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Angioimmunoblastic T-cell Lymphoma (angioimmunoblastic t-cell + lymphoma)
Selected AbstractsAngioimmunoblastic T-cell lymphoma with cutaneous involvementJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 6 2001R Mahendran [source] No correlation between immunoglobulin heavy chain rearrangements and the prognosis of angioimmunoblastic T-cell lymphomaEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 2 2009Daisuke Niino No abstract is available for this article. [source] Cutaneous involvement by angioimmunoblastic T-cell lymphoma: a unique histologic presentation, mimicking an infectious etiologyJOURNAL OF CUTANEOUS PATHOLOGY, Issue 2006Anu G. Jayaraman The cutaneous findings most commonly consist of a maculopapular eruption on the trunk. However, purpura, infiltrated or urticarial plaques, papulovesicular lesions, nodules, and erythroderma have also been reported. Histologic findings in the lymph node are characteristic, while those in the skin may show one of four patterns. Here, we review the previously reported histologic patterns and present a case of AILT involving the skin with a unique histologic appearance of necrotizing granulomas with abundant histiocytes and eosinophils, mimicking an infectious etiology. [source] Identification of CXCL13 as a new marker for follicular dendritic cell sarcoma,THE JOURNAL OF PATHOLOGY, Issue 3 2008W Vermi Abstract The homeostatic chemokine CXCL13 is preferentially produced in B-follicles and is crucial in the lymphoid organ development by attracting B-lymphocytes that express its selective receptor CXCR5. Follicular dendritic cells (FDCs) have been identified as the main cellular source of this chemokine in lymphoid organs. Recently, genome-wide approaches have suggested follicular CD4 T-helper cells (THF) as additional CXCL13 producers in the germinal centre and the neoplastic counterpart of THF (CD4+ tumour T-cells in angioimmunoblastic T-cell lymphoma) retains the capability of producing this chemokine. In contrast, no data are available on CXCL13 expression on FDC sarcoma (FDC-S) cells. By using multiple approaches, we investigated the expression of CXCL13 at mRNA and protein level in reactive and neoplastic FDCs. In reactive lymph nodes and tonsils, CXCL13 protein is mainly expressed by a subset of FDCs in B-cell follicles. CXCL13 is maintained during FDC transformation, since both dysplastic FDCs from 13 cases of Castleman's disease and neoplastic FDCs from ten cases of FDC-S strongly and diffusely express this chemokine. This observation was confirmed at mRNA level by using RT-PCR and in situ hybridization. Of note, no CXCL13 reactivity was observed in a cohort of epithelial and mesenchymal neoplasms potentially mimicking FDC-S. FDC-S are commonly associated with a dense intratumoural inflammatory infiltrate and immunohistochemistry showed that these lymphocytes express the CXCL13 receptor CXCR5 and are mainly of mantle zone B-cell derivation (IgD+ and TCL1+). In conclusion, this study demonstrates that CXCL13 is produced by dysplastic and neoplastic FDCs and can be instrumental in recruiting intratumoural CXCR5+ lymphocytes. In addition to the potential biological relevance of this expression, the use of reagents directed against CXCL13 can be useful to properly identify the origin of spindle cell and epithelioid neoplasms. Copyright © 2008 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] A rare cause of bilateral parotid enlargement: angioimmunoblastic T-cell lymphoma,ANZ JOURNAL OF SURGERY, Issue 10 2009J. Jayarajan MBBS (Hons) No abstract is available for this article. [source] Toxic epidermal necrolysis secondary to angioimmunoblastic T-cell lymphomaAUSTRALASIAN JOURNAL OF DERMATOLOGY, Issue 3 2005Brad Jones SUMMARY A 67-year-old man presented with a history of lymphadenopathy, fevers and separate skin eruptions of erythrodermic spongiotic dermatitis initially and subsequent toxic epidermal necrolysis. Initial lymph node biopsies showed non-specific granulomatous changes, and skin biopsies and bone marrow aspirate were not diagnostic. His toxic epidermal necrolysis responded well to 3 days of intravenous immunoglobulin. The patient was discharged from hospital and reviewed regularly as an outpatient. Due to persisting lymphadenopathy, further lymph node biopsy led to the diagnosis of angioimmunoblastic T-cell lymphoma, a rare form of peripheral T-cell lymphoma with a poor prognosis. At the time of diagnosis his condition deteriorated rapidly and he died soon after. [source] Frequent occurrence of B-cell lymphomas in angioimmunoblastic T-cell lymphoma and proliferation of Epstein,Barr virus-infected cells in early casesBRITISH JOURNAL OF HAEMATOLOGY, Issue 6 2007Klaus Willenbrock Summary Secondary lymphomas occurring in the setting of angioimmunoblastic T-cell lymphoma (AILT) are considered to be rare. Their occurrence has been attributed to Epstein,Barr virus (EBV)-associated lymphoproliferations. A previous study detected a dysregulated hypermutation process in B-cells of AILT. The present study aimed at estimating the frequency of B-cell lymphomas in AILT. By studying the expression of EBV and activation-induced cytidine deaminase (AID) as an indicator of hypermutating cells, we assessed whether B-cell lymphoproliferations in AILT were strictly associated with EBV and whether hypermutation might contribute to lymphomagenesis. Among 161 cases of AILT, diagnosed between 1996 and 2005 at the lymph node registry, Frankfurt, Germany, 19 cases were detected that also had B-cell non-Hodgkin lymphoma (NHL) and two cases had classical Hodgkin lymphoma (HL). EBV was detected in tumour cells of 7/18 NHL and both HL, suggesting that factors other than EBV contribute to lymphomagenesis. AID was expressed in AILT in large cells disseminated in the tissue, implying that the process of somatic hypermutation is ongoing in AILT, although the GC architecture is disrupted. This might be relevant in the development of secondary lymphomas. [source] | ||||||||||||||||||||||