Oligoclonal populations of T and B cells in a case of angioimmunoblastic T-cell lymphoma predominantly infiltrated by T cells of the VB5.1 family.

Hodges, Elizabeth; Quin, Christine T.; Wright, Dennis H.; Smith, Joan K.

doi:10.1136/mp.50.1.15

Cited by 25 publications

(10 citation statements)

References 9 publications

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“…Incidence of Ig clonality was highest in AILT (32%), close to the frequencies identified by Smith et al 28 and Lome-Moldonado et al, 35 but higher than reported by Frizzera. 27 In this entity, Ig clonality most likely corresponds to expanded B-cell clones 28,[35][36][37][38] in line with the occurrence of secondary Epstein-Barr viruspositive B-cell lymphoma after AILT. 38,39 Also in T-LGL the association with B-cell proliferations is described.…”

Section: Anaplastic Large Cell Lymphomamentioning

confidence: 96%

Powerful strategy for polymerase chain reaction-based clonality assessment in T-cell malignancies Report of the BIOMED-2 Concerted Action BHM4 CT98-3936

White²,

et al. 2006

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Polymerase chain reaction (PCR) assessment of clonal T-cell receptor (TCR) and immunoglobulin (Ig) gene rearrangements is an important diagnostic tool in mature T-cell neoplasms. However, lack of standardized primers and PCR protocols has hampered comparability of data in previous clonality studies. To obtain reference values for Ig/TCR rearrangement patterns, 19 European laboratories investigated 188 T-cell malignancies belonging to five World Health Organization-defined entities. The TCR/Ig spectrum of each sample was analyzed in duplicate in two different laboratories using the standardized BIOMED-2 PCR multiplex tubes accompanied by international pathology panel review. TCR clonality was detected in 99% (143/145) of all definite cases of T-cell prolymphocytic leukemia, T-cell large granular lymphocytic leukemia, peripheral T-cell lymphoma (unspecified) and angioimmunoblastic T-cell lymphoma (AILT), whereas nine of 43 anaplastic large cell lymphomas did not show clonal TCR rearrangements. Combined use of TCRB and TCRG genes revealed two or more clonal signals in 95% of all TCR clonal cases. Ig clonality was mostly restricted to AILT. Our study indicates that the BIOMED-2 multiplex PCR tubes provide a powerful strategy for clonality assessment in T-cell malignancies assisting the firm diagnosis of T-cell neoplasms. The detected TCR gene rearrangements can also be used as PCR targets for monitoring of minimal residual disease.

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Section: Anaplastic Large Cell Lymphomamentioning

confidence: 96%

Powerful strategy for polymerase chain reaction-based clonality assessment in T-cell malignancies Report of the BIOMED-2 Concerted Action BHM4 CT98-3936

White²,

et al. 2006

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“…Our own series included 43 cases (41%) with a sizable CD8 ϩ T cell population, a feature also reported previously. 12,13,23,30,[32][33][34][35]47,48 . As these CD8…”

Section: All Ailt Are Derived From Cd4 ϩ T-lymphocytesmentioning

confidence: 99%

Angioimmunoblastic T cell lymphoma is derived from mature T‐helper cells with varying expression and loss of detectable CD4

Lee

Rüdiger

Odenwald

et al. 2002

Intl Journal of Cancer

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Angioimmunoblastic T cell lymphoma (AILT) is Key words: angioimmunoblastic T-cell lymphoma; immunohistochemistry; double labeling; clinicopathologic correlationAngioimmunoblastic lymphadenopathy with dysproteinemia was originally described by various groups 1-3 as a systemic lymphoproliferative disorder characterized by generalized lymphadenopathy, hepatosplenomegaly, fever, skin rash, anemia and immunologic abnormalities. Histologically, the lymph node structure is diffusely effaced by a hypocellular infiltrate including a mixture of small, medium-sized and large atypical lymphoid cells, plasma cells, eosinophils and histiocytes and a proliferation of high endothelial venules. 4 For some years it could not be clarified whether the disease should be considered a lymphoma 1,5,6 or an abnormal hyperimmune reaction, 2,4 because the fatal outcome was mostly attributed to severe infection rather than lymphoproliferation. 2,4 Subsequent studies, however, showed evidence of a clonal process demonstrating chromosomal abnormalities characteristic for T cell lymphoma 7-9 or a clonal rearrangement of T cell receptor genes. 10 -16 Based on these and immunophenotypic studies, the disease was incorporated into the updated Kiel classification of non-Hodgkin's lymphoma as "T cell lymphoma of angioimmunoblastic type". 17 Angioimmunoblastic lymphoma (AILT) has also been recognized by the REAL 18 and the World Health Organization (WHO) classification 19 as a separate disease entity of peripheral T cell lymphoma (PTCL). A morphological variant, AILT with hyperplastic germinal centers has been described recently. 20 It remains controversial whether the disease represents a homogeneous entity or should be divided into a preneoplastic and a neoplastic phase because some cases lack definite cytologic atypia and approximately 20 -30% of AILT showed no obvious evidence of clonality. [12][13][14][15][21][22][23][24][25] Criteria to predict an indolent clinical course have been proposed and were based on the absence of clear cells and lack of clonal T cell receptor gene rearrangement. 6,12,13,26 -29 Based on clinical data, others suggested the presence of clustered or sheet-like proliferations of immunoblasts or pale cells of T cell nature as a distinguishing criterion for AILD-like T cell lymphoma from reactive angioimmunoblastic lymphadenopathy. 6,28 The predictive value of these prognostic factors has not been settled so far.Ongoing research on AILT has also focused on the functional immunophenotype of putative tumor cells. These investigations proved to be rather difficult because of the morphologic heterogeneity of the cellular composition in AILT. Additionally, the nuclear morphology is not well preserved in frozen tissue sections. Although in most series the majority of cases seemed to be derived from CD4ϩ T cells, a minority of tumors was regarded to be CD8 ϩ . 12,13,16,20,23,24,27,30 -39 . In some studies, a considerable number of T cells was thought to be part of the reactive inflammatory background infiltrate of T cell lympho...

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“…[7][8][9][10][11][12][13][14][15][16] In addition, clonal rearrangements have been shown to regress or appear during the course of the disease, suggesting that these cases may harbor multiple clones 11 similar to those found in cases with acquired immunosuppression. 13,16 This conclusion is supported by cytogenetic studies that reveal a characteristic chromosome pattern consistent with the frequent presence of karyotypically unrelated abnormal clones, which may also appear and regress in a high proportion of AILD cases. 9,17 Given the heterogeneous nature of AILD it is reasonable to propose that a relationship between reactive and clonal T and B cell lymphoproliferations exist in this entity.…”

mentioning

confidence: 99%

Frequent T and B Cell Oligoclones in Histologically and Immunophenotypically Characterized Angioimmunoblastic Lymphadenopathy

Smith¹,

Hodges²,

Quin³

et al. 2000

The American Journal of Pathology

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The identification of clonal rearrangements of T cell receptor (TCR) genes is central to the diagnosis of T cell lymphomas. However, in angioimmunoblastic lymphadenopathy (AILD), first described as a nonneoplastic proliferation associated with immunodeficiency, the heterogeneity of TCR and IgH gene rearrangements suggest that some cases may harbor multiple lymphoid clones. In this study we have isolated DNA from archival paraffin biopsy material from 22 cases of AILD identified on the basis of classical histological and immunohistochemical features with the aim of establishing the occurrence of clones and oligoclones, the frequency of TCR and immunoglobulin heavy chain (IgH) variable (v) gene use, and the relationship of these findings to the presence of Epstein-Barr virus. DNA extracted from the biopsies was amplified using the polymerase chain reaction (PCR) and sequenced to detect functional and nonfunctional gene rearrangements. Epstein-Barr virusencoded short RNA species (EBERs) were detected using in situ hybridization combined with immunochemistry to identify the phenotype of the EpsteinBarr virus-infected cells. Fifty-seven clonal products were found in 20/22 patients: TCR␥ clonal products were identified in 16/22, TCR␤ clonal products in 16/22 and IgH clonal products in 6/22 cases. Oligoclonal PCR products were seen for TCR in 3/22 and for IgH in 3/22 cases. In one biopsy PCR products from all reactions were polyclonal. Sequence analysis revealed functional TCR␥, TCR␤, and IgH sequences in 6/12, 9/11, and 8/8 cases, respectively. Functional TCR and/or IgH oligoclones were detected in 6/20 (30%) cases. In addition, nonfunctional TCR and IgH sequences were found in 11 cases. EBERs were identified in 18/20 cases varying from occasional to 25 to 30% nuclei staining and were associated with both T and B cells, although the majority were of indetermi- Early reports of AILD stressed the nonneoplastic nature of this disease, 1,2 noting that neither the cytology nor the pattern of infiltration seen in biopsies or autopsies was that of a neoplasm. The disease was thought to be due to abnormal immune regulation, the majority of patients dying of infections, often with opportunistic organisms.2 An association with lymphoma was, however, noted by Lukes and Tindle, 3 who reported the development of immunoblastic lymphoma in 3 of their 32 patients. Subsequently, there has been controversy over the separation of AILD from AILD with immunoblastic lymphoma (IBL) based on histological features such as atypical clear cells, which has contributed to the variation in the reported incidence of lymphoma in AILD from 0 to 35%. 4 -6 In addition, both groups show clonality or lack of clonality. 4,7 Frizzera et al 8 has proposed that three AILDrelated disorders can be recognized as AILD, AILD-like dysplasia, and AILD-like peripheral T cell lymphoma (PTCL) based on a combination of morphology, phenotype, clonal-

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Oligoclonal populations of T and B cells in a case of angioimmunoblastic T-cell lymphoma predominantly infiltrated by T cells of the VB5.1 family.

Cited by 25 publications

References 9 publications

Powerful strategy for polymerase chain reaction-based clonality assessment in T-cell malignancies Report of the BIOMED-2 Concerted Action BHM4 CT98-3936

Powerful strategy for polymerase chain reaction-based clonality assessment in T-cell malignancies Report of the BIOMED-2 Concerted Action BHM4 CT98-3936

Angioimmunoblastic T cell lymphoma is derived from mature T‐helper cells with varying expression and loss of detectable CD4

Frequent T and B Cell Oligoclones in Histologically and Immunophenotypically Characterized Angioimmunoblastic Lymphadenopathy

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