SwePub
Sök i LIBRIS databas

  Utökad sökning

WFRF:(Rubin Mark A.)
 

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

  • Ceder, YvonneLund 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 Groups (författare)

The Molecular Evolution of Castration-resistant Prostate Cancer

  • Artikel/kapitelEngelska2016

Förlag, utgivningsår, omfång ...

  • Elsevier BV,2016
  • 8 s.

Nummerbeteckningar

  • LIBRIS-ID:oai:lup.lub.lu.se:e2544ab0-bc8b-4f5b-bcfa-76d5350273e2
  • https://lup.lub.lu.se/record/e2544ab0-bc8b-4f5b-bcfa-76d5350273e2URI
  • https://doi.org/10.1016/j.euf.2016.11.012DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:for swepub-publicationtype
  • Ämneskategori:ref swepub-contenttype

Anmärkningar

  • 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.

Ämnesord och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Bjartell, AndersLund University,Lunds universitet,Urologisk cancerforskning, Malmö,Forskargrupper vid Lunds universitet,Urological cancer, Malmö,Lund University Research Groups(Swepub:lu)kir-abj (författare)
  • Culig, ZoranMedical University of Innsbruck (författare)
  • Rubin, Mark AWeill Cornell Medicine (författare)
  • Tomlins, ScottUniversity of Michigan (författare)
  • Visakorpi, TapioTampere University Hospital,University of Tampere (författare)
  • Avdelningen för translationell cancerforskningInstitutionen för laboratoriemedicin (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:European Urology Focus: Elsevier BV2:5, s. 506-5132405-4569

Internetlänk

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