenname: Lucia surname: Cerundolo fullname: Cerundolo, Lucia organization: University of Oxford – sequence: 6 givenname: Hans surname: Lilja fullname: Lilja, Hans organization: Lund University – sequence: 7 givenname: Remko surname: Prevo fullname: Prevo, Remko organization: University of Oxford – sequence: 8 givenname: Guillaume surname: Rieunier fullname: Rieunier, Guillaume organization: University of Oxford – sequence: 9 givenname: Valentine surname: Macaulay fullname: Macaulay, Valentine organization: University of Oxford – sequence: 10 givenname: Geoffrey S. surname: Higgins fullname: Higgins, Geoffrey S. organization: University of Oxford – sequence: 11 givenname: Clare L. surname: Verrill fullname: Verrill, Clare L. organization: University of Oxford – sequence: 12 givenname: Alastair D. surname: Lamb fullname: Lamb, Alastair D. organization: University of Oxford – sequence: 13 givenname: Vincent T. surname: Cunliffe fullname: Cunliffe, Vincent T. organization: University of Sheffield – sequence: 14 givenname: Chas surname: Bountra fullname: Bountra, Chas organization: University of Oxford – sequence: 15 givenname: Freddie C. surname: Hamdy fullname: Hamdy, Freddie C. organization: University of Oxford – sequence: 16 givenname: Richard J. orcidid: 0000-0002-8330-9251 surname: Bryant fullname: Bryant, Richard J. email: richard.bryant@nds.ox.ac.uk organization: University of Oxford |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31104332$$D View this record in MEDLINE/PubMed https://gup.ub.gu.se/publication/281881$$DView record from Swedish Publication Index (Göteborgs universitet) |
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| Copyright | 2019 The Authors. Published by Wiley Periodicals, Inc. 2019 The Authors. The Prostate Published by Wiley Periodicals, Inc. 2019. This article is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| Copyright_xml | – notice: 2019 The Authors. Published by Wiley Periodicals, Inc. – notice: 2019 The Authors. The Prostate Published by Wiley Periodicals, Inc. – notice: 2019. This article is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| CorporateAuthor | Institutionen för translationell medicin Department of Translational Medicine Lunds universitet Profile areas and other strong research environments Clinical Chemistry, Malmö Lund University Strategiska forskningsområden (SFO) EpiHealth: Epidemiology for Health Faculty of Medicine Strategic research areas (SRA) Medicinska fakulteten Klinisk kemi, Malmö Profilområden och andra starka forskningsmiljöer |
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| Keywords | radiotherapy prostate cancer enhancer of zeste 2 |
| Language | English |
| License | Attribution 2019 The Authors. The Prostate Published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
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| Snippet | Background
Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy... Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy metastatic... BackgroundEnhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy... Background Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy... Background: Enhancer of zeste 2 (EZH2) promotes prostate cancer progression. We hypothesized that increased EZH2 expression is associated with postradiotherapy... |
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| SubjectTerms | androgen biochemical failure Biopsy Bone Neoplasms - metabolism Bone Neoplasms - secondary Cancer and Oncology Cancer och onkologi Cell Line, Tumor Clinical Medicine Colonies Disease Progression DNA-damage Endocrinology & Metabolism enhancer of zeste 2 Enhancer of Zeste Homolog 2 Protein - metabolism group protein ezh2 Histone H3 histone methyltransferase activity Humans Immunohistochemistry Klinisk medicin Lysine Male Medical and Health Sciences Medicin och hälsovetenskap Metastases Metastasis Methylation Multivariate analysis Neoplasm Grading Nephrology Njurmedicin Original proliferation Prostate - metabolism Prostate - pathology Prostate cancer Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Prostatic Neoplasms - radiotherapy Radiation therapy Radioresistance Radiosensitivity radiotherapy risk Soft Tissue Neoplasms - metabolism Soft Tissue Neoplasms - secondary Statistical analysis suppression Urology & Nephrology valproic acid |
| Title | Increased EZH2 expression in prostate cancer is associated with metastatic recurrence following external beam radiotherapy |
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