Absence of the JAK2 V617F activating mutation in classical Hodgkin lymphoma and primary mediastinal B-cell lymphoma [11]

Leukemia

Volumn 20, Issue 1, 2006, Pages 157-158

  Melzner, I ^a   Weniger, M A ^a   Menz, C K ^a   Möller, Peter ^a  

^a UNIVERSITY OF ULM   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

GENOMIC DNA; JANUS KINASE 2; STAT5 PROTEIN; SUPPRESSOR OF CYTOKINE SIGNALING 1;

B CELL LYMPHOMA; CARCINOGENESIS; CONTROLLED STUDY; ENZYME ACTIVITY; ENZYME MECHANISM; GENE MUTATION; GENE SILENCING; HODGKIN DISEASE; HUMAN; HUMAN CELL; LETTER; LYMPHOMA CELL LINE; MEDIASTINUM CANCER; POLYMERASE CHAIN REACTION; PRIORITY JOURNAL; REED STERNBERG CELL;

EID: 33644987681     PISSN: 08876924     EISSN: 14765551     Source Type: Journal    
DOI: 10.1038/sj.leu.2404036     Document Type: Letter

References (10)

1. Kube D, Holtick U, Vockerodt M, Ahmadi T, Haier B, Behrmann I et al. STAT3 is constitutively activated in Hodgkin cell lines. Blood 2001; 98: 762-770.
2. Guiter C, Dusanter-Fourt I, Copie-Bergman C, Boulland ML, Le Gouvello S, Gaulard P et al. Constitutive STAT6 activation in primary mediastinal large B-cell lymphoma. Blood 2004; 104: 543-549.
3. Rosenwald A, Wright G, Leroy K, Yu X, Gaulard P, Gascoyne RD et al. Molecular diagnosis of primary mediastinal B cell lymphoma identifies a clinically favorable subgroup of diffuse large B cell lymphoma related to Hodgkin lymphoma. J Exp Med 2003; 198: 851-862.
4. Steensma DP, Dewald GW, Lasho TL, Powell HL, McClure RF, Levine RL et al. The JAK2 V617F activating tyrosine kinase mutation is an infrequent event in both 'atypical' myeloproliferative disorders and myelodysplastic syndromes. Blood 2005; 106: 1207-1209.
5. Levine RL, Loriaux M, Huntly BJ, Loh M, Beran M, Stoffregen E et al. The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemia. Blood 2005 Aug 4; [E-pub ahead of print] PMID: 16081687 [PubMed - as supplied by publisher].
6. Kralovics R, Passamonti F, Buser AS, Teo SS, Tiedt R, Passweg JR et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. N Engl J Med 2005; 352: 1779-1790.
7. James C, Ugo V, Le Couedic JP, Staerk J, Delhommeau F, Lacout C et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature 2005; 434: 1144-1148.
8. Melzner I, Bucur AJ, Bruderlein S, Dorsch K, Hasel C, Barth TF et al. Biallelic mutation of SOCS-1 impairs JAK2 degradation and sustains phospho-JAK2 action in the MedB-1 mediastinal lymphoma line. Blood 2005; 105: 2535-2542.
9. Melzner I, Bucur AJ, Weniger MA, Brüderlein S, Dorsch K, Hasel C et al. Biallelic deletion within 16p13.13 including SOCS-1 in Karpas1106P mediastinal B-cell lymphoma line is associated with delayed degradation of JAK2 protein. Int J Cancer, (Published online: 14 November 2005, doi: 10.1002/ijc.21485)
10. Weniger MA, Melzner I, Menz CK, Wegener S, Bucur AJ, Dorsch K et al. Mutations of the tumor suppressor gene SOCS-1 in classical Hodgkin lymphoma are frequent and associated with nuclear phospho-STAT5 accumulation. Oncogene, in press.