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Autor     Steven P. Balk and Karen E. Knudsen
Titel    AR, the cell cycle, and prostate cancer
Zeitschrift    Nuclear Receptor Signaling
Ausgabe    6
Datum    1. February 2008
Nummer    e001
Seiten    12
Anmerkung    PMCID: PMC2254330
DOI    10.1621/nrs.06001
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2254330/pdf/nrs06001000.pdf

Literaturverz.   

yes
Fußnoten    yes
Fragmente    6


Fragmente der Quelle:
[1.] Rlm/Fragment 004 02 - Diskussion
Zuletzt bearbeitet: 2014-12-10 23:43:34 Singulus
Balk and Knudsen 2008, Fragment, Gesichtet, Rlm, SMWFragment, Schutzlevel sysop, Verschleierung

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Androgens bind to a specific androgen receptor (AR), a ligand-dependent transcription factor which controls the expression of a large number of downstream target genes. The androgen receptor (AR) is a critical effector of prostate cancer development and progression and for this reason , [sic] AR ablation is the first line of therapeutic intervention in the treatment of disseminated prostate cancers. However, recurrent tumors arise within a median of 2-3 years wherein androgen signaling has been inappropriately restored (2).

2)Feldman BJ,Feldman D,The development of androgen-independent prostate cancer. ) Nat Rev Cancer. 2001 Oct;1(1):34-45.

The androgen receptor (AR) is a critical effector of prostate cancer development and progression.The dependence of this tumor type on AR activity is exploited in treatment of disseminated prostate cancers, wherein ablation of AR function (achieved either through ligand depletion and/or the use of AR antagonists) is the first line of therapeutic intervention.

However, recurrent tumors arise within a median of 2-3 years, wherein androgen signaling has been inappropriately restored [Feldman and Feldman, 2001].

Androgen exerts its biological effects through the androgen receptor (AR), a member of the nuclear receptor superfamily that acts as a ligand dependent transcription factor [Evans, 1988; Mangelsdorf et al., 1995; Shand and Gelmann, 2006; Trapman and Brinkmann, 1996].

Anmerkungen
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(SleepyHollow02) Singulus

[2.] Rlm/Fragment 010 13 - Diskussion
Zuletzt bearbeitet: 2014-12-01 14:06:10 Singulus
Balk and Knudsen 2008, Fragment, Gesichtet, KomplettPlagiat, Rlm, SMWFragment, Schutzlevel sysop

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While the subsets of AR target genes that underlie each cellular outcome have yet to be clearly defined, discovery of at least one major AR-dependent target gene, prostate specific antigen (PSA) has had a major impact on disease management (12).

10) Riegman PH, Vlietstra RJ, van der Korput JA, Brinkmann AO, Trapman J The promoter of the prostate-specific antigen gene contains a functional androgen responsive element. Mol Endocrinol.1991 Dec;5(12):1921-30.

12) Ryan CJ, Smith A, Lal P, Satagopan J, Reuter V, Scardino P, Gerald W, Scher HI. Persistent prostate-specific antigen expression after neoadjuvant androgen depletion: an early predictor of relapse or incomplete androgen suppression Urology. 2006 Oct;68(4):834-9

While the subsets of AR target genes that underlie each cellular outcome have yet to be clearly defined, discovery of at least one major AR-dependent target gene, prostate specific antigen (PSA) [Riegman et al., 1991], has had a major impact on disease management.

Riegman, P. H., Vlietstra, R. J., van der Korput, J. A., Brinkmann, A. O. and Trapman, J. (1991) The promoter of the prostate-specific antigen gene contains a functional androgen responsive element Mol Endocrinol 5, 1921-30.

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(Graf Isolan), SleepyHollow02

[3.] Rlm/Fragment 011 03 - Diskussion
Zuletzt bearbeitet: 2014-12-01 14:07:06 Singulus
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Specifically, serum PSA is monitored clinically to detect early stage disease, track tumor burden, monitor the efficacy of therapeutic intervention, and detect the emergence of recurrent tumors post-therapy (13,14).

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.

12) Ryan CJ, Smith A, Lal P, Satagopan J, Reuter V, Scardino P, Gerald W, Scher HI. Persistent prostate-specific antigen expression after neoadjuvant androgen depletion: an early predictor of relapse or incomplete androgen suppression Urology. 2006 Oct;68(4):834-9

13) Reigman PJH, Vliestra RJ, van der Korput JAGM, Romijn JC, Trapman J Characterization of the prostate specific antigen gene: a novel kallikrein-like gene. Biochem Biophys Res Commun 159:95–102

14) Lilja H A kallikrein-like serine protease in prostatic fluid cleaves the predominant seminal vesicle protein. J Clin Invest 76: 1899–1903

Specifically, serum PSA is monitored clinically to detect early stage disease, track tumor burden, monitor the efficacy of therapeutic intervention, and detect the emergence of recurrent tumors post-therapy [Nash and Melezinek, 2000; Ryan et al., 2006].

Nash, A. F. and Melezinek, I. (2000) The role of prostate specific antigen measurement in the detection and management of prostate cancer Endocr Relat Cancer 7, 37-51.

Ryan, C. J., Smith, A., Lal, P., Satagopan, J., Reuter, V., Scardino, P., Gerald, W. and Scher, H. I. (2006) Persistent prostate-specific antigen expression after neoadjuvant androgen depletion: an early predictor of relapse or incomplete androgen suppression Urology 68, 834-9.

Anmerkungen

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In the original article, this passage follows immediately after the one documented in Rlm/Fragment_010_13.

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(Graf Isolan), SleepyHollow02

[4.] Rlm/Fragment 021 09 - Diskussion
Zuletzt bearbeitet: 2014-12-01 14:01:28 Singulus
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Transitions into and within the mitotic cell cycle are dictated by the coordinate activation of cyclin-dependent kinase (CDK)/cyclin complexes, wherein cyclin binding induces the catalytic activity of the kinase (31,32). Mitogenic signaling pathways generally induce cell cycle progression through ordered activation of CDK-cyclin complexes, whereas anti-mitogenic signals that result from extracellular events (e.g., nutrient depletion) or intracellular insults (e.g., DNA damage) typically serve to attenuate CDK function. Although the signals that dictate commitment to the cell cycle are often cell type-specific, the core machinery that drives the cell cycle engine is well conserved.

31) Lee YM, Sicinski P Targeting cyclins and cyclin-dependent kinases in cancer: lessons from mice, hopes for therapeutic applications in human. Cell Cycle. 2006 Sep;5(18):2110-4. Epub 2006 Sep 15.

32) Malumbres M,, Barbacid M Cell cycle kinases in cancer. Curr Opin Genet Dev.2007 Feb;17(1):60-5.

Transitions into and within the mitotic cell cycle are dictated by the coordinate activation of cyclin-dependent kinase (CDK)/cyclin complexes, wherein cyclin binding

induces the catalytic activity of the kinase [Lee and Sicinski, 2006; Malumbres and Barbacid, 2007; Sherr, 1996; Sherr and Roberts, 2004]. Mitogenic signaling pathways generally induce cell cycle progression through ordered activation of CDK-cyclin complexes, whereas anti-mitogenic signals that result from extracellular events (e.g., nutrient depletion) or intracellular insults (e.g., DNA damage) typically serve to attenuate CDK function. Although the signals that dictate commitment to the cell cycle are often cell type-specific, the core machinery that drives the cell cycle engine is well conserved.


Lee, Y. M. and Sicinski, P. (2006) Targeting cyclins and cyclin-dependent kinases in cancer: lessons from mice, hopes for therapeutic applications in human Cell Cycle 5, 2110-4.

Malumbres, M. and Barbacid, M. (2007) Cell cycle kinases in cancer Curr Opin Genet Dev 17, 60-5.

Sherr, C. J. (1996) Cancer cell cycles Science 274, 1672-7.

Sherr, C. J. and Roberts, J. M. (2004) Living with or without cyclins and cyclin-dependent kinases Genes Dev 18, 2699-711.

Anmerkungen

Although identical with identical references nothing has been marked as a citation.

The source is mentioned in passing on the next page.

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(Graf Isolan), SleepyHollow02

[5.] Rlm/Fragment 022 01 - Diskussion
Zuletzt bearbeitet: 2014-12-01 14:03:26 Singulus
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Prior to mitogenic stimulation cells can exit the cell cycle and enter into a resting stage deemed “G0. At this stage, several key gatekeepers of cell cycle transitions are invoked to prevent unscheduled cell cycle progression (33).

Figure 3:(from Balk et all2008) AR-cell cycle crosstalk.

Activated AR stimulates the accumulation of cyclin D1 (D1), through mammalian Target of Rapamycin (mTOR), to activate CDK4 and promote phosphorylation of the retinoblastoma (RB) tumor suppressor. In addition, AR-induced expression of p21Cip1 and degradation of p27Kip1 further enhance cycD1/CDK4 and cycE/CDK2-dependent inactivation of RB and allow expression of E2F target genes like cyclin A (CycA). Cyclin A in turn activates CDK2 to drive G1-S phase transition. Subsequently engaged components of the cell cycle machinery then impinge on AR to regulate the androgen response. Elevated cyclin D1 acts as in a negative feedback loop to attenuate AR activity, thereby modulating androgen action. In G2-phase, CDK1 promotes the phosphorylation and activation of AR. However, AR is degraded in M-phase and is purposed to be a “licensing factor” for DNA replication. Components that suppress AR function are outlined in red, whereas positive effectors of AR activity are outlined in green.


33) Balk SP, Knudsen KE AR, the cell cycle, and prostate cancer. Nucl Recept Signal. 2008 Feb 1;6:e001.

[Page 2]

Prior to mitogenic stimulation cells can exit the cell cycle and

[Page 3]

enter into a resting stage deemed “G0”. At this stage, several key gatekeepers of cell cycle transitions are invoked to prevent unscheduled cell cycle progression.

[Page 4]

Figure 1. AR-cell cycle crosstalk. Activated AR stimulates the accumulation of cyclin D1 (D1), through mammalian Target of Rapamycin (mTOR), to activate CDK4 and promote phosphorylation of the retinoblastoma (RB) tumor suppressor. In addition, AR-induced expression of p21Cip1 and degradation of p27Kip1 further enhance cycD1/CDK4 and cycE/CDK2-dependent inactivation of RB and allow expression of E2F target genes like cyclin A (CycA). Cyclin A in turn activates CDK2 to drive G1-S phase transition. Subsequently engaged components of the cell cycle machinery then impinge on AR to regulate the androgen response. Elevated cyclin D1 acts as in a negative feedback loop to attenuate AR activity, thereby modulating androgen action. In G2-phase, CDK1 promotes the phosphorylation and activation of AR. However, AR is degraded in M-phase and is purposed to be a “licensing factor” for DNA replication. Components that suppress AR function are outlined in red, whereas positive effectors of AR activity are outlined in green.



Anmerkungen

Although the texts are identical the citations have not been marked as such.

The source is only mentioned in passing.

Sichter
(Graf Isolan), SleepyHollow02

[6.] Rlm/Fragment 023 01 - Diskussion
Zuletzt bearbeitet: 2014-12-01 14:04:40 Singulus
Balk and Knudsen 2008, Fragment, Gesichtet, Rlm, SMWFragment, Schutzlevel sysop, Verschleierung

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Mechanistic investigations have showed that AR plays a master regulation of G1-S phase progression, able to induce signals that promote G1 cyclin-dependent-Kinase activity and finally, phosphorylation /inactivation of the receptor of the retinoblastoma tumor suppressor protein (34).

34) E. Cifuentes, R. Croxen, M Menon, E. R. Barrack, And G. Prem-Veer Reddy. Synchronized Prostate Cancer Cells for Studying Androgen Regulated Events in Cell Cycle Progression From G1 Into S Phase.. J Cell Physiol. 2003 Jun;195(3):337-45.

Mechanistic investigation has revealed that AR acts as a master regulator of G1-S phase progression, able to induce signals that promote G1 cyclin-dependent kinase (CDK) activity, induce phosphorylation/inactivation of the retinoblastoma tumor suppressor (RB), and thereby govern androgen-dependent proliferation.
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(Graf Isolan), SleepyHollow02

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