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Androgen Receptor and PIN1 in Prostate Cancer

von Dott. Raffaele La Montagna

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[1.] Rlm/Fragment 006 02 - Diskussion
Zuletzt bearbeitet: 2015-02-08 20:28:32 Schumann
Feldman and Feldman 2001, Fragment, Gesichtet, Rlm, SMWFragment, Schutzlevel sysop, Verschleierung

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Verschleierung
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SleepyHollow02
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 6, Zeilen: 2-18
Quelle: Feldman and Feldman 2001
Seite(n): 38, 41, Zeilen: 38: left col: 2 ff.; 41: right col: 4 ff.
Some of these tumors, at least initially, have adapted to the low androgen environment, others acquire mutations that allow them to circumvent the normal growth regulation by androgens. It seems that many cases of AIPC do not develop from a loss of androgen signaling, but rather from the acquisition of genetic changes that lead to aberrant activation of the androgen-signaling axis. These changes are usually missense mutations in the AR gene that decrease the specificity of ligand binding and allow inappropriate activation by various non-androgen steroids and androgen antagonists (4) . In other cases some growth factors such as insulin-like growth-factor- 1 (IGF- 1), keratinocyte growth factor (KGF) and epidermal growth factor (EGF), can activate the AR, creating an outlaw receptor, and can therefore induce AR target genes in the absence of androgen (5). These are just some of the mechanisms in which cells can use to escape androgen ablation and it is also possible that a single cancer uses several mechanisms either initially or in a multistep progression to AIPC.

4) Buchanan, G. et al. Collocation of androgen receptor gene mutations in prostate cancer. Clin. Cancer Res. 7, 1273–1281 (2001).

5) Culig, Z. et al. Androgen receptor activation in prostatic tumor cell lines by insulin-like growth factor-I, keratinocyte growth factor, and epidermal growth factor. Cancer Res. 54, 5474–5478 (1994)

Whereas some of these tumours, at least initially, have adapted to the low-androgen environment, others acquire mutations that allow them to circumvent the normal growth regulation by androgens. It seems that many cases of AIPC do not develop from a loss of androgen signalling, but rather from the acquisition of genetic changes that lead to aberrant activation of the androgen signalling axis21. These changes are usually missense mutations in the AR gene that decrease the specificity of ligand binding and allow inappropriate activation by various non-androgen steroids and androgen antagonists.

[page 41:]

Certain growth factors, such as insulin-like growth-factor-1 (IGF- 1), keratinocyte growth factor (KGF) and epidermal growth factor (EGF), can activate the AR, creating an outlaw receptor, and can therefore induce AR target genes in the absence of androgen59. [...] It is also possible, if not likely, that a single cancer uses several mechanisms either initially or in a multistep progression to AIPC


59. Culig, Z. et al. Androgen receptor activation in prostatic tumor cell lines by insulin-like growth factor-I, keratinocyte growth factor, and epidermal growth factor. Cancer Res. 54, 5474–5478 (1994). Early description of growth-factor activation of AR in the absence of ligand, developing the basis for the outlaw AR pathway.

Anmerkungen
Sichter
(SleepyHollow02) Singulus

[2.] Rlm/Fragment 006 18 - Diskussion
Zuletzt bearbeitet: 2014-12-10 23:19:52 Hindemith
Fragment, Gesichtet, Rlm, SABiosciences Androgen Signaling 2009, SMWFragment, Schutzlevel sysop, Verschleierung

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SleepyHollow02
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Seite: 6, Zeilen: 18-20
Quelle: SABiosciences Androgen Signaling 2009
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The appropriate regulation of androgen activity is necessary for a range of developmental and physiological processes, particularly male sexual development and maturation. The appropriate regulation of androgen activity is necessary for a range of developmental and physiological processes, particularly male sexual development and maturation.
Anmerkungen

The source is not mentioned. To be continued on the following page.

Sichter
(SleepyHollow02), Hindemith


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