Leukaemic Reticuloendotheliosis (‘Hairy’ Cell Leukaemia): A Distinct Clinico‐Pathological Entity

Catovsky, Daniel; Pettit, John E.; Galton, D. A. G.; Spiers, A. S. D.; Harrison, C. V.

doi:10.1111/j.1365-2141.1974.tb00445.x

Cited by 170 publications

(44 citation statements)

References 38 publications

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“…Other studies confirmed the increase in the collagen fibrils in the intercellular space around the HCs but did not find evidence that HCs give rise to these fibrils (10). These studies also showed that HCs are not argyrophilic (29), suggesting that they may not be the direct source of reticulin fibers. Since no massive increase in fibroblast numbers is observed in the BM of HCL patients (10), the increased production of reticulin and ECM proteins might be due to an accelerated differentiation of fibroblasts into matrix-producing cells rather than to an increased proliferation.…”

Section: Introductionmentioning

confidence: 72%

TGF-β1 induces bone marrow reticulin fibrosis in hairy cell leukemia

Shehata¹,

Schwarzmeier²,

Hilgarth³

et al. 2004

J. Clin. Invest.

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Nonstandard abbreviations used: B cell chronic lymphocytic leukemia (B-CLL); bone marrow (BM); BM fibroblast (BMF); BM mononuclear cell (BMMC); BM plasma (BMP); BM stromal cell (BMSC); hairy cell (HC); HC leukemia (HCL); healthy donor (HD); peripheral blood plasma (PBP); procollagen type III aminoterminal propeptide (PIIINP). Conflict of interest:The authors have declared that no conflict of interest exists. IntroductionHairy cell leukemia (HCL) is a chronic lymphoproliferative disorder characterized by the presence of hairy cells (HCs) in peripheral blood, bone marrow (BM), and spleen and is invariably associated with a unique type of BM fibrosis (1-3). Although a rare disease (2% of adult leukemia), HCL represents an excellent model for cancer biotherapy (4) and for understanding the deregulation of cytokines and growth factors in human neoplasia (5-7). The fibrotic process and the associated structural abnormality in BM of HCL patients are mainly due to accumulation of fine argyrophilic reticulin fibers, although collagen fibers can be observed in the advanced stages of the disease (8-11). The composition of reticulin fibers in HCL is not well defined. In normal and fibrotic BM, the distribution of reticulin fibers is identical to that of type III collagen and its precursor, type III procollagen (12,13). Electron microscopic studies of human tissues revealed that reticulin fibers are individual collagen fibrils or small bundles of these fibrils embedded in the interfibrillar matrix of proteoglycans (14-16) and that they are composed mainly of type III collagen surrounding a core of type I collagen fibrils (17,18). In addition to reticulin fibrosis, it has been recently demonstrated that the glycoprotein fibronectin, which is produced and assembled by HCs, contributes to the fibrotic process in BM of HCL patients (19). This process was also found to be particularly enhanced by bFGF, which is endogenously produced by the HCs (20). Since reticulin and fibronectin fibers were found to represent different structures in myelofibrotic BM (21), it appears that BM fibrosis in HCL is a complex process that involves accumulation and assembly of collagenous ECM components (reticulin) (22) and noncollagenous ECM components (fibronectin).In BM, HCs are found in association with randomly dispersed fibroblastoid cells and are surrounded by reticulin fibers (9, 10, 23, 24). These fibroblastoid cells, which have been found in close association with collagen fibers, are the matrix-producing cells and are responsible for the synthesis of reticulin and collagen (9,(25)(26)(27)(28). Other studies confirmed the increase in the collagen fibrils in the intercellular space around the HCs but did not find evidence that HCs give rise to these fibrils (10). These studies also showed that HCs are not argyrophilic (29), suggesting that they may not be the direct source of reticulin fibers. Since no massive increase in fibroblast numbers is observed in the BM of HCL patients (10), the increased production of reticulin and ECM proteins mig...

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Section: Introductionmentioning

confidence: 72%

TGF-β1 induces bone marrow reticulin fibrosis in hairy cell leukemia

Shehata¹,

Schwarzmeier²,

Hilgarth³

et al. 2004

J. Clin. Invest.

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“…Generally, they are considered as precursors of mature viruses [1]. Virus A particles are invariably present in murine tumor plasma cells but nei ther in normal murine nor in human plasmocytes [5,8,10]. The presence of virus-like particles in tumor plasma cells in a case of 'hairy cell' leu kemia is suggestive for a viral nature of this neoplastic disease.…”

Section: Discussionmentioning

confidence: 99%

“…Except for filopodia, 'hairy cells' do not show any constant morphological features typical for a specific cell type. 'Hairy cells' were supposed to be (a) abnormal lymphocytes [5,7]; (b) reticulum cells [3,9], or (c) histiocytes [2].…”

Section: Discussionmentioning

confidence: 99%

Virus-Bearing Plasma Cells in Peripheral Blood of a Patient with ‘Hairy Cell’ Leukemia

Pedio¹,

Rüttner²,

Spycher³

et al. 1975

Acta Haematol

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Electron-microscopic examination of peripheral blood from a patient with ‘hairy cell’ leukemia revealed classical ‘hairy cells’, atypical lymphoid cells and numerous pathological plasma cells. Osmiophilic granular material coated the cell surface of ‘hairy cells’ and lymphoid cells but not the plasmalemma of the plasma cells. The most important features of the plasma cells were cytoplasmic protrusions and masses of oncogenic virus A particles in their endoplasmic reticular cisternae.

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“…Blood buffy coat was obtained in four cases diagnosed by current clinical and morphological criteria (8,9). In our experimental conditions these abnormal nononuclear cells exhibited three main characteristics (Fig.…”

Section: Hairy Cell Leukemiamentioning

confidence: 99%

Surface Features of Cells in Human Lymphoproliferative Disorders. An Immunoelectron Microscopy Study

Gourdin

Reyes

Lejonc

et al. 1976

Modern Trends in Human Leukemia II

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SummaryPeroxidase conjugated antibodies were applied to cell suspensions in order to detect surface associated immunoglobulins. Ce11 suspensions were fixed prior to incubation with reagents, a procedure avoiding membrane alterations induced by antibodies to surface component. By immunoelectron microscopy an identification of B lymphocytes could be made with simultaneous observation of their surface architecture.Basic findings were that normal circulating human B lymphocytes had a villous surface. This relationship was not confirmed however by examinating samples from various B and T cell proliferations establishing that surface morphology is not sufficient to categorize cells in disease.Specimens from hairy cell leukemia were also examined. Despite salient surface characteristics as revealed by the present method, the categorization of cells remains unclear.

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Leukaemic Reticuloendotheliosis (‘Hairy’ Cell Leukaemia): A Distinct Clinico‐Pathological Entity

Cited by 170 publications

References 38 publications

TGF-β1 induces bone marrow reticulin fibrosis in hairy cell leukemia

TGF-β1 induces bone marrow reticulin fibrosis in hairy cell leukemia

Virus-Bearing Plasma Cells in Peripheral Blood of a Patient with ‘Hairy Cell’ Leukemia

Surface Features of Cells in Human Lymphoproliferative Disorders. An Immunoelectron Microscopy Study

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