Journal of Bone Research

Journal of Bone Research
Open Access

ISSN: 2572-4916

+44 1478 350008

Letter to Editor - (2013) Volume 1, Issue 3

A General View on Bone Marrow Research

Tejinde Gaurey*
Assistant Professor, Department of Haematology, University of California, USA
*Corresponding Author: Tejinde Gaurey, Assistant Professor, Department of Haematology, University of California, USA Email:

Abstract

The hyper cellular marrow of CML shows pan myelosis and a virtual absence of adipocytes. There is granulocytic and/or megakaryocytic proliferation, eosinophilia and basophilia, occasionally with pseudo- Gaucher / sea-blue histiocytes and fibrosis. Past studies divided CML into two histological subtypes: a commoner granulocytic variant (~83%) showing unilinear granulopoietic hyperplasia, and a bilinear megakaryocytic type (~41%) additionally showing megakaryocytic hyperplasia, altered topology and pleomorphism with ineffective diminished erythropoiesis and grade 2-4 reticulin

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Dear Editor

The hyper cellular marrow of CML shows pan myelosis and a virtual absence of adipocytes. There is granulocytic and/or megakaryocytic proliferation, eosinophilia and basophilia, occasionally with pseudo- Gaucher / sea-blue histiocytes and fibrosis. Past studies divided CML into two histological subtypes: a commoner granulocytic variant (˜83%) showing unilinear granulopoietic hyperplasia, and a bilinear megakaryocytic type (˜41%) additionally showing megakaryocytic hyperplasia, altered topology and pleomorphism with ineffective diminished erythropoiesis and grade 2-4 reticulin [1]. The clinical significance of this distinction (apart from the higher grade of fibrosis encountered in the megakaryocytic-type) remains controversial. Manifest myelofibrosis is an adverse morphological factor associated with larger spleens, increased circulating blast percentages, lower hemoglobin levels and additional karyotypic abnormalities. Grading of collagen density, whether semi-quantitative or by computerized morphometry, reveals that even slight increase in reticulin (compatible with doubled normal values) is associated with significantly worsened prognosis [2]. Thiele et al. recommended that myelofibrosis should be included in any staging system in CML relating to survival [3]. Imatinib mesylate therapy significantly decreases cellularity, neutrophil granulopoiesis, abnormal micromegakaryocytes, microvessel density and cell proliferation indices with regression of myelofibrosis. There is an increase in erythroid precursors and reactive lymphoid nodules with enhanced apoptosis. Myeloblasts, CD34+ cells and immature myelomonocytic cells also decrease in patients who go into complete or partial remission [4]. Imatinib-associated marrow aplasia has been described. Interferon-alpha induces apoptosis, resulting in reduced cellularity, expansion of normal erythropoiesis with increased ironladen histiocytes and reticulum cells. Busalfan promotes myelofibrosis while hydroxyurea prevents it in a significant number of patients. In a study on 363 BMBs taken sequentially before and after allogeneic bone marrow transplantation, there was a significant correlation of marrow fibrosis, CD61+ cells and peripheral blood platelet counts with delayed haemopoietic reconstitution and leukemic relapse [5]. Apart from assessing cellularity and fiber content, the BMB is also suitable for immunohistochemisty (angiogenesis, apoptosis, proliferation indices) and morphometric studies as well as Fluorescent In-Situ Hybridization (FISH). Application of FISH to paraffin sections for demonstrating bcr/abl in intact cells, though not recommended for diagnosis, has been used as an adjunct to cytogenetic studies and to demonstrate the common stem cell origin of the CML clone. FISH for bcr/abl on BMBs was also found to be useful to monitor therapeutic efficacy of Imatinib [6]. The BMB remains a valuable investigation in CML, both for the wealth of prognostic information conveyed as well as its usefulness in investigating scientific queries.

References

  1. Thiele J, Kvasnicka HM, Beelen DW, Flucke U, Spoer C, et al. (2001) Megakaryopoiesis and myelofibrosis in chronic myeloid leukemia after allogeneic bone marrow transplantation: an immunohistochemical study of 127 patients. Mod Pathol 14: 129-138.
  2. Knox WF, Bhavnani M, Davson J, Geary CG (1984) Histological classification of chronic granulocytic leukaemia. Clin Lab Haematol 6: 171-175.
  3. Thiele J, Kvasnicka HM (2006) A critical reappraisal of the WHO classification of the chronic myeloproliferative disorders. Leuk Lymphoma 47: 381-396.
  4. Thiele J, Kvasnicka HM, Schmitt-Graeff A, Kriener S, Engels K, et al. (2005) Bone marrow changes in chronic myelogenous leukaemia after long-term treatment with the tyrosine kinase inhibitor STI571: an immunohistochemical study on 75 patients. Histopathology 46: 540-550.
  5. Kvasnicka HM, Thiele J, Schmitt-Graeff A, Diehl V, Niederle N, et al. (2003) Impact of bone marrow morphology on multivariate risk classification in chronic myelogenous leukemia. Acta Haematol 109: 53-56.
  6. Thiele J, Kvasnicka HM, Varus E, Ollig E, Schmitt-Graeff A, et al. (2004) Megakaryocyte features and bcr/abl translocation in chronic myeloid leukemia following imatinib mesylate (STI571) therapy--a fluorescence in-situ hybridization study. Leuk Lymphoma 45: 1627-1631.
Citation: Gaurey T (2013) A General View on Bone Marrow Research. J Bone Marrow Res 1:129.

Copyright: © 2013 Gaurey T. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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