SwePub
Sök i LIBRIS databas

  Utökad sökning

WFRF:(Rubin Mark A.)
 

Sökning: WFRF:(Rubin Mark A.) > The Molecular Evolu...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004056naa a2200349 4500
001oai:lup.lub.lu.se:e2544ab0-bc8b-4f5b-bcfa-76d5350273e2
003SwePub
008190626s2016 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/e2544ab0-bc8b-4f5b-bcfa-76d5350273e22 URI
024a https://doi.org/10.1016/j.euf.2016.11.0122 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a for2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a 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
2451 0a The Molecular Evolution of Castration-resistant Prostate Cancer
264 1b 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 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Cancer och onkologi0 (SwePub)302032 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Cancer and Oncology0 (SwePub)302032 hsv//eng
700a 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
700a Culig, Zoranu Medical University of Innsbruck4 aut
700a Rubin, Mark Au Weill Cornell Medicine4 aut
700a Tomlins, Scottu University of Michigan4 aut
700a Visakorpi, Tapiou Tampere University Hospital,University of Tampere4 aut
710a Avdelningen för translationell cancerforskningb Institutionen för laboratoriemedicin4 org
773t European Urology Focusd : Elsevier BVg 2:5, s. 506-513q 2:5<506-513x 2405-4569
856u http://dx.doi.org/10.1016/j.euf.2016.11.012y FULLTEXT
8564 8u https://lup.lub.lu.se/record/e2544ab0-bc8b-4f5b-bcfa-76d5350273e2
8564 8u https://doi.org/10.1016/j.euf.2016.11.012

Hitta via bibliotek

Till lärosätets databas

Sök utanför SwePub

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy