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C Nezelof

Publications and source records attributed to C Nezelof.

At least 19 recordsLinked to original sources
PubMed1999

[Dynamic studies of Langerhans cell histiocytosis cells. Their contribution to the current concept of the disease. Report of a series of 38 cases].

In vitro explantation of 38 fragments of eosinophilic granuloma of bones was attempted. A satisfactory growth was obtained in nearly 90% of cases. This short-term culture maintained the ultrastructural characteristics and, to a lesser extent, the cytochemical features of the Langerhans cells, confirming the Langerhans cell origin of this cell proliferation. In addition, this procedure was able to demonstrate an immunodependent erythrophagocytosis (3/3) and a preferential fixation of labelled precursors (Glycerol, choline of lipid metabolism as well as labelled dopamine (2/2). All attempts to obtain a permanent cell line and graft to nude mice (even irradiated) failed. Under the in vitro conditions, the Langerhans cells do not divide up but can be readily identified up to 2 or 3 weeks. The contrast between the evident in vivo proliferation and the in vitro quiescent state suggests that some undetermined growth-factors targeted to the Langerhans cell system are missing in our commonly used culture media. The in vitro culture procedure could be of some help to their identification.

Animals↗
PubMed1998

Langerhans cell histiocytosis research. Past, present, and future.

This article reviews the various investigative events that led to the endorsement of the term Langerhans cell histiocytosis for the various clinicopathologic conditions previously called Hand-Schüller-Christian disease, Abt-Letterer-Siwe disease, eosinophilic granuloma of bone, and histiocytosis X. The different denominations reflect the changing conceptual approaches to the so-called reticuloendothelial system and the successive acquisition of new ultrastructural and immunocytochemical data.

Adult↗
PubMed1998

Malignant histiocytosis. Histologic, cytochemical, chromosomal, and molecular data with a nosologic discussion.

Although myelomonoblastic leukemia is thought to originate from a malignant transformation of the stem cell of the mononuclear phagocyte system, malignant histiocytosis (MH) is classically assumed to represent a malignant change of the terminal and fixed elements of this system. Indeed, MH is characterized by the proliferation of large, clear, pleomorphic, "histiocytic-like" HLADR and CD30+ cells resulting in a nodal and extranodal disseminated neoplasm affecting preferentially and severely children and young adults. Although there is broad agreement on the clinicopathologic presentation of this condition, there is currently quite a controversy over the T-lymphoid or histiocytic origin of the proliferative cells that results in a nosologic discussion between the anaplastic large cell lymphoma (ALCL) advocates and the MH supporters. This article has dealt mainly with this nosologic discussion and with the contributions provided by the investigations performed on MH permanent cell lines. These in vitro studies have demonstrated that the proliferation is characterized by a unique chromosomal abnormality, the 5q35bp usually associated with a t(2;5) translocation generating a fusion gene NPM/ALK and the subsequent translation of p80 protein. Although it is known that no single chromosomal abnormality is strictly restricted to a cell lineage, this 5q35bp and associated translocations seem today to represent the hallmark for this condition. In view of these chromosomal aberrations, the CD30+ ALCLs represent a heterogeneous group because 15% to 50% express the NPM/ALK fusion gene. In addition, these in vitro investigations have shown that 5q35bp proliferative cells are glass-adherent, can develop an immunodependent phagocytosis, and are able to reduce NBT and produce TNF-alpha. More significantly, they express constitutively the c-fms (the receptor of the macrophage growth factor) and, under TPA stimulation, are able to modulate the expression of this receptor and its ligand, as well as TNF-alpha and IL-1. None of these cell lines express CD3, but several express CD68 and CD71. In contrast, genomic investigations have shown the underlying existence of monoallelic and even biallelic gene rearrangements for TCR beta and IgJH. In view of these discrepancies between the genomic and phenotypic features of these cells, the histogenetic debate should remain open but must take into account these new chromosomal and molecular data.

Adult↗
PubMed1997

Contemporary classification of histiocytic disorders. The WHO Committee On Histiocytic/Reticulum Cell Proliferations. Reclassification Working Group of the Histiocyte Society.

Pathologists and pediatric hematologist/ oncologists of the World Health Organization's Committee on Histiocytic/Reticulum Cell Proliferations and the Reclassification Working Group of the Histiocyte Society present a classification of the histiocytic disorders that primarily affect children. Nosology, based on the lineage of lesional cells and biological behavior, is related to the ontogeny of histiocytes (macrophages and dendritic cells of the immune system). Dendritic cell-related disorders of varied biological behavior are dominated by Langerhans cell histiocytosis, but separate secondary proliferations of dendritic cells must be differentiated. Juvenile xanthogranuloma represents a disorder of dermal dendrocytes, another dendritic cell of skin. The hemophagocytic syndromes are the most common of the macrophage-related disorders of varied biological behavior. Guidelines for distinguishing the exceedingly rare malignant diseases of histiocytes from large cell lymphomas through the use of a battery of special studies are provided.

Cell Lineage↗
PubMed1994

Malignant histiocytosis and large cell anaplastic (Ki-1) lymphoma in childhood: guidelines for differential diagnosis--report of the Histiocyte Society.

A workshop of the Histiocyte Society was recently held, in order to discuss the problems and confusion of malignant histiocytosis (MH) and large cell anaplastic (Ki-1) lymphoma (LCAL). The aims of this workshop were to clarify the terminology for malignant histiocytic disorders and LCAL and to produce reliable criteria for diagnosis of both MH and LCAL. This article summarises the conclusions reached.

Antigens, CD↗
PubMed1993

FLT4 receptor tyrosine kinase gene mapping to chromosome band 5q35 in relation to the t(2;5), t(5;6), and t(3;5) translocations.

FLT4 is a recently cloned receptor tyrosine kinase cDNA, which is characterized by seven immunoglobulin-like loops in its extracellular domain. We have previously mapped the FLT4 gene to chromosome segment 5q33-qter using somatic cell hybrids. Here we have refined the localization to band 5q35 by fluorescence in situ hybridization and show that the gene is translocated to chromosomes 2 and 6 in the t(2;5)(p23;q35) and t(5;6)(q35;p21) translocations, respectively, of Ki-I-positive lymphomas, as well as to chromosome 3 in the t(3;5)(q25.1;q34) translocation, which is occasionally found in myelodysplastic syndromes and acute myeloid leukemia. No evidence was obtained for a rearrangement or deregulation of the translocated FLT4 gene. We further show that abundant FLT4 mRNA expression occurs only in erythroid and megakaryoblastoid cell lines among nine leukemia cell lines studied.

Chromosome Mapping↗