BRCA1 and implications for response to chemotherapy in ovarian cancer.

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BRCA1 and implications for response to chemotherapy in ovarian cancer.

  • In Contrast
  • Respectively
  • In Addition
  • Objectives: Treatment Of Epithelial Ovarian Cancer (Eoc) Remains A Challenge
  • Despite Advances In Surgery And Chemotherapy
  • Hereditary Ovarian Cancer Is Primarily Due To Germline Mutations In The Brca1 Tumour Suppressor Gene
  • Sporadic Eoc Tumours Display Signi?Cant Of Loss Of Brca1 Function Due To Epigenetic Inactivation Of
  • This Article Reviews The Preclinical And Clinical Evidence To Support A Role For Brca1 As A Potentia
  • <Br/><Br/>Methods: We Conducted A Medline And Pubmed Search For Reports Between 1990 And 2008 Using
  • Brca1 And Sporadic Ovarian Cancer
  • Ovarian Cancer And Chemotherapy
  • Ovarian Cancer And Taxanes
  • Ovarian Cancer And Platinums
  • Ovarian Cancer And Clinical Response
  • Brca1 And Dna Damage
  • Brca1 And Dna Repair
  • Brca1 And Mitotic Checkpoint
  • If Reports Identi?Ed By These Criteria Referred To Other Papers Not In The Initial Search
  • Then These Were Also Reviewed If Relevant To Brca1 And Ovarian Cancer
  • <Br/><Br/>Results: The Brca1 Pathway Plays A Signi?Cant Role In The Development Of Both Hereditary A
  • Evidence Suggests That Brca1 Is A Potential Biomarker Of Response To Platinum Chemotherapy In Eoc Wi
  • Initial Evidence Suggests That Loss Of Brca1 Function Results In Reduced Response To Antimicrotubule
  • The Ability Of Brca1 To Differentially Modulate Response To These Agents Involves Loss Of Brca1 Medi
  • <Br/><Br/>Conclusions: Standard ?Rst Line Treatment Of Eoc Consists Of A Combination Of Platinum And
  • However Clinically Useful Biomarkers For Predicting Response To These Agents Have Yet To Be Establis
  • Brca1 May Prove Useful As A Biomarker In Eoc For Assigning Chemotherapy Treatments Based On The Pres


Chapter 2 Androgen Action During Prostate Carcinogenesis Diping Wang and Donald J. Tindall Abstract Androgens are critical for normal prostate development and function, as well as prostate cancer initiation and progression. Androgens function mainly by regulating target gene expression through the androgen receptor (AR). Many studies have shown that androgen-AR signaling exerts actions on key events during prostate carcinogenesis. In this review, androgen action in distinct aspects of prostate carcinogenesis, including (i) cell proliferation, (ii) cell apoptosis, and (iii) prostate cancer metastasis will be discussed. Key words: Androgen receptor, prostate cancer, androgen metabolism, androgen signaling, castration-resistant prostate cancer. 1. Androgen Signaling Androgens are the male sex hormones, which control the differ- entiation and maturation of male reproductive organs, including the prostate gland. Testosterone is the principal androgen in cir- culation and is synthesized by Leydig cells in the testes, under the regulation of luteinizing hormone (LH), which is further regulated by gonadotropin-releasing hormone (GnRH). Adrenal glands also synthesize a small amount of androgens, such as dehy- droepiandrosterone (DHEA) and androstenedione (4-dione) (1). Testosterone enters prostate cells by passive diffusion, where it is converted enzymatically by 5-α reductases to the more potent androgen dihydrotestosterone (DHT) (2). Binding of androgens to the androgen receptor (AR), a ligand-modulated transcrip- tion factor, induces a conformational change in the AR, causing release of heat shock proteins and translocation of the AR to the F. Saatcioglu (ed.), Androgen Action, Methods in Molecular Biology 776, DOI 10.1007/978-1-61779-243-4_2, © Springer Science+Business Media, LLC 2011 25 26 Wang and Tindall nucleus, where it transcriptionally regulates the expression of tar- get genes (3). In addition to the classic genomic effects of sex steroids, accu- mulating

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