Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Letter to the Editor
  • Published:

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

Leukemia volume 20, pages 157–158 (2006)Cite this article

Alterations of JAK/STAT signaling molecules have been reported for several lymphomas including primary mediastinal B-cell lymphoma (PMBL) and classical Hodgkin lymphoma (cHL), where constitutive activation of STATs was found.1, 2 PMBL is a rather rare disease, however, there is increasing evidence that it is closely related to the far more frequent cHL.3 One common characteristic of these two entities is a frequent gain of 9p24 involving JAK2 which consequently has attracted considerable attention as potential trigger in the pathogenesis of these lymphomas. Recent publications revealed a substantial role for a gain of function mutation of JAK2 that results in constitutive activation of the tyrosine kinase, phosphorylation of STAT5, and expression of genetic markers in diverse myeloproliferative disorders, such as polycythemia vera, acute and chronic myeloid leukemia.4, 5, 6, 7 However, it was not found in acute and chronic lymphocytic leukemia.5

Our results demonstrate the absence of the G → T mutation in both alleles of JAK2 since BsaXI completely cleaved the PCR product yielded from DNA of all cell lines, PMBLs, and cHLs (Figure 1b).

This is a preview of subscription content, access via your institution

Relevant articles

Open Access articles citing this article.

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Figure 1

References

  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.

    Article  CAS  Google Scholar 

  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.

    Article  CAS  Google Scholar 

  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.

    Article  CAS  Google Scholar 

  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.

    Article  CAS  Google Scholar 

  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.

    Article  CAS  Google Scholar 

  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.

    Article  CAS  Google Scholar 

  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.

    Article  CAS  Google Scholar 

  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 Nov 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.

Download references

Author information

Author notes

  1. I Melzner and M A Weniger: These authors have equally contributed to this work.

Authors and Affiliations

  1. Department of Pathology, University of Ulm, Ulm, Germany

    I Melzner, M A Weniger, C K Menz & P Möller

Authors
  1. I Melzner
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. M A Weniger
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. C K Menz
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. P Möller
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to P Möller.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Melzner, I., Weniger, M., Menz, C. et al. Absence of the JAK2 V617F activating mutation in classical Hodgkin lymphoma and primary mediastinal B-cell lymphoma. Leukemia 20, 157–158 (2006). https://doi.org/10.1038/sj.leu.2404036

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/sj.leu.2404036

This article is cited by

Search

Advanced search

Quick links