2AF0 Nevalainen, Marja - Thomas Jefferson University - Thomas Jefferson University
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Marja Nevalainen, MD, PhD

Contact Dr. Nevalainen

Kimmel Cancer Center
233 S. Tenth Street, Suite 309B
Philadelphia, PA 19107

(215) 503-9250
(215) 503-9245 fax

Most Recent Peer-reviewed Publications

  1. Peptidylarginine deiminase 3 (PAD3) is upregulated by prolactin stimulation of CID-9 cells and expressed in the lactating mouse mammary gland
  2. Structure-based screen identifies a potent small molecule inhibitor of Stat5a/b with therapeutic potential for prostate cancer and chronic myeloid leukemia
  3. Inhibition of Stat5a/b enhances proteasomal degradation of androgen receptor liganded by antiandrogens in prostate cancer
  4. Jak2-Stat5a/b Signaling Induces Epithelial-to-Mesenchymal Transition and Stem-Like Cell Properties in Prostate Cancer
  5. Pharmacologic suppression of JAK1/2 by JAK1/2 inhibitor AZD1480 potently inhibits IL-6-induced experimental prostate cancer metastases formation
  6. Transcription factors Stat5a/b and Stat3 in prostate cancer growth and metastases
  7. Pharmacologic inhibition of Jak2-Stat5 signaling by Jak2 inhibitor AZD1480 potently suppresses growth of both primary and castrate-resistant prostate cancer
  8. STAT5A/B gene locus undergoes amplification during human prostate cancer progression
  9. Nuclear Stat5a/b predicts early recurrence and prostate cancer-specific death in patients treated by radical prostatectomy
  10. Signal transducer and activator of transcription-5 mediates neuronal apoptosis induced by inhibition of Rac GTPase activity
  11. Reply to A. Italiano
  12. Prolactin regulation of the prostate gland: A female player in a male game
  13. Signal transducer and activator of transcription 5a/b: Biomarker and therapeutic target in prostate and breast cancer
  14. Loss of nuclear localized and tyrosine phosphorylated Stat5 in breast cancer predicts poor clinical outcome and increased risk of antiestrogen therapy failure
  15. Targeting transcription factor stat5a/b as a therapeutic strategy for prostate cancer
  16. Robust gene network analysis reveals alteration of the STAT5a network as a hallmark of prostate cancer.
  17. N-terminal truncation of Stat5a/b circumvents PIAS3-mediated transcriptional inhibition of Stat5 in prostate cancer cells
  18. Activating mutation (V617F) in the tyrosine kinase JAK2 is absent in locally-confined or castration-resistant prostate cancer
  19. Stat5 promotes metastatic behavior of human prostate cancer cells in vitro and in vivo
  20. Transcription factor Stat3 stimulates metastatic behavior of human prostate cancer cells in vivo, whereas Stat5b has a preferential role in the promotion of prostate cancer cell viability and tumor growth
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