Enhanced sensitivity to androgen withdrawal due to overexpression of interleukin-6 in androgen-dependent human prostate cancer LNCaP cells. - Wikidata - awgldk - TriplyDB

Enhanced sensitivity to androgen withdrawal due to overexpression of interleukin-6 in androgen-dependent human prostate cancer LNCaP cells.

Enhanced sensitivity to androgen withdrawal due to overexpression of interleukin-6 in androgen-dependent human prostate cancer LNCaP cells.

http://www.wikidata.org/entity/Q37424118

about

Acquired resistance to temsirolimus in human renal cell carcinoma cells is mediated by the constitutive activation of signal transduction pathways through mTORC2.IL-6/IL-6R as a potential key signaling pathway in prostate cancer development.Characterization of mechanism involved in acquired resistance to sorafenib in a mouse renal cell cancer RenCa model.Acquired resistance to sunitinib in human renal cell carcinoma cells is mediated by constitutive activation of signal transduction pathways associated with tumour cell proliferation.β4-integrin-mediated cytotoxic activity of AexU in human prostate cancer PC3 cells.Interleukin-6 gene -174G>C and -636G>C promoter polymorphisms and prostate cancer risk.Inhibition of tumor growth and sensitization to chemotherapy by RNA interference targeting interleukin-6 in the androgen-independent human prostate cancer PC3 model.

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Enhanced sensitivity to androgen withdrawal due to overexpression of interleukin-6 in androgen-dependent human prostate cancer LNCaP cells.

http://www.wikidata.org/entity/Q37424118

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 20 October 2009

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Enhanced sensitivity to androg ...... n prostate cancer LNCaP cells.

@en

Enhanced sensitivity to androg ...... n prostate cancer LNCaP cells.

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type

label

Enhanced sensitivity to androg ...... n prostate cancer LNCaP cells.

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Enhanced sensitivity to androg ...... n prostate cancer LNCaP cells.

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prefLabel

Enhanced sensitivity to androg ...... n prostate cancer LNCaP cells.

@en

Enhanced sensitivity to androg ...... n prostate cancer LNCaP cells.

@nl

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British Journal of Cancer

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Enhanced sensitivity to androg ...... n prostate cancer LNCaP cells.

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H Miyake

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J Furukawa

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M E Gleave

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M Fujisawa

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S L Ettinger

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T Terakawa

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P2860

Interleukin-6- and cyclic AMP-mediated signaling potentiates neuroendocrine differentiation of LNCaP prostate tumor cells.

Castration-induced up-regulation of insulin-like growth factor binding protein-5 potentiates insulin-like growth factor-I activity and accelerates progression to androgen independence in prostate cancer models

Interleukin-6 activates phosphatidylinositol-3 kinase, which inhibits apoptosis in human prostate cancer cell lines

Activation of the androgen receptor N-terminal domain by interleukin-6 via MAPK and STAT3 signal transduction pathways

Ligand-independent activation of the androgen receptor by interleukin-6 and the role of steroid receptor coactivator-1 in prostate cancer cells

Vascular endothelial growth factor-mediated autocrine stimulation of prostate tumor cells coincides with progression to a malignant phenotype

Docetaxel and estramustine compared with mitoxantrone and prednisone for advanced refractory prostate cancer

Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer

Overexpression of vimentin contributes to prostate cancer invasion and metastasis via src regulation.

Mechanisms involved in the progression of androgen-independent prostate cancers: it is not only the cancer cell's fault.

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1731-1739

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scholarly article

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10.1038/SJ.BJC.6605358

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1028659814

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19844233

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