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  • 1
    Electronic Resource
    Electronic Resource
    Cathepsin D and E co-expression in sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease) and Langerhans' cell histiocytosis: further evidences of a phenotypic overlap between these histiocytic disorders (1994)
    Springer
    Virchows Archiv 424 (1994), S. 601-606 
    Details
    ISSN: 1432-2307
    Keywords: Cathepsin D ; Cathepsin E ; Rosai-Dorfman disease ; Langerhans' cell histiocytosis ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nosological classification of sinus histiocytosis with massive lymphadenopathy (SHML; Rosai-Dorfman disease) is difficult, and the normal cellular counterpart of Rosai-Dorfman (RD) cells is uncharacterised. The peculiar S-100+ phenotype of RD cells suggests a relationship with the dendritic cell family. Recent investigations have revealed cathepsin E to be selectively concentrated in antigen-presenting cells, whereas cathepsin D was found to be expressed in cells of macrophage lineage. Cathepsin D and E distribution was investigated by immunohistochemistry in a series of SHML biopsies and in two types of dendritic cell proliferative lesions: dermatopathic lymphadenitis (DL) and Langerhans' cell histiocytosis (LCH). In SHML biopsies, RD cells and monocyte-related elements of the sinuses and pulp coexpressed cathepsin D and E. LCH cells also stained for both these aspartic proteinases. Conversely, in DL cathepsin E and D were localised to separate cells that resembled Langerhans' cells (LC) or macrophages, respectively, in morphology and distribution. Our data outline the peculiar immunophenotype of RD and LCH cells and suggest that caution should be exercised in the identification of their normal cellular counterpart. The common expression of cathepsin D and E and of S-100 protein suggests some phenotypic overlap between SHML and LCH cells, despite their striking morphological divergence.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00195773
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Cathepsin D and E co-expression in sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease) and Langerhans' cell histiocytosis: further evidences of a phenotypic overlap between these histiocytic disorders (1994)
    Springer
    Virchows Archiv 424 (1994), S. 601-606 
    Details
    ISSN: 1432-2307
    Keywords: Cathepsin D ; Cathepsin E ; Rosai-Dorfman disease ; Langerhans' cell histiocytosis ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nosological classification of sinus histiocytosis with massive lymphadenopathy (SHML; Rosai-Dorfman disease) is difficult, and the normal cellular counterpart of Rosai-Dorfman (RD) cells is uncharacterised. The peculiar S-100+ phenotype of RD cells suggests a relationship with the dendritic cell family. Recent investigations have revealed cathepsin E to be selectively concentrated in antigen-presenting cells, whereas cathepsin D was found to be expressed in cells of macrophage lineage. Cathepsin D and E distribution was investigated by immunohistochemistry in a series of SHML biopsies and in two types of dendritic cell proliferative lesions: dermatopathic lymphadenitis (DL) and Langerhans' cell histiocytosis (LCH). In SHML biopsies, RD cells and monocyte-related elements of the sinuses and pulp coexpressed cathepsin D and E. LCH cells also stained for both these aspartic proteinases. Conversely, in DL cathepsin E and D were localised to separate cells that resembled Langerhans' cells (LC) or macrophages, respectively, in morphology and distribution. Our data outline the peculiar immunophenotype of RD and LCH cells and suggest that caution should be exercised in the identification of their normal cellular counterpart. The common expression of cathepsin D and E and of S-100 protein suggests some phenotypic overlap between SHML and LCH cells, despite their striking morphological divergence.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01069739
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Npm/alk fusion mRNA expression in Hodgkin and Reed–Sternberg cells is rare but does occur: Results from single-cell cDNA analysis (1997)
    Springer
    Annals of oncology 8 (1997), S. 83-87 
    Details
    ISSN: 1569-8041
    Keywords: clonal heterogeneity ; Hodgkin's disease ; NPM/ALK ; single cell PCR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: The translocation t(2;5)(p23;q35) leads to the fusion of the nucleophosmin gene (NPM) on chromosome 5q35 to the recently described receptor kinase ALK 2p23. It is characteristic of a subgroup of CD30+large-cell anaplastic non-Hodgkin's lymphoma (ALCL). Since some cases of Hodgkin's disease (HD) and ALCL share common features, a common pathogenesis has been proposed in a report of the expression of NPM/ALK fusion mRNA in11/13 Hodgkin's lymphomas. Patients and methods: We approached this question by micro manipulatory isolation of single Hodgkin and Reed–Sternberg (H-RS) cells and subsequent RT-PCR amplification of NPM/ALK fusion cDNA from these single cells. Results: Specificity of cell selection was shown by the HD-specific pattern of EBV-gene expression in single H-RS cells. In 4 out of 7 cases, NPM/ALK fusion cDNA was detected in the RNA from whole lymph node tissue. In2 out of 9 cases, NPM/ALK fusion sequences were amplified from single H-RS cells, albeit in a very low frequency (〈5%). Conclusions: These data indicate that NPM/ALK fusion transcripts do not play an early role in the pathogenesis of HD. Whether the rare expression of NPM/ALK is the result of clonal heterogeneity or an indication for clonal evolution and progression toward ALCL can only be answered by the repeated analysis of indicator cases during the course of the disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008246719680
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Npm/alk fusion mRNA expression in Hodgkin and Reed–Sternberg cells is rare but does occur: Results from single-cell cDNA analysis (1997)
    Springer
    Annals of oncology 8 (1997), S. 83-87 
    Details
    ISSN: 1569-8041
    Keywords: clonal heterogeneity ; Hodgkin's disease ; NPM/ALK ; single cell PCR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: The translocation t(2;5)(p23;q35) leads to the fusion of thenucleophosmin gene (NPM) on chromosome 5q35 to the recently describedreceptor kinase ALK 2p23. It is characteristic of a subgroup of CD30+large-cell anaplastic non-Hodgkin's lymphoma (ALCL). Since some cases ofHodgkin's disease (HD) and ALCL share common features, a common pathogenesishas been proposed in a report of the expression of NPM/ALK fusion mRNA in11/13 Hodgkin's lymphomas. Patients and methods: We approached this question by micromanipulatoryisolation of single Hodgkin and Reed–Sternberg (H-RS) cells andsubsequent RT-PCR amplification of NPM/ALK fusion cDNA from these singlecells. Results: Specificity of cell selection was shown by the HD-specificpattern of EBV-gene expression in single H-RS cells. In 4 out of 7 cases,NPM/ALK fusion cDNA was detected in the RNA from whole lymph node tissue. In2 out of 9 cases, NPM/ALK fusion sequences were amplified from single H-RScells, albeit in a very low frequency (〈5%). Conclusions: These data indicate that NPM/ALK fusion transcripts donot play an early role in the pathogenesis of HD. Whether the rare expressionof NPM/ALK is the result of clonal heterogeneity or an indication for clonalevolution and progression toward ALCL can only be answered by the repeatedanalysis of indicator cases during the course of the disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008246719680
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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