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Autor     Brian J. Feldman and David Feldman
Titel    THE DEVELOPMENT OF ANDROGEN-INDEPENDENT PROSTATE CANCER
Zeitschrift    Nat Rev Cancer
Datum    October 2001
Seiten    34-45
URL    http://www.nature.com/nrc/journal/v1/n1/pdf/nrc1001-034a.pdf

Literaturverz.   

yes
Fußnoten    yes
Fragmente    4


Fragmente der Quelle:
[1.] Rlm/Fragment 005 05 - Diskussion
Zuletzt bearbeitet: 2014-12-01 13:39:34 Singulus
Feldman and Feldman 2001, Fragment, Gesichtet, Rlm, SMWFragment, Schutzlevel sysop, Verschleierung

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Quelle: Feldman and Feldman 2001
Seite(n): 36, 37, Zeilen: 36: right col. 14-16, 21-25, 28-33; 37: left col. 1-7, 25-31
One possible mechanism by which a prostate cancer circumvents the effects of androgen ablation therapy is by increasing its sensitivity to very low levels of androgens. There are several potential mechanisms that would allow increased tumor-cell proliferation, despite low circulating androgens in the patient. One mechanism to accomplish this is by increasing the expression of the AR itself. Approximately 30% of tumors that become androgen independent after ablation therapy have amplified the AR gene (3). A second hypersensitive mechanism for tumor progression results in high-level expression of the AR, increased stability, and enhanced nuclear localization of AR in recurrent tumor cells. A third hypersensitive mechanism to circumvent androgen ablation therapy is by increasing the local production of androgens, to compensate for the overall decline in circulating testosterone. Prostate cells could increase the rate of conversion of testosterone to the more potent hormone DHT by increasing 5α-reductase activity.

3) Koivisto, P. et al. Androgen receptor gene amplification: a possible molecular mechanism for androgen deprivation therapy failure in prostate cancer. Cancer Res. 57, 314–319.

[Page 36]

Type 1: the hypersensitive pathway

One possible mechanism by which a prostate cancer circumvents the effects of androgen ablation therapy is by increasing its sensitivity to very low levels of androgens. [...]

AR amplification. There are several potential mechanisms that would allow increased tumour-cell proliferation, despite low circulating androgens in the patient. One mechanism to accomplish this is by increasing the expression of the AR itself. [...] Approximately 30% of tumours that become androgen independent after ablation therapy have amplified the AR gene, resulting in increased AR expression, whereas none of the primary tumours from the same patients before androgen ablation had an AR gene amplification15,25.

[Page 37]

Increased AR sensitivity. A second hypersensitive mechanism for tumour progression was found in animal models of the transition from androgen-dependent prostate cancer to apparent AIPC27.This pathway results in high-level expression of the AR, increased stability, and enhanced nuclear localization of AR in recurrent tumour cells. [...]

Increased androgen levels. A third hypersensitive mechanism to circumvent androgen ablation therapy is by increasing the local production of androgens, to compensate for the overall decline in circulating testosterone. Prostate cells could increase the rate of conversion of testosterone to the more potent hormone DHT by increasing 5α-reductase activity.


15. Koivisto, P. et al. Androgen receptor gene amplification: a possible molecular mechanism for androgen deprivation therapy failure in prostate cancer. Cancer Res. 57, 314–319.

25. Visakorpi, T. et al. In vivo amplification of the androgen receptor gene and progression of human prostate cancer. Nature Genet. 9, 401–406 (1995). This study defined the amplified AR as a mechanism for the hypersensitive pathway.

27. Gregory, C. W., Johnson, R. T. Jr, Mohler, J. L., French, F. S. & Wilson, E. M. Androgen receptor stabilization in recurrent prostate cancer is associated with hypersensitivity to low androgen. Cancer Res. 61, 2892–2898.

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[2.] 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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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.

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[3.] Rlm/Fragment 010 04 - Diskussion
Zuletzt bearbeitet: 2014-12-10 23:37:06 Singulus
Feldman and Feldman 2001, Fragment, Gesichtet, Rlm, SMWFragment, Schutzlevel sysop, Verschleierung

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Testosterone — the main circulating androgen — is secreted primarily by the testes, but is also formed by peripheral conversion of adrenal steroids. It circulates in the blood, where it is bound to albumin and sex-hormone-binding globulin (SHBG), with a small fraction dissolved freely in the serum. When free testosterone enters into prostate cells , it is converted to dihydrotestosterone (DHT) by the enzyme 5α-reductase (SRD5A2). DHT is the more active hormone, having fivefold higher affinity for the androgen receptor (AR) than does testosterone(11).

11) Nash AF , Melezinek I. The role of prostate specific antigen measurement in the detection and management of prostate cancer. Endocr Relat Cancer. 2000 Mar;7(1):37-51.

Testosterone — the main circulating androgen — is secreted primarily by the testes, but is also formed by peripheral conversion of adrenal steroids4. It circulates in the blood, where it is bound to albumin and sex-hormone-binding globulin (SHBG), with a small fraction dissolved freely in the serum. When free testosterone enters prostate cells (BOX 2), 90% is converted to dihydrotestosterone (DHT) by the enzyme 5α-reductase (SRD5A2). DHT is the more active hormone, having fivefold higher affinity for the androgen receptor (AR) than does testosterone.

4. Griffin, J. E. & Wilson, J. D. in Williams Testbook of Endocrinology 9th edn (eds Wilson, J. D., Foster, D. W., Kronenberg, H. M. & Larsen, P. R.) 819–876 (W. B. Saunders & Co., Philadelphia, 1998).

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[4.] Rlm/Fragment 013 01 - Diskussion
Zuletzt bearbeitet: 2014-12-10 23:28:43 Singulus
Feldman and Feldman 2001, Fragment, Gesichtet, KomplettPlagiat, Rlm, SMWFragment, Schutzlevel sysop

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Fig2. Androgen action. Testosterone circulates in the blood bound to albumin (not shown) and sex-hormone-binding globulin (SHBG), and exchanges with free testosterone. Free testosterone enters prostate cells and is converted to dihydrotestosterone (DHT) by the enzyme 5α-reductase. Binding of DHT to the androgen receptor (AR) induces dissociation from heat-shock proteins (HSPs) and receptor phosphorylation. The AR dimerizes and can bind to androgen-response elements in the promoter regions of target genes. Co-activators (such as ARA70) and corepressors (not shown) also bind the AR complex, facilitating or preventing, respectively, its interaction with the general transcription apparatus (GTA). Activation (or repression) of target genes leads to biological responses including growth, survival and the production of prostate-specific antigen (PSA). Figure 1 Androgen action. Testosterone circulates in the blood bound to albumin (not shown) and sex-hormone-binding globulin (SHBG), and exchanges with free testosterone. Free testosterone enters prostate cells and is converted to dihydrotestosterone (DHT) by the enzyme 5α-reductase. Binding of DHT to the androgen receptor (AR) induces dissociation from heat-shock proteins (HSPs) and receptor phosphorylation. The AR dimerizes and can bind to androgen-response elements in the promoter regions of target genes6. Co-activators (such as ARA70) and corepressors (not shown) also bind the AR complex, facilitating or preventing, respectively, its interaction with the general transcription apparatus (GTA). Activation (or repression) of target genes leads to biological responses including growth, survival and the production of prostate-specific antigen (PSA).

6. Brinkmann, A. O. et al. Mechanisms of androgen receptor activation and function. J. Steroid Biochem. Mol. Biol. 69, 307–313 (1999).

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