Search PubMed⌕ Search

Biomedical subjects

E S Jaffe

Publications and source records attributed to E S Jaffe.

At least 181 records · Page 10Linked to original sources
PubMed1994

Epstein-Barr virus is infrequently identified in non-Hodgkin's lymphomas associated with Hodgkin's disease.

Epstein-Barr virus (EBV) was identified in a subset of cases of Hodgkin's disease (HD) and in some non-Hodgkin's lymphomas (NHLs), particularly those associated with immunodeficiency. Because patients with HD have associated immune system defects, we hypothesized that EBV might be involved in NHLs associated with HD. Using fixed paraffin sections and in situ hybridization for EBV EBER1 RNA, we studied 12 cases of composite NHL + HD, two patients with NHL who simultaneously also had HD involving a different site (simultaneous HD and NHL), 14 NHLs arising in patients who previously had HD, and seven NHLs from patients who subsequently developed HD. Epstein-Barr virus was identified most frequently in composite NHL + HD. Five (42%) cases of composite NHL + HD contained EBV in Reed-Sternberg and Hodgkin cells, four of which also had EBV-positive NHLs, diffuse mixed or large-cell type, with 10 to more than 50 EBV-positive cells per x400 microscopic field. These results suggest that in this subset of four cases, both the NHL and HD components may have arisen from the same EBV-infected progenitor cell. We did not find EBV in two cases of simultaneous NHL and HD or in seven NHLs preceding development of HD. We identified EBV in only two of 14 NHLs following HD, one small noncleaved cell lymphoma and one plasmacytoma, both containing more than 50 EBV-positive cells per x400 microscopic field. These results suggest that EBV plays a minimal role in NHLs associated with HD, with the exception of composite NHL + HD. Hodgkin's disease-associated immune defects may be involved in the pathogenesis of a subset of NHLs following HD, but the exact pathogenesis of most NHLs associated with HD remains uncertain. Parallels with the high-grade Burkitt-like lymphomas associated with human immunodeficiency virus infection are noted.

Adult↗
PubMed1994

Malignant lymphomas of B-cell lineage with marked tissue eosinophilia. A report of five cases.

Tissue eosinophilia is commonly seen in Hodgkin's disease and non-Hodgkin's lymphomas of T-cell lineage. In contrast, eosinophilia is infrequent in non-Hodgkin's lymphomas of B-cell origin. We describe five-B-cell lymphomas with exuberant tissue eosinophils. According to the Working Formulation, three were classified as large-cell immunoblastic, one as small lymphocytic lymphoma/chronic lymphocytic leukemia, and one as low-grade, not further subclassified, with features of monocytoid B-cell lymphoma. Immunophenotypic studies in each case revealed B-cell lineage; neoplastic cells expressed monotypic immunoglobulin light chain (four of five cases) or pan-B-cell antigens (five of five cases) and were negative for T-cell antigens. Southern blot hybridization in one case revealed immunoglobulin gene rearrangements, further confirming B-cell lineage. Eosinophilopoiesis is stimulated by interleukin 5 (IL-5), and Epstein-Barr virus (EBV) has been shown to upregulate IL-5 production. Therefore, both EBV infection and IL-5 expression were investigated as possibly pathogenetic mechanisms for the eosinophilia. However, both in situ hybridization studies for EBV mRNA and IL-5 mRNA were negative in the neoplastic cells. In one tumor, IL-5 was abundant in the cytoplasm of the eosinophils, a pattern similar to that seen in five cases of Hodgkin's disease studied with the same technique. Although rare, marked tissue eosinophilia may be associated with B-cell non-Hodgkin's lymphomas. Immunophenotypic or molecular genetic analyses are needed to make the correct diagnosis.

Adult↗
PubMed1994

Bilateral adrenal hemorrhage and adrenal insufficiency in a patient with lymphomatous adrenal infiltration following administration of a fusion toxin (DAB486 interleukin-2).

DAB486IL-2 is a novel fusion toxin in which the ADP-ribosyltransferase and membrane-translocating domains of diphtheria toxin have been combined with the interleukin-2 (IL-2) gene, creating a recombinant protein capable of selectively intoxicating cells bearing the high-affinity IL-2 receptor. Clinical activity has been documented in Hodgkin disease and the non-Hodgkin lymphomas; toxicities have been minimal and include mild hepatic transaminitis, proteinuria, and hypersensitivity reactions. In this report, a patient with tumor-stage cutaneous T-cell lymphoma developed clinical adrenal failure with bilateral adrenal hemorrhage and necrosis 7 weeks after completing a 5-day course of treatment with DAB486IL-2. The relationship of fusion toxin therapy to the development of this unusual toxicity is discussed.

Adrenal Gland Diseases↗
PubMed1994

Diffuse small noncleaved-cell, non-Burkitt's lymphoma in adults: a high-grade lymphoma responsive to ProMACE-based combination chemotherapy.

PURPOSE: To review the efficacy of cyclophosphamide, doxorubicin, etoposide, methotrexate with leucovorin, and prednisone (ProMACE)-based combination chemotherapy programs in the treatment of patients with diffuse small noncleaved-cell non-Burkitt's lymphoma. PATIENTS AND METHODS: Thirty-three patients with diffuse small noncleaved-cell non-Burkitt's lymphoma were accrued: eight with localized disease were treated with modified ProMACE-mechlorethamine, vincristine, procarbazine, and prednisone (MOPP) plus involved-field radiation therapy, and 25 with advanced-stage disease were treated with ProMACE/MOPP flexitherapy (n = 8), ProMACE-MOPP (n = 9), or ProMACE-cytarabine, bleomycin, vincristine, and methotrexate with leucovorin (CytaBOM) (n = 8). The median follow-up duration is 10 years. RESULTS: All eight patients with localized disease achieved a complete response, none have relapsed, and one died of intercurrent illness. Among patients with advanced-stage disease, five of eight (63%) flexitherapy-treated patients, six of nine (67%) ProMACE-MOPP-treated patients, and eight of eight (100%) ProMACE-CytaBOM-treated patients achieved a complete response. If the two ProMACE-MOPP-based groups are considered together, disease-free and overall survival rates at 15 years are projected at 61% and 35%, respectively. In contrast, only one patient has relapsed from a ProMACE-CytaBOM-induced complete remission, and overall survival of ProMACE-CytaBOM-treated patients (88%) is significantly higher than that for flexitherapy and ProMACE-MOPP (P2 = .04). CONCLUSION: Adult patients with diffuse small non-cleaved-cell non-Burkitt's lymphoma may be effectively treated with regimens that are effective in other aggressive lymphomas (eg, diffuse large-cell lymphoma).

Adult↗
PubMed1994

Immunodeficiency-associated malignant lymphoma. Three cases showing genotypic evidence of both T- and B-cell lineages.

Dual rearrangement of both immunoglobulin and T-cell receptor (TCR) genes has been described in up to 30% of precursor lymphoid neoplasms, but this phenomenon occurs rarely in lymphomas with a mature phenotype. We describe three cases of immunodeficiency-associated lymphomas, two in patients with acquired immunodeficiency syndrome (AIDS) and one in a patient with a renal transplant, in which both immunoglobulin and TCR gene rearrangements were identified. Two cases exhibited clonal JH, clonal JK, and clonal TCR beta gene rearrangements; the other case had clonal JK and TCR beta gene rearrangements with deletion of JH. Two of these bigenotypic lesions exhibited a B-cell phenotype, and the other exhibited evidence of both a B- and T-cell phenotype, containing cytoplasmic CD3 as well as monoclonal kappa light chain. In addition, two of the cases exhibited the presence of clonal Epstein-Barr viral DNA. These observations suggest that lymphomas arising in immunodeficiency states may be more prone to disordered differentiation than those arising in an intact immune system.

Adult↗
PubMed1994

An investigation of the viral pathogenesis of Kikuchi-Fujimoto disease. Lack of evidence for Epstein-Barr virus or human herpesvirus type 6 as the causative agents.

Histiocytic necrotizing lymphadenitis of Kikuchi and Fujimoto is a well-defined clinicopathologic entity of unknown cause. Both the Epstein-Barr virus (EBV) and human herpesvirus type 6 (HHV-6) have been suggested as potential etiologic agents. Twenty cases of Kikuchi-Fujimoto disease were studied for the presence of EBV DNA and HHV-6 DNA by the polymerase chain reaction (PCR), and in situ hybridization in the case of EBV. Cellular DNA from sections of formalin-fixed, paraffin-embedded lymph node tissue was amplified using the PCR technique and oligonucleotide primers to the EBV BamH1 W, lymphocyte-determined membrane antigen, or the EBNA-1 region. These studies were performed in three separate laboratories. In addition, 12 cases were examined by in situ hybridization, eight of which had shown at least one positive PCR signal for EBV. The presence of HHV-6 was assessed by PCR using primers to part of the pZVH14 sequence. Biopsy specimens from eight patients (40%) showed a strong positive signal for EBV in at least one laboratory, while an additional three specimens (15%) showed a weaker positive signal. Five cases studied showed rare positive cells by in situ hybridization, and one case had scattered positive cells. All samples lacked HHV-6 genomic templates. These findings indicate that HHV-6 does not play a role in the pathogenesis of Kikuchi-Fujimoto disease and do not implicate EBV as a causal agent for Kikuchi-Fujimoto disease, since EBV was detected in only a fraction of cases with a low number of positive cells detected by in situ hybridization. Further, some discrepancies were identified in the positive results for EBV in samples studied by multiple laboratories. These results indicate that inconsistent results by PCR may occur with very low levels of viral genomes and that different laboratories perform DNA amplification at different efficiencies. Alternatively, laboratory contamination may give rise to false-positive results. Therefore, a positive result for EBV should be interpreted with caution and should be confirmed by repeated study (PCR) or by independent methodology (in situ hybridization).

Adolescent↗
PubMed1993

Role of HTLV-I in development of non-Hodgkin lymphoma in Jamaica and Trinidad and Tobago. The HTLV Lymphoma Study Group.

Human T-cell lymphotropic virus type I (HTLV-I) has been implicated in the aetiology of adult T-cell leukaemia/lymphoma in Japan and elsewhere, particularly the Caribbean. We have carried out parallel case-control studies in Jamaica and in Trinidad and Tobago to quantify the role of HTLV-I in the development of non-Hodgkin lymphoma (NHL). 135 cases of NHL were enrolled in Jamaica and 104 in Trinidad and Tobago. Controls were selected from patients treated in the same wards or clinics at the same time as the cases. Overall, patients with NHL were 10 times more likely than were controls to be seropositive for HTLV-I (Jamaica odds ratio 10.3 [95% CI 6.0-18.0], Trinidad and Tobago 14.4 [7.6-27.2]). In both countries the association between NHL and HTLV-I was greatest for T-cell lymphomas (18.3 [9.5-35.6] and 63.3 [25-167]). Among T-cell lymphomas especially, there was no significant difference between men and women in the association between NHL and HTLV-I, but there was a significant inverse relation between age and likelihood of HTLV-I seropositivity. B-cell lymphomas were predominant in the older age groups and were not associated with HTLV-I seropositivity. These findings are consistent with the hypothesis that early life exposure to HTLV-I is important for risk of subsequent ATL. Prevention of vertical transmission of HTLV-I could reduce by 70-80% cases of NHL in people under 60 years in this region.

Adult↗
PubMed1993

p53 mutation is associated with progression in follicular lymphomas.

The majority of low-grade follicular lymphomas will eventually transform to an aggressive intermediate, or high-grade lymphoma. The molecular mechanisms responsible for this transformation have not been determined. We studied serial biopsies from 34 patients with follicular lymphomas that underwent histologic transformation, for abnormalities of the p53 tumor suppressor gene by a combination of immunohistochemistry, single strand conformation polymorphism analysis (SSCP), and sequencing. We found overexpression of p53 in 10 of the 34 transformed aggressive lymphomas, 9 of which contained mutations identified by SSCP analysis and subsequent sequencing. Matched pretransformation low-grade follicular lymphoma biopsies were available for 7 of the 10 cases. None of six studied by immunohistochemistry showed overexpression of p53 and only 1 of 4 studied by SSCP/sequencing showed the presence of mutation in the pretransformation biopsy. Interestingly, an eighth p53 positive transformed lymphoma recurred with a clonally related, p53 negative low-grade lymphoma 5 years after the patient had achieved a complete remission. Immunohistochemistry also showed that several pretransformation biopsies from p53 positive transformed cases showed rare p53 positive cells and in one case we could document an increase in their number over time. Twenty-five additional low-grade follicular lymphoma biopsies were also examined. Three patients had lymphomas positive for p53 mutation. One of the three subsequently transformed within a year of the biopsy studied; the second patient had an earlier (unavailable) biopsy at a different site that showed transformed histology. The third patient was treated with ProMACE-MOPP combination chemotherapy and attained a complete remission. We conclude that (1) mutations of p53 are associated with histologic transformation in approximately 25% to 30% of follicular lymphomas and (2) p53 positive cells can be detected before histologic transformation, but do not comprise a significant percentage of the neoplastic cell population (identifiable by SSCP) until late in the disease, just before or after histologic progression. Finally, the data also suggest that p53 positive low-grade lymphomas are at risk for progression and that in this subset, aggressive therapy may be warranted.

Base Sequence↗
PubMed1993

Molecular analysis of the BCL-3 locus at chromosome 17q22 in B-cell neoplasms.

To better understand the role of the BCL-3 locus at chromosome 17q22 in the pathogenesis and progression of leukemias and lymphomas, we examined its genomic configuration in 264 B-cell malignancies and its expression in a smaller subset. Cases studied included 39 chronic lymphocytic leukemias, 58 low-grade follicular lymphomas, 20 mantle cell lymphomas, 30 small noncleaved cell lymphomas, 25 acute lymphoblastic leukemias, 10 acquired immunodeficiency syndrome--related non-Hodgkin's lymphomas, and 44 diffuse mixed- or diffuse large-cell lymphomas. In addition, 38 aggressive lymphomas (transformed follicular lymphomas) derived from previously indolent follicular lymphomas were examined. Southern blot analysis showed BCL-3 locus rearrangement in 4 cases (1.5%), ie, in 3 transformed follicular lymphomas and in 1 indolent follicular lymphoma. All 4 also had BCL-2 rearrangements consistent with their follicular center cell origin. None of the BCL-3 rearranged cases showed MYC gene rearrangement, as reported for the original leukemia that led to the discovery of BCL-3. Pretransformation specimens of all three transformed follicular lymphomas showed the presence of the BCL-3 alteration before histologic progression. In 1 case, serial pretransformation biopsies showed that the BCL-3 rearrangement was acquired during the indolent follicular phase of the patient's disease. Thirty lymphomas, including 2 of the 4 with BCL-3 rearrangement, were also examined for BCL-3 message. All 30, including the 2 with BCL-3 rearrangements, expressed the normal 1.7-kb BCL-3 transcript, at approximately equivalent levels. The data indicate that, although BCL-3 locus alterations are found in only a small fraction of B-cell lymphoid malignancies, they occur primarily in a subset of follicular center cell lymphomas. Interestingly, these alterations appear to be acquired during the indolent (follicular) phase of the disease and they are maintained when histologic transformation takes place. The data also suggest that BCL-3 locus alterations do not result in gross changes of BCL-3 gene expression and do not necessarily involve the MYC gene. Although the preferential involvement of BCL-3 alterations in a small subset of follicular lymphomas that transform suggests a possible link between these abnormalities and progression, further studies are needed to ensure that these alterations are biologically relevant and not simply a manifestation of genomic instability.

B-Cell Lymphoma 3 Protein↗
PubMed1993

B-cell lymphoma after angioimmunoblastic lymphadenopathy: a case with oligoclonal gene rearrangements associated with Epstein-Barr virus.

We describe a patient with angioimmunoblastic lymphadenopathy with dysproteinemia (AILD), who subsequently developed large-cell immunoblastic lymphoma of B-cell immunophenotype. At the time of the initial diagnosis, histologic examination of an inguinal lymph node showed typical features of AILD, and there was no evidence of a monoclonal B-cell population by immunohistochemical analysis. In situ hybridization and Southern blot analysis for Epstein-Barr virus (EBV) were negative. At autopsy 2 years later, the patient had widespread lymph node and organ involvement by large-cell immunoblastic lymphoma of B-cell immunophenotype. Southern blot analysis performed on DNA extracted from lymph nodes, liver, and spleen showed two patterns of Ig heavy chain and kappa light chain gene rearrangements. The T-cell receptor beta chain gene was in the germline configuration. Analysis with an EBV terminal repeat region probe showed two clonal populations that paralleled the Ig gene rearrangement studies. Double-labeling immunohistochemistry and in situ hybridization confirmed the presence of EBV within the neoplastic B cells. The data support the hypothesis that EBV was not etiologically related to AILD in this case, and that EBV proliferation may occur after the onset of the disease. Further, the data suggest that some B-cell lymphomas that arise in the setting of AILD resemble EBV-associated B-cell lymphomas that arise in other immunodeficiency states.

Blotting, Southern↗
PubMed1993

Small noncleaved cell lymphoma associated with florid epithelioid granulomatous response. A clinicopathologic study of seven patients.

The finding of epithelioid granulomas has been widely reported in solid tumors and in hematologic malignancies. This phenomenon has been especially well studied in Hodgkin's disease, where its presence has been shown to confer a favorable prognosis. Such granulomas have not, however, been as extensively studied in other forms of hematologic malignancy, particularly in small noncleaved cell lymphoma. We report seven cases of small noncleaved cell lymphoma that were associated with a marked epithelioid granulomatous response. Detailed clinical data, including follow-up, were available in five of the seven patients. Three had localized disease (stage I), whereas two had advanced disease (stages III-A and IV-B, respectively). All five patients achieved a complete remission and are alive without evidence of disease (median follow-up, 6 years). These findings suggest that the epithelioid granulomas may be a manifestation of a host response that confers an improved prognosis in this subtype of non-Hodgkin's lymphoma.

Adult↗
PubMed1993

Malignant lymphomas involving the ovary. A clinicopathologic analysis of 39 cases.

We report 39 patients with non-Hodgkin's lymphoma who initially presented with ovarian enlargement. Fifteen patients had unilateral (10 left, four right, one unknown) and 24 had bilateral ovarian masses. The median size of the tumors was 8 cm (range, 2 to 23 cm). Histologically, using the Working Formulation, 21 lesions (54%) were classified as small noncleaved cell, Burkitt's type; 12 (31%) as large cell (nine diffuse, three focally follicular); three (8%) as diffuse mixed, small and large cell; two (5%) as large cell immunoblastic; and one (2%) as follicular and diffuse small cleaved cell. Twenty-six tumors were analyzed immunophenotypically, 25 (96%) of which were B-cell neoplasms. However, combining histologic and immunohistochemical findings, 37 neoplasms were of B-cell lineage, one diffuse large-cell lymphoma was not analyzed, and one large-cell immunoblastic lymphoma (with features of anaplastic large-cell lymphoma) was of T-cell lineage with an aberrant immunophenotype. On the basis of staging studies and clinical follow-up, we conclude that only four (10%) of the neoplasms in this study most likely arose in the ovary. The primary neoplasms, three diffuse large-cell and one diffuse mixed small- and large-cell, were B-cell neoplasms. Three of four patients with primary neoplasms were apparently cured at last follow-up following surgical excision and chemotherapy. The remainder of the lymphomas in this study, most commonly of small noncleaved cell, Burkitt's type, appear to be systemic tumors that involved the ovaries secondarily. Approximately 40% of patients with systemic neoplasms were alive without evidence of disease at last follow-up.

Adolescent↗
PubMed1993

Epstein-Barr virus-associated T-cell lymphoma in a renal transplant patient.

Posttransplant lymphoproliferative disorders in organ allograft recipients are most commonly of B cell origin, whereas T cell lymphomas are rarely described. We report a case of T cell immunoblastic large cell lymphoma associated with Epstein-Barr virus (EBV) that occurred in a recipient of a cadaveric renal transplant 7 years posttransplantation. On paraffin immunophenotyping, none of the neoplastic cells stained with the T cell-associated markers used, but did show strong CD30 expression. Flow cytometric studies revealed a predominance of T cells without definite evidence of T cell neoplasia. Frozen section immunophenotyping studies revealed a T cell phenotype with aberrant expression, and genotypic studies demonstrated T cell receptor beta gene rearrangement with germline configuration of immunoglobulin heavy chain and kappa light chain genes, confirming a T lineage. EBV-encoded RNA transcripts were demonstrated within the neoplastic cells by in situ hybridization. Southern blot analysis using probes derived from the terminal repeat region of the virus detected a single restriction band indicating a clonal population. We believe this is the first case of a posttransplant T cell lymphoma in which the EBV genome has been demonstrated. This case also illustrates the pitfalls of paraffin immunophenotyping in the diagnosis of T cell lymphoma.

Adult↗
PubMed1993

Parameters affecting the development of non-Hodgkin's lymphoma in patients with severe human immunodeficiency virus infection receiving antiretroviral therapy.

PURPOSE: To investigate the occurrence of non-Hodgkin's lymphoma (NHL) in human immunodeficiency virus (HIV)-infected patients receiving long-term antiretroviral therapy and factors associated with the development of these lymphomas. PATIENTS AND METHODS: The charts of 55 patients with advanced HIV infection receiving zidovudine (formerly known as azidothymidine [AZT])-based therapy and 61 patients receiving dideoxyinosine (ddI) were examined for the occurrence of NHL. Stored samples from the AZT-based treatment cohort were examined retrospectively for parameters predictive of the subsequent development of lymphoma. RESULTS: Eight of 55 patients receiving AZT-based therapy developed NHL, yielding an estimated probability of 12% (95% confidence interval [CI], 4.7% to 27.1%) after 24 months, and 29.2% (95% CI, 15.2% to 48.7%) after 36 months. Four of 61 patients receiving ddI developed NHL, yielding a 6.2% (95% CI, 2.1% to 17%) estimated probability after 24 months, and 9.5% (95% CI, 3.6% to 22.8%) after 36 months. The difference between these cohorts was not significant (two-tailed P [P2] = .13). Patients with less than 50 CD4 cells/microL developed NHL at a significantly higher rate (P2 = .0085). This was particularly true for patients who presented with primary CNS lymphoma (PCNSL). For patients receiving AZT-based therapy, pretreatment serum interleukin-6 (IL-6) levels were somewhat higher in those who subsequently developed NHL than in those who did not (P2 = .048). CONCLUSION: HIV-infected patients with profound immunodeficiency, especially those with less than 50 CD4 cells/microL, are at substantial risk of developing NHL and particularly PCNSL. Additional studies are needed to define the role of other factors such as IL-6 in the pathogenesis of these opportunistic tumors.

CD4-Positive T-Lymphocytes↗
PubMed1993

EPOCH chemotherapy: toxicity and efficacy in relapsed and refractory non-Hodgkin's lymphoma.

PURPOSE: Based on in vitro evidence that tumor cells are less resistant to prolonged exposure to low concentrations of the natural product class, compared with brief higher concentration exposure, we developed a chemotherapy regimen (etoposide, vincristine, doxorubicin, cyclophosphamide, and prednisone [EPOCH]) in which the natural products are administered as a continuous infusion. PATIENTS AND METHODS: This is a phase II study of etoposide, vincristine, and doxorubicin, administered as a 96-hour continuous infusion, with intravenous (IV) bolus cyclophosphamide and oral prednisone (EPOCH) in 74 consecutive patients who relapsed from or failed to respond to most of the same drugs administered on a bolus schedule. Patients with aggressive lymphomas who achieved a good response after EPOCH were eligible to undergo bone marrow transplantation. RESULTS: Patients with intermediate- or high-grade lymphoma comprised 76% of this series and 77% had stage IV disease. Seventy-one percent had previously received all of the drugs contained in the EPOCH regimen and 92% had received at least four of the drugs. Seventy patients were assessable for response, of whom 19 (27%) achieved a complete remission (CR) and 42 (60%) a partial remission (PR). Among 21 patients who had no response to prior chemotherapy, 15 (71%) responded, but only one achieved a CR. Patients who relapsed from an initial CR had a 100% response rate, with 76% CRs. With a median potential follow-up duration of 19 months, there was a 28% probability of being event-free at 1 year. Toxicity was primarily hematologic with neutropenia during 51% of cycles, but only a 17% incidence of febrile neutropenia. Gastrointestinal, neurologic, and cardiac toxicity were minimal. CONCLUSION: EPOCH chemotherapy was well tolerated and highly effective in patients who were resistant to or relapsed from the same drugs administered on a bolus schedule, suggesting that continuous infusion of the natural drug component of this regimen is capable of partially reversing drug resistance and reducing toxicity. Dose-intensity (DI) was > or = that achieved in primary treatment regimens for aggressive lymphomas.

Adult↗
PubMed1993

Follicular center cell lymphoma with the t(14;18) translocation in which the rearranged BCL-2 gene is silent.

Using reverse transcription and the polymerase chain reaction (RT-PCR), we determined the level of expression of BCL-2/IgH in 18 follicular center cell lymphomas containing a t(14;18) translocation involving the major breakpoint region and five non-neoplastic lymph nodes. BCL-2/IgH transcripts were demonstrated in 16 follicular center cell lymphoma cases (five high, 11 low) and were not present in any of the five non-neoplastic lymph nodes. In the two follicular lymphoma cases in which BCL-2/IgH transcripts could not be detected by RT-PCR, PCR amplification of genomic DNA indicated this was not due to primer selection. In addition, non-expression was confirmed at the protein level by immunoperoxidase studies. We therefore conclude that these represent true negative cases. This is the first time primary follicular lymphoma cases have been quantitatively studied at the RNA level for expression of BCL-2. We conclude that RT-PCR is a sensitive method for determining levels of expression of this oncogene and may be useful in studying the involvement of BCL-2 in follicular lymphoma.

Adult↗
PubMed1993

Low-grade B-cell lymphoma of mucosa-associated lymphoid tissue arising in the kidney.

We describe a malignant lymphoma arising in the kidney that exhibited clinical and histologic features of low-grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT). Clinically, the neoplasm involved the kidney and one perirenal lymph node (stage IIE) and did not recur or disseminate following nephrectomy, lymphadenectomy, and local radiation therapy. Histologically, the neoplasm recapitulated the features of low-grade B-cell lymphomas of MALT at other sites. The neoplastic cells resembled centrocyte-like cells, some of which formed lymphoepithelial lesions with renal tubules, and reactive lymphoid follicles were scattered within the neoplasm. The neoplastic cells expressed monotypic cytoplasmic Ig kappa. Low-grade B-cell MALT lymphomas arising in the kidney are rare. Their occurrence further demonstrates the diversity of anatomical sites that may be involved by MALT lymphomas. In addition, this neoplasm also had histologic and cytologic features resembling those of monocytoid B-cell lymphoma, supporting the hypothesis that low-grade B-cell lymphomas of MALT and monocytoid B-cell lymphomas are closely related and may be two morphological manifestations of the same neoplasm.

Aged↗