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.

  • Correspondence
  • Published:

Reduced expression of H19 in bone marrow cells from chronic myeloproliferative disorders

Leukemia volume 17, pages 815–816 (2003)Cite this article

TO THE EDITOR

From the paternally imprinted and maternally expressed H19 gene, an untranslated RNA is generated that exerts growth regulatory functions during embryogenesis and acts as a potential tumor suppressor in some types of cancer. It is a developmentally regulated gene and, thus, abundantly expressed in several fetal tissues, and repressed in most organs after birth.1 It has been elucidated that the untranslated RNA retains a high potency of antiproliferative effects and acts directly as a tumor suppressor.2 So far, no H19 protein could be identified.2 Little is known about the role of H19 in normal and neoplastic hematopoiesis. In precursor cells of patients with polycythemia vera, a reduced expression of H19 could be demonstrated.3 To assess the level of H19 in total bone marrow cells, we quantitatively focused on its expression in reactive lesions and chronic myeloproliferative disorders (CMPD). A total of 59 formalin-fixed, paraffin-embedded (FFPE) bone marrow trephines with histopathologically proven and clinically untreated CMPD (17 polycythemia vera (PV), 11 essential thrombocythemia (ET), 11 chronic myeloid leukemia (CML), 10 idiopathic myelofibrosis (IMF) in the cellular phase, 10 IMF with demonstrable fiber increase), 12 cases with chronic myelomonocytic leukemia (CMML), and 33 control cases (bone marrow biopsies with no evidence of a neoplastic disease) were retrieved from the Bone Marrow Registry, Institute of Pathology, Medizinische Hochschule Hannover. Total RNA was extracted using an optimized protocol for the extraction of RNA from FFPE archival tissues.5 Total RNA (1 μg), pretreated with RNase-free DNase (RQ1, Promega, USA), was transcribed to the complementary DNA (cDNA) according to the manufacture's protocol using SuperScript II Rnase− Reverse Transcriptase (Invitrogen, Karlsruhe, Germany).

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. Looijenga LHJ, Verkerk AJMH, de Groot N, Hochberg AA, Oosterhuis JW . H19 in normal development and neoplasia. Mol Reprod Dev 1997; 46: 419–439.

    Article  CAS  Google Scholar 

  2. Hao Y, Crenshaw T, Moulton T, Newcomb E, Tycko B . Tumour-suppressor activity of H19 RNA. Nature 1993; 365: 764–767.

    Article  CAS  Google Scholar 

  3. Núnêz C, Bashein AM, Brunet CL, Hoyland JA, Freemont AJ, Bickle AM et al. Expression of the imprinted tumour-suppressor gene H19 is tightly regulated during normal haematopoiesis and is reduced in haematopoietic precursors of patients with the myeloproliferative disease polycythaemia vera. J Pathol 2000; 190: 61–68.

    Article  Google Scholar 

  4. Livak KJ, Schmittgen TD . Analysis of relative gene expression data using real-time quantitative PCR and the 2−ΔΔC - method. Methods 2001; 25: 402–408.

    Article  CAS  Google Scholar 

  5. Bock O, Kreipe H, Lehmann U . One-step extraction of RNA from archival biopsies. Analyt Biochem 2001; 295: 116–117.

    Article  CAS  Google Scholar 

  6. Wilkin F, Paquette J, Ledru E, Mamelin C, Pollak M, Deal CL . H19 sense and antisense transgenes modify insulin-like growth-factor-II mRNA levels. Eur J Biochem 2000; 267: 4020–4027.

    Article  CAS  Google Scholar 

  7. Morison IM, Eccles MR, Reeve AE . Imprinting of insulin-like growth factor 2 is modulated during hematopoiesis. Blood 2000; 96: 3023–3028.

    CAS  PubMed  Google Scholar 

  8. Rhandawa GS, Cui H, Barletta JA, Strichman-Almashanu LZ, Talpaz M, Kantarjian HM et al. Loss of imprinting in disease progression in chronic myelogenous leukemia. Blood 1998; 91: 3144–3147.

    Google Scholar 

  9. Wu H, Weksberg R, Minden MD, Squire JA . Loss of imprinting of human insulin-like growth factor II gene, IGF2, in acutemyeloid leukemia. Biochem Biophys Res Commun 1997; 231: 466–472.

    Article  CAS  Google Scholar 

  10. Steenman MJ, Rainier S, Dobry CJ, Grundy P, Horon IL, Feinberg AP . Loss of imprinting of IGF2 is linked to reduced expression and abnormal methylation of H19 in Wilms’ tumour. Nature Genet 1994; 7: 433–439.

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Institute of Pathology, Medizinische Hochschule Hannover, Hannover, Germany

    Oliver Bock, Jerome Schlué & Hans Kreipe

Authors
  1. Oliver Bock
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Jerome Schlué
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Hans Kreipe
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Bock, O., Schlué, J. & Kreipe, H. Reduced expression of H19 in bone marrow cells from chronic myeloproliferative disorders. Leukemia 17, 815–816 (2003). https://doi.org/10.1038/sj.leu.2402830

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/sj.leu.2402830

This article is cited by

Search

Advanced search

Quick links