Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied open-lung biopsies from 17 patients with pulmonary lymphomatoid granulomatosis (LYG) using paraffin-section immunostains and Epstein-Barr virus (EBV) RNA in situ hybridization to assess the phenotype of these unique tumors and to clarify the role of EBV infection. Histologically, all cases demonstrated the characteristic mixed mononuclear cell infiltrate of lymphomatoid granulomatosis with variable numbers of cytologically atypical large lymphoid cells in a background of small lymphocytes. Paraffin-section immunostains in all cases showed a predominance of T lymphocytes. A minor population of CD20-positive large B lymphocytes was identified in 11 cases; immunoglobulin light-chain restriction was demonstrated in four of these and immunoglobulin gene rearrangements in another case. Nuclear labelling for EBV RNA was detected in 10 of these 11 cases and was confined to the population of large B lymphocytes. Staining for CD20 was absent in the remaining six cases, as was nuclear labeling for EBV RNA. However, the large atypical lymphoid cells stained for T-cell-lineage-specific antibodies in three of these cases. We conclude that some cases of lymphomatoid granulomatosis are B-cell lymphoma associated with EBV infection, whereas others are of T-cell origin and are probably unrelated to EBV infection.
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PMID:Lymphomatoid granulomatosis. Evidence of immunophenotypic diversity and relationship to Epstein-Barr virus infection. 757 93

Although T-cell-rich B-cell lymphoma (TCRBCL) is a recently recognized form of non-Hodgkin's lymphoma (NHL), limited information regarding its incidence, cellular origin, morphologic spectrum, and biologic behavior is currently available. In this study, the clinicopathologic features of eight patients with TCRBCL are presented. This neoplasm comprised about 1% of all NHLs seen at Emory University Hospital over 2 years. The male-to-female ratio was 1.6, and the mean age at diagnosis was 60 years. At presentation, TCRBCL was nodal in 88% of the patients and widely disseminated in 50% of the patients. A complete remission was seen in three of the five patients treated with combination chemotherapy that was directed at intermediate grade NHL. Three patients received inadequate or incomplete chemotherapy. One of these patients later achieved a complete remission with more intensive therapy. Two of the patients were not evaluable for response to therapy. The actuarial and disease-free survival rates of the group at 5 years were 72% and 21%, respectively. Morphologically, the lymph nodes in seven of eight cases were diffusely obliterated, whereas one had markedly expanded interfollicular zones that lead to an initial diagnosis of T-zone lymphoma. All tumors were characterized by no more than 25% large lymphoid cells, which were scattered in a background of small lymphocytes with round or irregular nuclei. The presence of numerous histiocytes imparted a lymphoepithelioid appearance in two cases. Although immunoperoxidase stains of frozen tissue were initially suggestive of a peripheral T-cell lymphoma in some cases, paraffin immunoperoxidase stains clearly established the B-cell nature of the large cells, whereas most of the small cells were T lymphocytes. The clonal nature of the large cells was confirmed in seven cases by monotypic immunoglobulin (Ig) light chain restriction or Ig gene rearrangements. Epstein-Barr virus genomic DNA was detected in two of the six cases tested by polymerase chain reaction or Southern blot analysis, but no evidence of a bcl-2 rearrangement was found in any of the five cases examined. These findings indicate that TCRBCL is an uncommon form of NHL with a therapeutic response and overall survival consistent with intermediate grade lymphoma. Paraffin immunoperoxidase stains and occasionally genotypic analysis are required to exclude the diagnosis of PTCL or diffuse lymphocyte predominant Hodgkin's disease. The authors found no morphologic or molecular evidence to support a follicular center cell origin in these cases of TCRBCL.
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PMID:T-cell-rich B-cell lymphoma. A clinicopathologic study of eight cases. 781 42

Peripheral T-cell lymphomas (PTCLs) are regarded as diffuse proliferations. We describe an unusual paracortical nodular growth pattern in four nodal PTCLs that were initially interpreted as atypical lymphoid hyperplasia in three patients and small B-cell lymphoma with plasmacytic differentiation in a fourth. The nodules were vague to easily discernible and produced minimal to partial architectural distortion. Sinuses were often open, and scattered cortical lymphoid follicles with atretic to hyperplastic germinal centers were present. Clusters of tumor cells abutted some follicles in all cases, and in one case they exhibited focal T-zone expansion. Hypervascularity was not prominent, but a few nodules surrounded epithelioid venules, imparting an angiofollicular appearance. The nodules were composed primarily of small lymphocytes with irregular nuclei admixed with scattered large transformed cells, both cell types having clear cytoplasm. Paraffin immunoperoxidase showed that the nodules were composed of T cells. Dendritic cell networks were present only in follicular centers. Southern blot analysis found T-cell receptor gene rearrangements and a germline immunoglobulin gene configuration in all four nodes. These paracortical clear cell nodules of clonal T cells may be a special type of PTCL. Alternatively, they may represent early foci of lymphoma or they may be a subgroup of T-zone lymphoma. Paracortical nodular PTCL must be differentiated from atypical hyperplastic lesions and some B-cell lymphomas.
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PMID:Paracortical nodular T-cell lymphoma. Identification of an unusual variant of peripheral T-cell lymphoma. 787 27

Paraffin sections of 133 cases of non-Hodgkin's lymphoma (69 B-cell type and 64 T-cell type) were stained in a labeled streptavidin biotin immunoperoxidase technique with a panel of antibodies that recognized T-lymphocyte associated antigens. This study was done to determine the sensitivity and specificity of these reagents for phenotyping T-cell lymphomas. UCHL-1, polyclonal anti-CD3, Leu-22, and OPD4 stained 78%, 72%, 91%, and 69% of the cases of T-cell lymphomas, respectively. The phenotype of L-26 negative and CD3 or UCHL-1 positive accurately predicted T-cell phenotype in 95% (60 of 63) of the T-cell lymphomas and was not seen in any of the cases of B-cell lymphoma. Although Leu-22 was the most sensitive T-cell-associated marker in this series, its lack of specificity for T-lymphocytes limited its usefulness as part of a routine panel designed to distinguish between T-cell and B-cell lymphomas. In conjunction with other reports, this study supports the use of the T-cell markers CD3 and UCHL-1 in combination with the B-cell-associated marker L-26 to phenotype most efficiently non-Hodgkin's lymphomas in paraffin sections.
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PMID:Immunoperoxidase staining of non-Hodgkin's lymphomas for T-cell lineage associated antigens in paraffin sections. Comparison of the performance characteristics of four commercially available antibody preparations. 835 74

Histologic features of recurrent Hodgkin's disease (HD) after conventional therapy are well known, but few studies describe HD after bone marrow transplantation (BMT). Histologic material from 63 patients who underwent BMT performed to treat recurrent nodular sclerosing HD (NSHD) between 1985 and 1994 was examined; 13 of the 63 patients had histologically proved recurrent disease after BMT. Histologic material and clinical findings from the original diagnostic biopsy specimen and pre-BMT and post-BMT specimens were available from our study population of eight patients (five male, three female; age range, 16 to 38 years; median age, 27.5 years). Seven patients had recurrent NSHD after BMT; sites of recurrence included lymph nodes only (four patients), and lymph nodes and lung, lung and liver, and lung only (one patient each). In one patient, a high-grade non-Hodgkin's B-cell lymphoma developed in the large intestine 5 years after BMT. In another, disease progressed from grade 1 in the original biopsy specimen to grade 2 in both the pre-BMT and post-BMT recurrent HD biopsy specimens. Post-BMT biopsy specimens of recurrent HD with lung involvement revealed a substantial increase in sclerosis and fibroblastic features. Paraffin immunoperoxidase studies in seven patients demonstrated substantial change in phenotype of Reed-Stemberg cell variants in only one post-BMT recurrent HD specimen, which showed a +2 reaction with CD30 (Ki-1). No substantial differences in the reactive component were noted between the original biopsy specimen and pre-BMT and post-BMT specimens of recurrent disease. In summary, histologic findings of post-BMT recurrent NSHD do not differ significantly from those of the original diagnostic biopsy or pre-BMT recurrent HD specimens. The lung is the most common site of extranodal post-BMT recurrence. In one patient, high-grade non-Hodgkin's B-cell lymphoma developed after BMT performed to treat recurrent HD.
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PMID:Recurrent Hodgkin's disease after bone marrow transplantation. 898 Mar 71

The criteria for distinguishing benign lymphoepithelial lesions (BLEL) from low grade B-cell lymphomas of mucosa-associated lymphoid tissue (MALT) type in salivary glands and the significance of genotypically documented clonality in this setting are controversial. In addition, the clinical implications of a neoplastic diagnosis are unclear. The histopathologic features of 68 specimens from 49 patients with at least one salivary gland biopsy with LEL together with available clinical data were, therefore, reviewed. Paraffin section immunohistochemical (IHC) stains for kappa, lambda, CD3, CD20, and CD43; in situ hybridization (ISH) for kappa and lambda; and polymerase chain reaction (PCR) for immunoglobulin (Ig) HC rearrangement were performed. The 61 salivary gland specimens were classified as BLEL-13, BLEL with monocytoid B-cell (MBC) halos (BLEL-halo-8), low grade B-cell lymphoma of MALT type with confluent zones of MBC or other atypical lymphocytes (ML-MALT-24), low grade B-cell lymphoma of MALT type with monoclonal plasma cells (ML-MALT-PC-12), and high grade B-cell lymphoma of MALT type (MALT-high grade-4). Soft tissue and perineural invasion was not observed in BLEL and was most common in the MALT lymphomas. Lymph node involvement was identified in six patients at the time of their salivary gland MALT lymphomas but in none with BLEL. CD43+ B cells were seen most commonly in ML-MALT but were present in all other categories except MALT-high grade. Clonal B cells were identified by PCR in 5 of 12 BLEL, 5 of 8 BLEL-halo, 17 of 22 ML-MALT, 6 of 10 ML-MALT-PC, and 3 of 3 MALT-high grade biopsies. All ML-MALT-PC were clonal by ISH or IHC. Repeat biopsies in 14 patients most commonly showed a BLEL/ML-MALT lesion in an ipsilateral or contralateral salivary gland with one transformation to a MALT-high grade. Although only a few patients are known to have received chemoradiation or radiation therapy, most patients with low-grade lesions have pursued an indolent course. These data show the presence of two types of borderline lesions within the spectrum of lymphoid proliferations associated with salivary gland LEL. One has clonal B cells without histological features of neoplasia and the other nonconfluent MBC extending beyond the confines of LEL ("halos"). They share some features with the infrequent nonneoplastic BLEL and others with the more common low-grade B-cell lymphomas of MALT. A few high-grade B-cell lymphomas of MALT were also identified including a rare example of transformation from a low- to high-grade lesion. The optimal therapeutic approach for the borderline and low-grade lesions and the reason why so many of the lymphoproliferative lesions associated with LEL remain localized to the neck remain to be defined.
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PMID:Salivary gland lymphoid infiltrates associated with lymphoepithelial lesions: a clinicopathologic, immunophenotypic, and genotypic study. 922 40

The TCL1 gene, localized near the break point of chromosome 14q32.1 often involved in T cell leukemias, is also expressed in normal precursor T and B cells, and B cell lymphoma cell lines. We investigated the expression of the TCL1 protein in various types of B cell lymphomas according to the Revised European-American Classification of Lymphoid neoplasms. Paraffin-embedded tissue sections of lymphoma specimens were subjected to TCL1 immunohistochemistry, and positivity was scored on a three-tiered scale: - (< 25% cells), + (25-50% cells), and ++ (> 50% cells). The TCL1 protein was expressed in low-grade B cell lymphomas including mucosa-associated lymphoid tissue type in ocular adnexa (18/20, 90%). It was also expressed in follicular, lymphoplasmacytic, and mantle cell lymphoma, but not in high-grade diffuse large B cell lymphoma (2/11, 18%). These data suggest that the expression of the TCL1 gene characterizes low-grade B cell lymphomas, and may be involved in certain processes of lymphomatogenesis.
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PMID:Activation of the TCL1 protein in B cell lymphomas. 1079 82

Primary cutaneous B-cell lymphomas (PCBLs) may have particular clinicopathologic characteristics distinct from their lymph node-based counterparts. It has been suggested that PCBLs should have a separate classification system. The aim of this study was to determine whether the Revised European-American Lymphoid Neoplasms (REAL) classification is applicable to PCBL. Thirty-nine cases of PCBL from 36 patients, consisting of 20 men and 16 women (median age 66 yrs), were included in this study. Paraffin-section immunohistochemistry for CD3, CD5, CD10, CD20, CD43, Bcl-2, Bcl-6, and cyclin D1 was performed in all cases. Immunostaining for immunoglobulin light chains was also performed on cases histologically diagnosed as extranodal marginal zone lymphoma (MZL) and primary cutaneous B-cell lymphoma unclassifiable (PCBLu). Polymerase chain reaction (PCR) analysis of t(14;18) was performed in all cases. Immunoglobulin heavy chain gene rearrangement (VDJ) was tested by PCR on all follicle center lymphoma (FCL), MZL, and PCBLu cases. The 39 cases consisted of 15 (39%) FCLs, 13 (33%) diffuse large B-cell lymphomas (DLCL), 9 (23%) extranodal MZL, and 2 cases of PCBLu. Anatomically, 59% of PCBLs occurred in the head and neck, of which approximately 57% were FCL. Five of six cases presenting on the lower extremity were DLCL. Follow-up data was available from all 39 patients with a mean of 50.8 months. All but two patients are alive with or without disease at last contact. One patient with DLCL died of lung metastases and the other DLCL patient died of sepsis as a complication of therapy. In all 15 cases of FCL, CD10 and/or Bcl-6 expression supported the follicle center origin of the neoplastic cells. In contrast to previous reports, we found that 53% (8 of 15) of primary cutaneous FCL had either Bcl-2 protein expression or t(14;18). Our data indicate that many cases of primary cutaneous FCL have Bcl-2 alterations similar to their nodal counterpart. We found that 95% (37 of 39) of PCBLs could be classified according to the REAL classification, supporting its applicability in cutaneous lymphomas.
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PMID:Clinicopathologic reassessment of primary cutaneous B-cell lymphomas with immunophenotypic and molecular genetic characterization. 1125 30

Paraffin blocks and clinical data from 521 patients with lymphocyte predominance Hodgkin disease (LPHD) diagnosed between 1970 and 1994 were collected from 16 European and United States oncological centers to establish the pathologic and clinical characteristics of a large patient cohort, to determine how frequent T-cell-rich large B-cell lymphoma (TCRLBCL) is among LPHD, and to find differential diagnostic criteria distinguishing between the 2 lymphoma categories. For this purpose, conventionally and immunohistologically stained sections were reviewed by a panel of hematopathologists. The diagnosis of LPHD was confirmed in only 219 of the 388 assessable cases (56.5%). This low confirmation rate was due mainly to the presence of a new variant of classical Hodgkin disease (CHD), which resembled, in terms of nodular growth and lymphocyte-richness, nodular LPHD and, in terms of the immunophenotype of the tumor cells, CHD and was designated nodular lymphocyte-rich CHD (NLRCHD). The nodules of LRCHD consisted-as in nodular LPHD-predominantly of B cells but differed from those present in LPHD in that they represented expanded mantle zones with atrophic germinal centers. Clinically, patients with LPHD and NLRCHD showed similar disease characteristics at presentation but differed in the frequency of multiple relapses and prognosis after relapse. Patients with LPHD and NLRCHD clearly differed from patients with CHD with nodular sclerosis or mixed cellularity, as they presented with an earlier disease stage and infrequent mediastinal involvement. As 97% of the LPHD cases showed a complete or partial nodular growth pattern, their differentiation from TCRLBCL was a rare problem in the present series. (Blood. 2000;96:1889-1899)
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PMID:European Task Force on Lymphoma project on lymphocyte predominance Hodgkin disease: histologic and immunohistologic analysis of submitted cases reveals 2 types of Hodgkin disease with a nodular growth pattern and abundant lymphocytes. 1096 91

The objective of this study was to examine placentas after delivery from normal, healthy patients at term gestation. The placentas were from elective cesarean sections (n = 10, prior to the onset of labor) and spontaneous vaginal delivery (n = 10, after labor). We found that deoxyribonucleic acid laddering was present in all placentas and consistent with the pattern found in tissues that undergo apoptosis. Paraffin-embedded sections of placental villi stained by the in situ terminal deoxynucleotidyl transferase mediated biotinylated dUTP nick end labeling method revealed positive apoptotic nuclei in the placental villi. Reverse-transcriptase polymerase chain reaction demonstrated expression of messenger RNA for testosterone-repressed prostate message 2 and B cell lymphoma/leukemia-2 in the placenta. Our data demonstrate that apoptosis occurs in human term placenta.
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PMID:Apoptosis in human term placenta. A morphological and gene expression study. 1096 89


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