15 results on '"Castrate-resistant prostate cancer"'
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2. The molecular function of kallikrein‐related peptidase 14 demonstrates a key modulatory role in advanced prostate cancer
- Author
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Thomas Kryza, Nathalie Bock, Scott Lovell, Anja Rockstroh, Melanie L. Lehman, Adam Lesner, Janaththani Panchadsaram, Lakmali Munasinghage Silva, Srilakshmi Srinivasan, Cameron E. Snell, Elizabeth D. Williams, Ladan Fazli, Martin Gleave, Jyotsna Batra, Colleen Nelson, Edward W. Tate, Jonathan Harris, John D. Hooper, and Judith A. Clements
- Subjects
castrate‐resistant prostate cancer ,kallikrein‐related peptidase ,metastasis ,prostate cancer ,protease ,protease‐substrate ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Kallikrein‐related peptidase 14 (KLK14) is one of the several secreted KLK serine proteases involved in prostate cancer (PCa) pathogenesis. While relatively understudied, recent reports have identified KLK14 as overexpressed during PCa development. However, the modulation of KLK14 expression during PCa progression and the molecular and biological functions of this protease in the prostate tumor microenvironment remain unknown. To determine the modulation of KLK14 expression during PCa progression, we analyzed the expression levels of KLK14 in patient samples using publicly available databases and immunohistochemistry. In order to delineate the molecular mechanisms involving KLK14 in PCa progression, we integrated proteomic, transcriptomic, and in vitro assays with the goal to identify substrates, related‐signaling pathways, and functional roles of this protease. We showed that KLK14 expression is elevated in advanced PCa, and particularly in metastasis. Additionally, KLK14 levels were found to be decreased in PCa tissues from patients responsive to neoadjuvant therapy compared to untreated patients. Furthermore, we also identified that KLK14 expression reoccurred in patients who developed castrate‐resistant PCa. The combination of proteomic and transcriptomic analysis as well as functional assays revealed several new KLK14 substrates (agrin, desmoglein 2, vitronectin, laminins) and KLK14‐regulated genes (Interleukin 32, midkine, SRY‐Box 9), particularly an involvement of the mitogen‐activated protein kinase 1 and interleukin 1 receptor pathways, and an involvement of KLK14 in the regulation of cellular migration, supporting its involvement in aggressive features of PCa progression. In conclusion, our work showed that KLK14 expression is associated with the development of aggressive PCa suggesting that targeting this protease could offer a novel route to limit the progression of prostate tumors. Additional work is necessary to determine the benefits and implications of targeting/cotargeting KLK14 in PCa as well as to determine the potential use of KLK14 expression as a predictor of PCa aggressiveness or response to treatment.
- Published
- 2020
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3. The molecular function of kallikrein‐related peptidase 14 demonstrates a key modulatory role in advanced prostate cancer
- Author
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Martin E. Gleave, Colleen C. Nelson, Scott Lovell, Srilakshmi Srinivasan, Anja Rockstroh, Adam Lesner, Janaththani Panchadsaram, Jonathan M. Harris, Cameron Snell, Nathalie Bock, Edward W. Tate, Ladan Fazli, Judith A. Clements, Elizabeth D. Williams, Melanie Lehman, Lakmali Munasinghage Silva, John D. Hooper, Thomas Kryza, and Jyotsna Batra
- Subjects
0301 basic medicine ,Male ,Proteomics ,Cancer Research ,protease-substrate ,INVASION ,kallikrein‐related peptidase ,Metastasis ,Transcriptome ,ACTIVATION ,PATHWAY ,Prostate cancer ,MIDKINE ,0302 clinical medicine ,Cell Movement ,Tandem Mass Spectrometry ,castrate-resistant prostate cancer ,Databases, Genetic ,Tumor Microenvironment ,Neoplasm Metastasis ,Chromatography, High Pressure Liquid ,Research Articles ,Midkine ,biology ,protease‐substrate ,General Medicine ,prostate cancer ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,Immunohistochemistry ,Neoadjuvant Therapy ,Up-Regulation ,Gene Expression Regulation, Neoplastic ,Oncology ,030220 oncology & carcinogenesis ,Molecular Medicine ,GROWTH ,Kallikreins ,Life Sciences & Biomedicine ,Signal Transduction ,Research Article ,EXPRESSION ,Proteases ,Down-Regulation ,lcsh:RC254-282 ,03 medical and health sciences ,Cell Line, Tumor ,Genetics ,medicine ,castrate‐resistant prostate cancer ,Humans ,metastasis ,1112 Oncology and Carcinogenesis ,Oncology & Carcinogenesis ,Cell Proliferation ,Tumor microenvironment ,Science & Technology ,IDENTIFICATION ,Prostatic Neoplasms ,protease ,Kallikrein ,medicine.disease ,GENE ,Interleukin 32 ,SERINE-PROTEASE ,030104 developmental biology ,kallikrein-related peptidase ,KLK14 ,biology.protein ,Cancer research - Abstract
Kallikrein‐related peptidase 14 (KLK14) is one of the several secreted KLK serine proteases involved in prostate cancer (PCa) pathogenesis. While relatively understudied, recent reports have identified KLK14 as overexpressed during PCa development. However, the modulation of KLK14 expression during PCa progression and the molecular and biological functions of this protease in the prostate tumor microenvironment remain unknown. To determine the modulation of KLK14 expression during PCa progression, we analyzed the expression levels of KLK14 in patient samples using publicly available databases and immunohistochemistry. In order to delineate the molecular mechanisms involving KLK14 in PCa progression, we integrated proteomic, transcriptomic, and in vitro assays with the goal to identify substrates, related‐signaling pathways, and functional roles of this protease. We showed that KLK14 expression is elevated in advanced PCa, and particularly in metastasis. Additionally, KLK14 levels were found to be decreased in PCa tissues from patients responsive to neoadjuvant therapy compared to untreated patients. Furthermore, we also identified that KLK14 expression reoccurred in patients who developed castrate‐resistant PCa. The combination of proteomic and transcriptomic analysis as well as functional assays revealed several new KLK14 substrates (agrin, desmoglein 2, vitronectin, laminins) and KLK14‐regulated genes (Interleukin 32, midkine, SRY‐Box 9), particularly an involvement of the mitogen‐activated protein kinase 1 and interleukin 1 receptor pathways, and an involvement of KLK14 in the regulation of cellular migration, supporting its involvement in aggressive features of PCa progression. In conclusion, our work showed that KLK14 expression is associated with the development of aggressive PCa suggesting that targeting this protease could offer a novel route to limit the progression of prostate tumors. Additional work is necessary to determine the benefits and implications of targeting/cotargeting KLK14 in PCa as well as to determine the potential use of KLK14 expression as a predictor of PCa aggressiveness or response to treatment., Kallikrein‐related peptidase 14 (KLK14) is a secreted serine protease belonging to the kallikrein‐related‐peptidase family. We identified that KLK14 is overexpressed in advanced prostate cancer and acts on various substrates involved in adhesion, migration, and invasion of cancer cells, thus modulating genes and signaling pathways essential for prostate cancer progression. These results suggest that KLK14 is a potential target to control aggressiveness of prostate tumors.
- Published
- 2020
4. Pembrolizumab in men with heavily treated metastatic castrate‐resistant prostate cancer
- Author
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Patrick Healy, Sundhar Ramalingam, Santosh Gupta, Jason Zhu, Andrew J. Armstrong, Michael R. Harrison, Tian Zhang, Daniel J. George, Matthew D Tucker, William R. Berry, Yuan Wu, Stacey Lisi, Daniele Marin, and Rajan T. Gupta
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Male ,0301 basic medicine ,Oncology ,Cancer Research ,Castrate-resistant prostate cancer ,Pembrolizumab ,Prostate cancer ,chemistry.chemical_compound ,Antineoplastic Agents, Immunological ,0302 clinical medicine ,Clinical efficacy ,Neoplasm Metastasis ,Original Research ,Aged, 80 and over ,education.field_of_study ,mCRPC ,Middle Aged ,lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,prostate cancer ,LRP1b ,Prostatic Neoplasms, Castration-Resistant ,MutS Homolog 2 Protein ,Treatment Outcome ,030220 oncology & carcinogenesis ,Kallikreins ,pembrolizumab ,genomic profiling ,medicine.medical_specialty ,Population ,Antibodies, Monoclonal, Humanized ,lcsh:RC254-282 ,03 medical and health sciences ,Internal medicine ,medicine ,Humans ,Enzalutamide ,Radiology, Nuclear Medicine and imaging ,education ,Aged ,Retrospective Studies ,business.industry ,Clinical Cancer Research ,Microsatellite instability ,Sequence Analysis, DNA ,Prostate-Specific Antigen ,medicine.disease ,Survival Analysis ,030104 developmental biology ,Receptors, LDL ,chemistry ,MSH2 ,Mutation ,business - Abstract
Background Pembrolizumab is approved for patients with metastatic, microsatellite instability (MSI)‐high or mismatch repair‐deficient (dMMR) solid tumors. However, very few men with prostate cancer were included in these initial studies. Methods We performed a single institution retrospective review of men with metastatic castrate‐resistant prostate cancer (mCRPC) who were treated with pembrolizumab. The primary objective was to describe the clinical efficacy of pembrolizumab associated with patient and genomic characteristics. Results We identified 48 men who received ≥1 cycle of pembrolizumab for mCRPC. Of these, 94% (45/48) had ≥3 prior lines of therapy for mCRPC. Somatic tumor sequencing was available in 18/48 men (38%). We found that 17% (8/48) had a ≥50% confirmed PSA decline with pembrolizumab, and 8% (4/48) had a ≥90% PSA decline with durations of response ranging from 3.1 to 16.3 months. Two of these four men had mutations in LRP1b, one of whom also had MSH2 loss and was MSI‐H and TMB‐high. Despite prior progression on enzalutamide, 48% (23/48) of men were treated with concurrent enzalutamide. The median PSA progression‐free‐survival was 1.8 months (range 0.4‐13.7 months), with 31% of patients remaining on pembrolizumab therapy and 54% of men remain alive with a median follow‐up of 7.1 months. Conclusions In a heavily pretreated population of men with mCRPC, pembrolizumab was associated with a ≥50% PSA decline in 17% (8/48) of men, including a dramatic ≥90% PSA response in 8% (4/48), two of whom harbored pathogenic LRP1b mutations suggesting that LRP1b mutations may enrich for PD‐1 inhibitor responsiveness in prostate cancer.
- Published
- 2019
5. Management of advanced prostate cancer in a middle-income country: real-world consideration of the Advanced Prostate Cancer Consensus Conference 2017
- Author
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Rachael Kit Tsan Khong, Rohan Malek, Teng Aik Ong, Chong Beng Chua, Guan Chou Teh, Adlinda Alip, Fuad Ismail, Hwoei Fen Soo Hoo, Marniza Saad, Pei Jye Voon, Chit Sin Loh, Flora Li Tze Chong, Muthukkumaran Thiagarajan, Jasmine Lim, Noor Azam Nasuha, Murali Sundram, Khairul Asri Mohd Ghani, Ibtisam Md Noor, Chun Sen Lim, Azad Hassan Abdul Razack, Hui Meng Tan, Matin Mellor Abdullah, and Noor Ashani Md Yusoff
- Subjects
castration‐resistant prostate cancer ,Male ,medicine.medical_specialty ,Consensus ,Urology ,media_common.quotation_subject ,Locally advanced ,Castrate-resistant prostate cancer ,Reviews ,#pcsm ,cost and access to treatment ,Review ,Middle income country ,Health Services Accessibility ,high‐risk localized prostate cancer ,03 medical and health sciences ,Prostate cancer ,0302 clinical medicine ,Voting ,Health care ,Humans ,Medicine ,Generalizability theory ,030212 general & internal medicine ,Societies, Medical ,media_common ,business.industry ,Malaysia ,Consensus conference ,Prostatic Neoplasms ,castration‐naïve prostate cancer ,medicine.disease ,low‐middle income countries ,#ProstateCancer ,030220 oncology & carcinogenesis ,Family medicine ,Practice Guidelines as Topic ,oligometastatic prostate cancer ,business - Abstract
Objective To examine the results of the Malaysian Advanced Prostate Cancer Consensus Conference (MyAPCCC) 2018, held for assessing the generalizability of consensus reached at the Advanced Prostate Cancer Consensus Conference (APCCC 2017) to Malaysia, a middle-income country. Methods Six key sections were chosen: (1) high-risk localized and locally advanced prostate cancer, (2) oligometastatic prostate cancer, (3) castration-naive prostate cancer, (4) castrate resistant prostate cancer, (5) use of osteoclast-targeted therapy and (6) global access to prostate cancer drugs. There were 101 consensus questions, consisting of 91 questions from APCCC 2017 and 10 new questions from MyAPCCC 2018, selected and modified by the steering committee; of which, 23 questions were assessed in both ideal world and real-world settings. A panel of 22 experts, comprising of 11 urologists and 11 oncologists, voted on 101 predefined questions anonymously. Final voting results were compared with the APCCC 2017 outcomes. Results Most voting results from the MyAPCCC 2018 were consistent with the APCCC 2017 outcomes. No consensus was achieved for controversial topics with little level I evidence, such as management of oligometastatic disease. No consensus was reached on using high-cost drugs in castration-naive or castration-resistant metastatic prostate cancer in real-world settings. All panellists recommended using generic drugs when available. Conclusions The MyAPCCC 2018 voting results reflect the management of advanced prostate cancer in a middle-income country in a real-world setting. These results may serve as a guide for local clinical practices and highlight the financial challenges in modern healthcare.
- Published
- 2019
6. Patients' and partners' views of care and treatment provided for metastatic castrate-resistant prostate cancer in the UK
- Author
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Susan Catt, Malcolm David Mason, Valerie Jenkins, L. Matthews, Shirley May, and Heather Payne
- Subjects
Male ,medicine.medical_specialty ,Palliative care ,Decision Making ,Health Behavior ,Specialist nurse ,Castrate-resistant prostate cancer ,Systemic therapy ,Interviews as Topic ,03 medical and health sciences ,Prostate cancer ,0302 clinical medicine ,medicine ,Humans ,Pain Management ,Prospective Studies ,Neoplasm Metastasis ,Spouses ,Aged ,Aged, 80 and over ,Symptom management ,business.industry ,Cancer ,Middle Aged ,medicine.disease ,United Kingdom ,Prostatic Neoplasms, Castration-Resistant ,Oncology ,030220 oncology & carcinogenesis ,Family medicine ,Structured interview ,Quality of Life ,business ,Attitude to Health - Abstract
Objective\ud Documentations of the experiences of patients with advanced prostate cancer and their partners are sparse. Views of care and treatment received for metastatic castrate resistant prostate cancer (mCRPC) are presented here.\ud \ud Methods\ud Structured interviews conducted within 14 days of a systemic therapy for mCRPC starting and 3 months later explored: treatment decisions, information provision, perceived benefits and harms of treatment, and effects of these on patients’ and partners’ lives.\ud \ud Results\ud Thirty-seven patients and 33 partners recruited from UK cancer centres participated. The majority of patients (46%) reported pain was their worst symptom and many wanted to discuss its management (baseline-50%; 3 months-33%). Patients and partners believed treatment would: delay progression (>75%), improve wellbeing (33%), alleviate pain (≈12%) and extend life (15% -patients, 36% -partners). At 3 months most men (42%) said fatigue was the worst treatment-related side effect (SE), 27% experienced unexpected SEs, and 54% needed help with SEs. Most patients received SE information (85% written; 75% verbally); many additionally searched the internet (33%-patients; 55%-partners). Only 54% of patients said nurse support was accessible. \ud \ud Conclusion\ud Pain and other symptom management is not optimal. Increased specialist nurse provision and earlier palliative care links are needed. Dedicated clinics may be justified.
- Published
- 2019
7. Beyond the androgen receptor II: New approaches to understanding and treating metastatic prostate cancer; Report from the 2017 Coffey-Holden Prostate Cancer Academy Meeting
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Heather H. Cheng, Daniel E. Spratt, Leigh Ellis, Wassim Abida, Howard R. Soule, Andrea K. Miyahira, Jonathan W. Simons, Lauren C. Harshman, and Kenneth J. Pienta
- Subjects
Male ,0301 basic medicine ,Oncology ,medicine.medical_specialty ,Urology ,medicine.medical_treatment ,Castrate-resistant prostate cancer ,03 medical and health sciences ,Prostate cancer ,0302 clinical medicine ,Cancer immunotherapy ,Internal medicine ,medicine ,Animals ,Humans ,Neoplasm Metastasis ,business.industry ,Prostatic Neoplasms ,Immunotherapy ,medicine.disease ,Androgen receptor ,Clinical Practice ,Prostatic Neoplasms, Castration-Resistant ,030104 developmental biology ,Receptors, Androgen ,030220 oncology & carcinogenesis ,Immunology ,business ,Ovarian cancer - Abstract
Introduction The 2017 Coffey-Holden Prostate Cancer Academy (CHPCA) Meeting, “Beyond the Androgen Receptor II: New Approaches to Understanding and Treating Metastatic Prostate Cancer,” was held in Carlsbad, California from June 14-17, 2017. Methods The CHPCA is an annual scientific conference hosted by the Prostate Cancer Foundation (PCF) that is uniquely designed to produce extensive and constructive discussions on the most urgent and impactful topics concerning research into the biology and treatment of metastatic prostate cancer. The 2017 CHPCA Meeting was the 5th meeting in this annual series and was attended by 71 investigators focused on prostate cancer and a variety of other fields including breast and ovarian cancer. Results The discussions at the meeting were concentrated on topics areas including: mechanisms and therapeutic approaches for molecular subclasses of castrate resistant prostate cancer (CRPC), the epigenetic landscape of prostate cancer, the role of DNA repair gene mutations, advancing the use of germline genetics in clinical practice, radionuclides for imaging and therapy, advances in molecular imaging, and therapeutic strategies for successful use of immunotherapy in advanced prostate cancer. Discussion This article reviews the presentations and discussions from the 2017 CHPCA Meeting in order to disseminate this knowledge and accelerate new biological understandings and advances in the treatment of patients with metastatic prostate cancer.
- Published
- 2017
8. Implementing newer agents for the management of castrate-resistant prostate cancer: what is known and what is needed?
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Nicolas Mottet, Maria De Santis, Juan Morote, Filiberto Zattoni, Steven Joniau, and Noel W. Clarke
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Gynecology ,medicine.medical_specialty ,Prostate cancer ,business.industry ,Urology ,Castrate-resistant prostate cancer ,Effective treatment ,Medicine ,business ,Intensive care medicine ,medicine.disease - Abstract
Men receiving androgen-deprivation therapy will in time develop metastatic castrate-resistant prostate cancer (mCRPC). Whilst effective treatment options for mCRPC have traditionally been limited, new agents are becoming available. Since 2010, the number and class of agents available to treat mCRPC has increased dramatically. As such, there is a need for clear guidance on the optimum treatment and sequence of treatments for mCRPC before and after chemotherapy. This evidence-based statement, reflecting the views of the authors, provides suggestions on the continued relevance of conventional approaches to first- and second-line treatment in mCRPC, the potential role of novel treatments, and factors that may influence the choice of hormonal agents and/or chemotherapy.
- Published
- 2014
9. Castrate-resistant prostate cancer: the future of antiandrogens
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Justin Stebbing, Heba Alshaker, and Dmitri Pchejetski
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Oncology ,medicine.medical_specialty ,business.industry ,Antiandrogens ,Castrate-resistant prostate cancer ,Cancer ,medicine.disease ,Prostate cancer ,Internal medicine ,Epidemiology of cancer ,medicine ,Family history ,Risk factor ,business - Abstract
Prostate cancer is the most common non-cutaneous cancer in North American and European men and the second leading cause of male cancer-related death [1]. The lifetime probability of developing prostate cancer in the UK is 14% [1] and in 2010 there were there were 40,975 new cases, accounting for 10,721 deaths [2]. Prostate cancer is associated with many risk factors, including age, family history, ethnicity, diet, and weight and although it is estimated that not more than 5% of all prostate cancer cases are hereditary, family history is appropriately considered a relevant risk factor. Many genetic changes have been associated with prostate cancer, including mutations in P53, P21, and P73 and tumour suppressor genes [3].
- Published
- 2014
10. Metastatic castrate-resistant prostate cancer: a discussion of the physical and psychosocial effects
- Author
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Karen Flynn
- Subjects
Gerontology ,medicine.medical_specialty ,Nursing (miscellaneous) ,business.industry ,Service delivery framework ,Urology ,Psychological intervention ,Castrate-resistant prostate cancer ,Disease ,medicine.disease ,Prostate cancer ,Quality of life ,Nephrology ,Health care ,Physical therapy ,Medicine ,business ,Psychosocial - Abstract
Management options for metastatic castrate-resistant prostate cancer (mCRPC) have increased in recent years resulting in more men living for longer with the disease. The implications for patients and health care services are considered through an examination of the literature in relation to the physical and psychosocial effects of mCRPC and its treatment, looking at quality of life (QoL) and service delivery implications. QoL in advanced prostate cancer has been well documented in the literature but studies involving those with mCRPC are sparse. There is a lack of evidence regarding psychological distress and effective psychological interventions for men with mCRPC. There is a need for research to understand the impact of new treatments on QoL of men and their partners, to establish effective psychological interventions for men with mCRPC and to quantify the increased demand for services with prolonged survival. The purpose of this discussion paper is to examine the physical and psychosocial effects of both disease and treatment, alongside QoL issues and consideration of the implications for service delivery.
- Published
- 2013
11. Metastatic castrate-resistant prostate cancer: dawn of a new age of management
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Susan Masson and Amit Bahl
- Subjects
Gynecology ,Oncology ,medicine.medical_specialty ,business.industry ,Urology ,Internal medicine ,medicine ,Castrate-resistant prostate cancer ,business - Published
- 2012
12. Relationship between serum response factor and androgen receptor in prostate cancer
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Prencipe, Maria, O'Neill, Amanda, O'Hurley, Gillian, Nguyen, Lan K., Fabre, Aurélie, Gallagher, William M., and Watson, R. William
- Subjects
Androgen receptor ,Serum response factor ,urologic and male genital diseases ,Castrate-resistant prostate cancer - Abstract
Background: Serum response factor (SRF) is an important transcription factor in castrate-resistant prostate cancer (CRPC). Since CRPC is associated with androgen receptor (AR) hypersensitivity, we investigated the relationship between SRF and AR. Materials and Methods: Transcriptional activity was assessed by luciferase assay. Cell proliferation was measured by MTT and flow cytometry. Protein expression in patients was assessed by immunohistochemistry. Results: To investigate AR involvement in SRF response to androgen, AR expression was down-regulated using siRNA. This resulted in the abrogation of SRF induction post-DHT. Moreover, DHT stimulation failed to induce SRF transcriptional activity in AR-negative PC346 DCC cells, which was only restored following AR over-expression. Next, SRF expression was down-regulated by siRNA, resulting in AR increased transcriptional activity in castrate-resistant LNCaP Abl cells but not in the parental LNCaP. This negative feedback loop in the resistant cells was confirmed by immunohistochemistry which showed a negative correlation between AR and SRF expression in CRPC bone metastases and a positive correlation in androgen-naïve prostatectomies. Cell proliferation was next assessed following SRF inhibition, demonstrating that SRF inhibition is more effective than AR inhibition in castrate-resistant cells. Conclusion: Our data support SRF as a promising therapeutic target in combination with current treatments. Prostate 75:1704–1717, 2015. © 2015 Wiley Periodicals, Inc. European Commission - Seventh Framework Programme (FP7) Science Foundation Ireland Irish Cancer Society
- Published
- 2015
13. Botanicals inhibit castrate‐resistant prostate cancer via mechanisms involving AMPK, inhibition of lipogenesis, mTOR‐mediated proliferation, and histone modification
- Author
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Jay Whelan and Yi Zhao
- Subjects
Histone ,biology ,Chemistry ,Lipogenesis ,Genetics ,biology.protein ,Cancer research ,Castrate-resistant prostate cancer ,AMPK ,Molecular Biology ,Biochemistry ,PI3K/AKT/mTOR pathway ,Biotechnology - Published
- 2013
14. Medicinal herbs inhibit castrate‐resistant prostate cancer via mechanisms involving AMPK
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Jay Whelan and Yi Zhao
- Subjects
business.industry ,Genetics ,Castrate-resistant prostate cancer ,Cancer research ,Medicinal herbs ,Medicine ,AMPK ,business ,Molecular Biology ,Biochemistry ,Biotechnology - Published
- 2012
15. Enhanced effectiveness of using herbs versus their isolated bioactive compounds in a model of castrate‐resistant prostate cancer
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E-Chu Huang, Yi Zhao, and Jay Whelan
- Subjects
business.industry ,Genetics ,Cancer research ,Castrate-resistant prostate cancer ,Medicine ,business ,Molecular Biology ,Biochemistry ,Biotechnology - Published
- 2011
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