Activating Mutation (V617F) in the Tyrosine Kinase JAK2 is Absent in Locally-Confined or Castration-Resistant Prostate Cancer
Background: Transcription factor Stat5a/b is highly critical for the viability of human prostate cancer cells in vitro and for prostate tumor growth in vivo. Stat5 is constitutively active in clinical prostate cancers but not in the normal human prostate epithelium. Moreover, Stat5a/b activation in...
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| Format: | Article |
| Language: | English |
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Wiley
2010-01-01
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| Series: | Analytical Cellular Pathology |
| Online Access: | http://dx.doi.org/10.3233/ACP-CLO-2010-0534 |
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| author | Lei Gu Xian-Hua Zhu Tapio Visakorpi Kalle Alanen Tuomas Mirtti Tina Bocker Edmonston Marja T. Nevalainen |
| author_facet | Lei Gu Xian-Hua Zhu Tapio Visakorpi Kalle Alanen Tuomas Mirtti Tina Bocker Edmonston Marja T. Nevalainen |
| author_sort | Lei Gu |
| collection | DOAJ |
| description | Background: Transcription factor Stat5a/b is highly critical for the viability of human prostate cancer cells in vitro and for prostate tumor growth in vivo. Stat5 is constitutively active in clinical prostate cancers but not in the normal human prostate epithelium. Moreover, Stat5a/b activation in prostate cancer is associated with high histological grade of prostate cancer. However, the molecular mechanisms underlying constitutive activation of Stat5a/b in prostate cancer are unclear. The receptor-associated tyrosine kinase Jak2 is a known key activator of Stat5a/b in prostate cancer cells in response to ligand stimulation. Recently, a single gain-of-function point mutation of JAK2 was described in myeloproliferative diseases leading to constitutive Jak2 kinase activity, subsequent Stat5a/b activation and involvement of V617F Jak2 in the pathogenesis of myeloproliferative disorders. |
| format | Article |
| id | doaj-art-f029275c3ac84e32a006dfb22d95dfad |
| institution | Kabale University |
| issn | 2210-7177 2210-7185 |
| language | English |
| publishDate | 2010-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Analytical Cellular Pathology |
| spelling | doaj-art-f029275c3ac84e32a006dfb22d95dfad2025-02-03T01:26:37ZengWileyAnalytical Cellular Pathology2210-71772210-71852010-01-01332555910.3233/ACP-CLO-2010-0534Activating Mutation (V617F) in the Tyrosine Kinase JAK2 is Absent in Locally-Confined or Castration-Resistant Prostate CancerLei Gu0Xian-Hua Zhu1Tapio Visakorpi2Kalle Alanen3Tuomas Mirtti4Tina Bocker Edmonston5Marja T. Nevalainen6Department of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USADepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USAInstitute of Medical Technology, University of Tampere and Tampere University Hospital, Tampere, FinlandDepartment of Pathology, Institute of Biomedicine, University of Turku, Turku, FinlandDepartment of Pathology, Institute of Biomedicine, University of Turku, Turku, FinlandDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USADepartment of Cancer Biology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USABackground: Transcription factor Stat5a/b is highly critical for the viability of human prostate cancer cells in vitro and for prostate tumor growth in vivo. Stat5 is constitutively active in clinical prostate cancers but not in the normal human prostate epithelium. Moreover, Stat5a/b activation in prostate cancer is associated with high histological grade of prostate cancer. However, the molecular mechanisms underlying constitutive activation of Stat5a/b in prostate cancer are unclear. The receptor-associated tyrosine kinase Jak2 is a known key activator of Stat5a/b in prostate cancer cells in response to ligand stimulation. Recently, a single gain-of-function point mutation of JAK2 was described in myeloproliferative diseases leading to constitutive Jak2 kinase activity, subsequent Stat5a/b activation and involvement of V617F Jak2 in the pathogenesis of myeloproliferative disorders.http://dx.doi.org/10.3233/ACP-CLO-2010-0534 |
| spellingShingle | Lei Gu Xian-Hua Zhu Tapio Visakorpi Kalle Alanen Tuomas Mirtti Tina Bocker Edmonston Marja T. Nevalainen Activating Mutation (V617F) in the Tyrosine Kinase JAK2 is Absent in Locally-Confined or Castration-Resistant Prostate Cancer Analytical Cellular Pathology |
| title | Activating Mutation (V617F) in the Tyrosine Kinase JAK2 is Absent in Locally-Confined or Castration-Resistant Prostate Cancer |
| title_full | Activating Mutation (V617F) in the Tyrosine Kinase JAK2 is Absent in Locally-Confined or Castration-Resistant Prostate Cancer |
| title_fullStr | Activating Mutation (V617F) in the Tyrosine Kinase JAK2 is Absent in Locally-Confined or Castration-Resistant Prostate Cancer |
| title_full_unstemmed | Activating Mutation (V617F) in the Tyrosine Kinase JAK2 is Absent in Locally-Confined or Castration-Resistant Prostate Cancer |
| title_short | Activating Mutation (V617F) in the Tyrosine Kinase JAK2 is Absent in Locally-Confined or Castration-Resistant Prostate Cancer |
| title_sort | activating mutation v617f in the tyrosine kinase jak2 is absent in locally confined or castration resistant prostate cancer |
| url | http://dx.doi.org/10.3233/ACP-CLO-2010-0534 |
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