Mutation screening of the androgen receptor promoter and untranslated regions in prostate cancer

Waltering, Kati K.; Wallén, Mika J.; Tammela, Teuvo L.J.; Vessella, Robert L.; Visakorpi, Tapio

doi:10.1002/pros.20387

Cited by 16 publications

(12 citation statements)

References 30 publications

(42 reference statements)

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“…Although no functional analysis was described, it is interesting that the C214A change could disrupt a potential, but functionally unconfirmed, Sp1 binding site (see Wang and Ferrari 2006). However, a later study examining tumour and normal prostate tissue, together with five prostate cancer cell lines and xenograft samples, concluded that mutations were only present in cultured cell lines (DU145 and LAPC4) and a small number of xenografts (Waltering et al 2006). There was no evidence of recurrent mutations in the promoter, 5' and 3 UTRs in patient samples.…”

Section: Clinical Mutations In the 5'utrmentioning

confidence: 96%

Tissue control of androgen action: The ups and downs of androgen receptor expression

Hunter

Hay

Esswein

et al. 2018

Molecular and Cellular Endocrinology

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Please cite this article as: Hunter, I., Hay, C.W., Esswein, B., Watt, K., McEwan, I.J., Tissue control of androgen action: The ups and downs of androgen receptor expression, Molecular and Cellular Endocrinology (2017), doi: 10.1016/j.mce.2017 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Section: Clinical Mutations In the 5'utrmentioning

confidence: 96%

Tissue control of androgen action: The ups and downs of androgen receptor expression

Hunter

Hay

Esswein

et al. 2018

Molecular and Cellular Endocrinology

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“…In addition, 44 unselected, genome Phi-amplified (GenomiPhi Amplification kit, Amersham, GE Healthcare, UK), prostate tumour samples from the Tampere region (Waltering et al, 2006) were analysed. Of these, 28 were previously untreated cancers (primary), 12 were hormone-refractory, and four were characterised as benign prostate hyperplasia.…”

Section: Sample Materialsmentioning

confidence: 99%

Mutation analysis of aryl hydrocarbon receptor interacting protein (AIP) gene in colorectal, breast, and prostate cancers

et al. 2007

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Germline mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene were recently identified in individuals with pituitary adenoma predisposition (PAP). These patients have prolactin (PRL) or growth hormone (GH) oversecreting pituitary adenomas, the latter exhibiting acromegaly or gigantism. Loss-of-heterozygosity (LOH) analysis revealed that AIP is lost in PAP tumours, suggesting that it acts as a tumour-suppressor gene. Aryl hydrocarbon receptor interacting protein is involved in several pathways, but it is best characterised as a cytoplasmic partner of the aryl hydrocarbon receptor (AHR). To examine the possible role of AIP in the genesis of common cancers, we performed somatic mutation screening in a series of 373 colorectal cancers (CRCs), 82 breast cancers, and 44 prostate tumour samples. A missense R16H (47G4A) change was identified in two CRC samples, as well as in the respective normal tissues, but was absent in 209 healthy controls. The remaining findings were silent, previously unreported, changes of the coding, noncoding, or untranslated regions of AIP. These results suggest that somatic AIP mutations are not common in CRC, breast, and prostate cancers.

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“…5,6 Two important mechanisms underlying the development and progression of CRPC, which can be exploited therapeutically, are the overexpression of IL-6 and hypersensitivity or mutation of the androgen receptor, both of which contribute to CRPC. [22][23][24][25][26] Unfortunately, the current DTX regimen does not have a role in these mechanisms. It has been demonstrated that bicalutamide (BCL) can effectively block the effect of IL-6 on a mutated androgen receptor, resulting in the apoptosis of prostate cancer cell lines (DU-145 and LNCAP) in vitro.…”

Section: Introductionmentioning

confidence: 99%

Intermittent tri-weekly docetaxel plus bicalutamide in patients with castration-resistant prostate cancer: a single-arm prospective study using a historical control for comparison

Zhang²,

Tao-tao³

et al. 2013

Asian J Androl

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Whether continuous docetaxel (DTX) chemotherapy offers an advantage over intermittent therapy for castration-resistant prostate cancer (CRPC) is unknown. In this study, we evaluated the efficacy, toxicity and quality of life (QoL) of intermittent tri-weekly DTX with bicalutamide in CRPC. Forty-two patients (group A) with CRPC were enrolled. The patients received intravenous DTX (75 mg m 22 ) once tri-weekly with oral bicalutamide (50 mg) once daily. Patients had a DTX holiday when the prostate-specific antigen (PSA) level declined o50%. DTX was restarted in patients with a PSA increase o25%. Sixty patients (group B) who had matching characteristics and had continuously received DTX without bicalutamide for 10-12 cycles were also enrolled. There were no statistically significant differences in progression-free survival (8 months vs. 9 months, P50.866) or overall survival (19 months vs. 21 months, P50.753) between groups A and B; however, the proportions of patients in group A with all grades of neutropenia (33% vs. 58%, P50.013) and nausea/vomiting (11% vs. 29%, P50.024) were significantly less compared to group B. A significant improvement in the global health and fatigue scores was recorded for group A post-chemotherapy compared to pre-chemotherapy (P,0.05). The fatigue, nausea/ vomiting and appetite loss scores in group B were increased post-chemotherapy compared to pre-chemotherapy (P,0.05). In conclusion, intermittent tri-weekly DTX plus bicalutamide is well tolerated and has the potential to achieve comparable disease control with an improvement in QoL for patients with CRPC.

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Mutation screening of the androgen receptor promoter and untranslated regions in prostate cancer

Abstract: Recurrent mutations in the promoter or UTRs of AR seem to be rare, and thus not likely mechanisms for the increased expression of the gene in the androgen ablation-resistant prostate cancer.

Cited by 16 publications

References 30 publications

Tissue control of androgen action: The ups and downs of androgen receptor expression

Tissue control of androgen action: The ups and downs of androgen receptor expression

Mutation analysis of aryl hydrocarbon receptor interacting protein (AIP) gene in colorectal, breast, and prostate cancers

Intermittent tri-weekly docetaxel plus bicalutamide in patients with castration-resistant prostate cancer: a single-arm prospective study using a historical control for comparison

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