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Clinical relevance of androgen receptor alterations in prostate cancer
Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
2017 (engelsk)Inngår i: Endocrine Connections, ISSN 2049-3614, E-ISSN 2049-3614, Vol. 6, nr 8, s. R146-R161Artikkel, forskningsoversikt (Fagfellevurdert) Published
Abstract [en]

Prostate cancer (PC) remains a leading cause of cancer-related deaths among men worldwide, despite continuously improved treatment strategies. Patients with metastatic disease are treated by androgen deprivation therapy (ADT) that with time results in the development of castration-resistant prostate cancer (CRPC) usually established as metastases within bone tissue. The androgen receptor (AR) transcription factor is the main driver of CRPC development and of acquired resistance to drugs given for treatment of CRPC, while a minority of patients have CRPC that is non-AR driven. Molecular mechanisms behind epithelial AR reactivation in CRPC include AR gene amplification and overexpression, AR mutations, expression of constitutively active AR variants, intra-tumoural and adrenal androgen synthesis and promiscuous AR activation by other factors. This review will summarize AR alterations of clinical relevance for patients with CRPC, with focus on constitutively active AR variants, their possible association with AR amplification and structural rearrangements as well as their ability to predict patient resistance to AR targeting drugs. The review will also discuss AR signalling in the tumour microenvironment and its possible relevance for metastatic growth and therapy.

sted, utgiver, år, opplag, sider
2017. Vol. 6, nr 8, s. R146-R161
Emneord [en]
prostate cancer, castration resistance, androgen receptor
HSV kategori
Identifikatorer
URN: urn:nbn:se:umu:diva-144124DOI: 10.1530/EC-17-0118ISI: 000418497500001PubMedID: 29030409OAI: oai:DiVA.org:umu-144124DiVA, id: diva2:1176778
Forskningsfinansiär
Swedish Research Council, K2013-64X-20407-04-3Swedish Cancer Society, CAN 2016/824Swedish Cancer Society, CAN 2013/1324Tilgjengelig fra: 2018-01-23 Laget: 2018-01-23 Sist oppdatert: 2019-05-10bibliografisk kontrollert

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