123 research outputs found

    Lymphocyte-rich classical Hodgkin lymphoma

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    Classical Hodgkin lymphoma

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    Lymphocyte-rich classical Hodgkin lymphoma accounts for a small fraction of all Hodgkin lymphomas. Lymphocyte-rich classical Hodgkin lymphoma is a rare variant of classical Hodgkin lymphoma which resembles nodular lymphocyte predominance Hodgkin lymphoma, in terms of nodular growth and lymphocyte-richness, and mimics cHL, in terms of the immunophenotype of the tumour cells. Lymphocyte-rich classical Hodgkin lymphoma tumour cells have lost the B-cell phenotype, but express CD30 and the B-cell transcription program. As regards to genetics and cytogenetics findings please refer to the general features described in the CARDS related to nodular lymphocyte predominance Hodgkin lymphoma and classical Hodgkin lymphoma

    Follicular dendritic cell in lymphomas of follicular origin

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    B-cell lymphomas of presumed follicular origin include follicular lymphoma (FL), mantle cell lymphoma (MCL) and marginal zone lymphoma (MZL). Within the microenvironment of all these follicle-derived lymphomas tumor cells show a strict topographical and functional relationship with FDCs, together with reactive lymphoid and stromal cells. The FDC patterns, as described for FL and MCL, are reminiscent of the distribution pattern of FDC meshwork seen in the GC or the mantle zone of the secondary lymphoid follicle, respectively

    Nodular lymphocyte-predominant Hodgkin lymphoma

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    Follicular lymphomas of germinal center (B- or T-cell) origin

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    Follicular lymphomas of germinal center (B- or T-cell) origin include follicular lymphoma (FL), nodular lymphocyte predominant Hodgkin lymphoma (NLPHL), and angioimmunoblastic T-cell lymphoma (AITL).Other lymphomas of presumed follicular origin comprise mantle cell lymphoma (MCL) and marginal zone lymphoma (MZL) (Fig. 1). In this article we describe the clinical, pathological and genetic features of follicular lymhomas of germinal center (B- or T-cell) origin

    Lymphocyte depletion classical Hodgkin lymphoma

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    HIV-associated lymphomas

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    Lymphoma remains the most frequent neoplastic cause of death among HIV-infected individuals. Lymphomas in patients infected with HIV are heterogeneous, not only pathologically but also in terms of pathogenetic pathways and cellular derivation. This CARD summarizes the association of the different types of HIV-associated lymphomas with known genetic lesions and/or oncogenic viruses. In the setting of HIV infection different, but not mutually exclusive, pathogenic pathways might occur. For a distinct pathway of AIDS-related lymphomagenesis there can be multiple associated genetic lesions in the tumor. Several of the HIV-associated lymphomas are also related to EBV and/or KSHV (HHV-8) infection

    Classification of Hodgkin lymphoma over years

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    Review on del(5)(q32q33) EBF1/PDGFRB fusion with clinical data and genes involved

    High serum levels of soluble CD40-L in patients with undifferentiated nasopharyngeal carcinoma: pathogenic and clinical relevance

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    BACKGROUND: Engagement of CD40 promotes survival of undifferentiated nasopharyngeal carcinoma (UNPC) cells and similar effects are induced by the EBV oncoprotein LMP-1 that is expressed in a fraction of cases. Considering that CD40 may be activated also by the soluble isoform of CD40L (sCD40L), we investigated the serum levels of sCD40L in a series of 61 UNPC patients from Italy, a non-endemic area for this disease. RESULTS: At diagnosis, serum samples of UNPC patients contained significantly higher levels of sCD40L than age-matched healthy controls (p < 0.001). High levels of sCD40L (i.e., >18 ng/ml) were more frequently found in patients <40 years of age (p = 0.03) and with distant metastases at presentation (p = 0.03). Serum levels of sCD40L were inversely associated with the expression of the EBV oncoprotein LMP-1 (p = 0.03), which mimics a constitutively activated CD40. The amount of sCD40L decreased in a fraction of patients treated with local radiotherapy alone. Moreover, CD40L(+ )lymphoid cells admixed to neoplastic UNPC cells were detected in cases with high serum levels of sCD40L, suggesting that sCD40L is probably produced within the tumor mass. CONCLUSION: sCD40L may contribute to CD40 activation in UNPC cells, particularly of LMP-1-negative cases, further supporting the crucial role of CD40 signalling in the pathogenesis of UNPC. sCD40L levels may be useful to identify UNPC patients with occult distant metastases at presentation
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