Sökning: WFRF:(Rubin Mark A.) > The Molecular Evolu...
Fältnamn | Indikatorer | Metadata |
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000 | 04056naa a2200349 4500 | |
001 | oai:lup.lub.lu.se:e2544ab0-bc8b-4f5b-bcfa-76d5350273e2 | |
003 | SwePub | |
008 | 190626s2016 | |||||||||||000 ||eng| | |
024 | 7 | a https://lup.lub.lu.se/record/e2544ab0-bc8b-4f5b-bcfa-76d5350273e22 URI |
024 | 7 | a https://doi.org/10.1016/j.euf.2016.11.0122 DOI |
040 | a (SwePub)lu | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a for2 swepub-publicationtype |
072 | 7 | a ref2 swepub-contenttype |
100 | 1 | a Ceder, Yvonneu Lund University,Lunds universitet,Avdelningen för translationell cancerforskning,Institutionen för laboratoriemedicin,Medicinska fakulteten,Medicinsk molekylärbiologi,Forskargrupper vid Lunds universitet,Division of Translational Cancer Research,Department of Laboratory Medicine,Faculty of Medicine,Medical Molecular Biology,Lund University Research Groups4 aut0 (Swepub:lu)klke-yol |
245 | 1 0 | a The Molecular Evolution of Castration-resistant Prostate Cancer |
264 | 1 | b Elsevier BV,c 2016 |
300 | a 8 s. | |
520 | a CONTEXT: Androgen deprivation therapy (ADT) is the backbone of treatment for advanced prostate cancer. However, castration-resistant prostate cancer (CRPC) nearly invariably develops through a range of different molecular mechanisms accompanied by progression to a more aggressive phenotype.OBJECTIVE: To understand the key molecular mechanisms leading to CRPC and the functional implications of this progression. Understanding molecular evolutionary mechanisms in CRPC is essential for the development of novel curative therapeutic approaches.EVIDENCE ACQUISITION: A systematic literature search to identify relevant original articles was conducted using PubMed. Findings verified in independent studies and supported by in vivo data were prioritised. From the eligible collection, 50 papers were selected.EVIDENCE SYNTHESIS: The majority of CRPC tumours harbour alterations in the androgen receptor (AR) at the DNA, RNA, and/or protein level, and/or other alterations involving the AR signalling pathway, so this central molecule is the focus of this review. To survive and resume growth despite low levels of circulating androgens, prostate cancer cells can also adapt androgen synthesis or induce alternative pathways.CONCLUSIONS: Despite more efficient ADT strategies, most evidence points to persistent AR signalling as a major mechanism of progression to CRPC. Resistance due to transdifferentiation or AR independence is also emerging as a mechanism of resistance. The diversity of potential resistance mechanisms supports the need for combination treatment and serial monitoring for adaptive treatment strategies.PATIENT SUMMARY: In this review, we summarise how prostate cancer cells evade androgen deprivation therapy and become more aggressive. Defining the molecular mechanisms will be critical for the development of new treatment approaches and hence improved survival. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Cancer och onkologi0 (SwePub)302032 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cancer and Oncology0 (SwePub)302032 hsv//eng |
700 | 1 | a Bjartell, Andersu Lund University,Lunds universitet,Urologisk cancerforskning, Malmö,Forskargrupper vid Lunds universitet,Urological cancer, Malmö,Lund University Research Groups4 aut0 (Swepub:lu)kir-abj |
700 | 1 | a Culig, Zoranu Medical University of Innsbruck4 aut |
700 | 1 | a Rubin, Mark Au Weill Cornell Medicine4 aut |
700 | 1 | a Tomlins, Scottu University of Michigan4 aut |
700 | 1 | a Visakorpi, Tapiou Tampere University Hospital,University of Tampere4 aut |
710 | 2 | a Avdelningen för translationell cancerforskningb Institutionen för laboratoriemedicin4 org |
773 | 0 | t European Urology Focusd : Elsevier BVg 2:5, s. 506-513q 2:5<506-513x 2405-4569 |
856 | 4 | u http://dx.doi.org/10.1016/j.euf.2016.11.012y FULLTEXT |
856 | 4 8 | u https://lup.lub.lu.se/record/e2544ab0-bc8b-4f5b-bcfa-76d5350273e2 |
856 | 4 8 | u https://doi.org/10.1016/j.euf.2016.11.012 |
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