Biomedical subjects

B Schnitzer

Publications and source records attributed to B Schnitzer.

At least 37 records · Page 2Linked to original sources

PubMed1997

The t(2;5)-associated p80 NPM/ALK fusion protein in nodal and cutaneous CD30+ lymphoproliferative disorders.

A high percentage of extracutaneous CD30+ anaplastic large cell lymphomas (nodal ALCL) carry a specific chromosomal translocation, t(2;5) (p23;q35), that results in abnormal expression of p80 NPM/ALK chimeric protein (p80). The protein p80 may be detected by immunohistochemistry using polyclonal (anti-p80) or monoclonal (ALK1) antibody directed against the ALK epitope. Although nodal ALCL, primary cutaneous ALCL, and lymphomatoid papulosis type A (lyp A) have similar histologic and immunohistochemical features, the expression of p80 in these cutaneous lesions has not been extensively studied. We immunostained tissues from 10 nodal ALCL, 8 primary cutaneous ALCL, 24 lyp A, and positive and negative controls using polyclonal rabbit anti-p80 and the avidin-biotin-peroxidase labeling method. Reactivity was determined by comparing staining intensity to positive controls [4 nodal ALCL with t(2;5)] and negative controls (21 non-ALCL lymphomas). Only cutaneous lesions staining positively with anti-p80 were further studied with the monoclonal antibody ALK1 and reverse transcription polymerase chain reaction (RT-PCR) for p80 messenger RNA. All positive controls (4/4), but none of the negative controls (0/21) nor lyp A (0/24), were immunoreactive for anti-p80. Sixty percent (6/10) of nodal ALCL and a single case (12%) of primary cutaneous ALCL were immunoreactive for anti-p80. In this exceptional cutaneous lesion, although we did not find NPM/ALK by RT-PCR, we detected strong expression of ALK using ALK1. We conclude that t(2;5) is rarely involved in the pathogenesis of cutaneous CD30+ lymphoproliferative disorders.

Anaplastic Lymphoma Kinase↗

PubMed1997

Ruptured spleens with expanded marginal zones do not reveal occult B-cell clones.

An indolent variant of splenic marginal zone lymphoma (SMZL) lacking massive splenomegaly has been described as an incidental finding in spleens removed for rupture or hypersplenism. We studied traumatically ruptured spleens with expanded marginal zones (MZs) to assess the incidence of occult monoclonal B-cell populations in this setting. Ninety-one ruptured or lacerated spleens removed from 1984 to 1995 were classified as to whether they had expanded MZs (> 12 cell layers thick). When available, paraffin-embedded, formalin-fixed tissue from cases with expanded MZs was examined for immunoglobulin heavy chain gene rearrangement by polymerase chain reaction (PCR) and stained for CD20, CD43, and kappa and lambda light chains. Splenectomies were performed for blunt (70 patients) and penetrating (7 patients) trauma, surgical misadventure (13 patients), or spontaneous rupture (1 patient). There were 58 men and 33 women in our study, ranging in age from 17 to 87 years (mean, 40 yr). Average spleen weight was 183 g (range, 44-505 g). Twenty-seven (30%) of 91 patients had expanded MZs. There were no significant differences in age, sex, spleen weight, or reason for excision between those cases with and without MZ expansion. Germinal centers varied from absent to inactive to floridly reactive. Paraffin blocks were available in 24 cases; the 20 with amplifiable DNA were polyclonal by PCR. Follow-up was available for 25 of the 27 patients with expanded MZs (range, 1-85 mo; median, 6 mo); lymphoma did not develop in anyone, although one patient's spleen was morphologically suspicious for lymphoma, showing involvement of red pulp by MZ-type B-cells; PCR revealed a polyclonal pattern. This patient's 3-year follow-up revealed no evidence of lymphoma. Traumatically ruptured spleens with expanded MZs do not seem to harbor occult B-cell clones, as detected by PCR. Although a few cases of incidentally removed spleens have been reported to contain low-stage SMZL, this seems to be an infrequent event.

Adolescent↗

PubMed1996

Detection of immunoglobulin heavy chain gene rearrangement by polymerase chain reaction in chronic active gastritis associated with Helicobacter pylori.

Chronic active gastritis associated with Helicobacter pylori (CAG-Hp) has been linked to the pathogenesis of gastric B-cell lymphomas of mucosa-associated lymphoid tissue (MALT). To determine whether monoclonal lymphoid populations are present in CAG-Hp and histological predictors of monoclonality exist, the authors examined 46 endoscopic biopsies from 41 patients with CAG-Hp. The authors scored gastric biopsies for the presence of lymphoepithelial lesions (LELs), intensity of lymphoid infiltrate, presence of lymphoid aggregates and germinal centers, coexpression of CD43 (Leu 22) on B cells, and cytoplasmic immunoglobulin light chain restriction in formalin-fixed, paraffin embedded tissues. DNA extracts from these routinely processed tissues were analyzed for immunoglobulin heavy chain (IgH) gene rearrangement by polymerase chain reaction (PCR). Histological features, immunophenotype, gene rearrangement status, and clinical information were correlated. Six of the 46 biopsies (13%) from six of 41 patients (15%) showed a monoclonal PCR pattern. Monoclonal PCR patterns correlated with the presence of LELs (P<.015) but not with intensity of lymphoid infiltrate, presence of germinal centers, or presence of lymphoid aggregates. LELs correlated with germinal centers (P<.003) and intensity of infiltrate (P<.0001). None of the cases showed cytoplasmic light chain restriction nor coexpression of CD43 on B cells by immunohistochemistry. Clinical follow-up was available in all six patients whose gastric biopsies had a monoclonal PCR pattern (median, 58 months; range, 1 to 66 months) and 33 of the 35 patients with biopsies showing a polyclonal PCR pattern (median, 41 months; range 0.1 to 63 months). No patient developed gastric lymphoma. Monoclonality of lymphoid cells was detected by IgH PCR in 13% of patients with CAG-Hp. Although the authors cannot exclude the possibility that some patients with monoclonal gastric lymphoid infiltrates may eventually develop overt lymphoma, no histological, immunophenotypic, nor clinical evidence of lymphoma was noted at presentation or on clinical follow-up. Given the high incidence of CAG-Hp in the general population and the relatively low incidence of gastric MALT lymphoma, clinicopathologic correlation is needed when interpreting tests for clonality in this setting. The presence of clonal IgH gene rearrangement in CAG-Hp supports the hypothesis that H pylori is involved in the pathogenesis of low grade gastric B-cell MALT lymphomas.

Adult↗

PubMed1996

Follicular lymphoma with involvement of the splenic marginal zone: a pitfall in the differential diagnosis of splenic marginal zone cell lymphoma.

Follicular lymphomas (FL) involving the spleen arise in and expand the germinal centers of the white pulp, whereas mantle cell lymphomas arise in the mantle zone and surround the benign germinal center. The recently described marginal zone cell lymphoma (MZCL) is a B-cell neoplasm characterized by concentric expansion of cells around the follicle, with or without infiltration of the mantle zone or germinal center. In addition, the immunoglobulin heavy chain gene is rearranged although none of the MZCL reported have been shown to be positive for the bcl-2 gene translocation by molecular studies. We report a patient with FL showing preferential involvement of the marginal zone of spleen morphologically mimicking a primary splenic MZCL. The patient reported here had a well-documented previous lymph node diagnosis of FL. The immunoglobulin heavy chain gene and bcl-2 gene rearrangement analysis confirmed the clonal origin of both the original FL, as well as the lymphoma, with a marginal zone pattern in the spleen.

Base Sequence↗

PubMed1996

Ki-1 anaplastic large cell lymphoma with a prominent leukemic phase.

Patients with Ki-1 (CD30)-positive anaplastic large cell lymphoma (ALCL) occasionally have rare circulating lymphoma cells. We report a case of ALCL with a prominent leukemic phase. A 36-year-old man presented with widespread ALCL involving lymph nodes, spleen, pleural fluid, cerebrospinal fluid, and bone marrow. His white blood cell count was 106,000/mm3 with 20% lymphoma cells. The circulating neoplastic cells were large, and had irregular nuclei with multiple small nucleoli, ample cytoplasm, and multiple clear cytoplasmic vacuoles. This case illustrates that ALCL may have a marked leukemic phase composed of large anaplastic cells.

Adult↗

PubMed1996

Analysis of immunoglobulin heavy chain gene rearrangement in myoepithelial sialadenitis by polymerase chain reaction.

Myoepithelial sialadenitis (MESA) can often be difficult to distinguish from low grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT). The authors have previously studied a series of 25 patients with MESA and identified histologic and immunologic features predictive of extrasalivary lymphoma (ESL). The authors have now analyzed formalin-fixed, paraffin-embedded salivary gland tissue from 21 of these patients (and 1 new patient) for immunoglobulin heavy chain (IgH) gene rearrangement by a semi-nested polymerase chain reaction (PCR) technique to compare monoclonality by IgH PCR with clinical outcome (median follow-up 6.7 years, range 3 months-19.4 years) and the paraffin section immunophenotype. The PCR technique employed consensus primers from variable (FR3A) and joining regions (LJH, VLJH) of the IgH gene. A monoclonal PCR product was detected in 16 of 28 specimens from 13 of 22 patients. By Fisher's exact test, a monoclonal PCR pattern did not correlate (P > .05) with development of ESL, broad strands of monocytoid B-cells, plasma cell light chain restriction by immunoperoxidase, or CD43 coexpression on monocytoid B cells by immunoperoxidase. This study suggests that the majority of MESA lesions harbor monoclonal B-cell populations and that clonality does not predict progression to clinically overt lymphoma. Acquired salivary gland MALT, in the form of MESA, may progress to a process that is clonal but not necessarily malignant. Extranodal lymphoma develops in a minority of patients with this lesion.

Adult↗

PubMed1995

Cyclin D1 protein expression in mantle cell lymphoma.

BACKGROUND: The t(11;14)(q13;q32) is a chromosomal abnormality usually associated with mantle cell (centrocytic) lymphomas, although it has occasionally been reported in other chronic lymphoproliferative disorders such as chronic lymphocytic leukemia, prolymphocytic leukemia, splenic lymphoma with villous lymphocytes, and multiple myeloma. This abnormality results in the translocation of the bcl-1 oncogene from chromosome 11 to the immunoglobulin heavy chain locus on chromosome 14. The bcl-1 oncogene is a member of the cyclin gene family, and high levels of cyclin D1 mRNA are consistently found in malignant B cell proliferations with t(11;14). PATIENTS AND METHODS: We examined cyclin D1 protein expression in 33 patients with low grade lymphoproliferative disorders and 2 patients with reactive hyperplasias by Western blot analysis using a polyclonal antibody. RESULTS: 8/11 mantle cell lymphomas, 0/11 chronic lymphocytic leukemias, 0/4 hairy cell leukemias, 0/2 Sezary syndrome, 0/2 monocytoid B-cell lymphomas, 0/3 follicular lymphomas, and 0/2 reactive hyperplasias had overexpression of cyclin D1. Cytogenetic analysis was performed in four cases of mantle cell lymphoma; three of these cases had the t(11;14), one of which was hypotetraploid with two copies of t(11;14). Immunophenotypically, all cases of mantle cell lymphoma and chronic lymphocytic leukemia had coexpression of CD5 and CD20. CONCLUSION: Mantle cell lymphoma may be difficult to discriminate from chronic lymphocytic leukemia, a more indolent disease, on morphologic and immunophenotypic grounds. Our findings suggest that analysis of cyclin D1 protein expression may be helpful in differentiating mantle cell lymphomas from other low grade lymphoproliferative disorders.

Antigens, Neoplasm↗

PubMed1995

Epstein-Barr virus and bcl-2 protein overexpression are not detected in the neoplastic cells of nodular lymphocyte predominance Hodgkin's disease.

Recent studies have indicated that nodular lymphocyte predominance Hodgkin's disease (nLP-HD) is a B-cell lymphoma. Although molecular events in the neoplastic transformation of B-cells are not well understood, Epstein-Barr virus infection and bcl-2 protein overexpression have been postulated to have etiologic roles in some lymphomas. Epstein-Barr virus has been demonstrated in the Reed-Sternberg cells of Hodgkin's disease cases (other than nLP-HD) as well as in some B-cell lymphomas; bcl-2 overexpression is found in the majority of follicular lymphomas. The biologic role for bcl-2 in HD is controversial. Some reports have indicated the presence of bcl-2 gene rearrangements, associated with the t(14;18) (q32;q21), detected by the polymerase chain reaction in HD; recent studies have failed to confirm this finding. Reports in the literature describe only a few such analyses in the nLP-HD subtype. To address these conflicting issues, we examined 12 cases of nLP-HD to determine whether bcl-2 protein expression (by immunohistochemistry) and Epstein-Barr virus (by in situ hybridization) could be detected in the Reed-Sternberg variants. None of the cases showed expression of bcl-2 protein or Epstein-Barr virus RNA in the neoplastic cells. Epstein-Barr virus does not appear to play an important role in the pathogenesis of nLP-HD. Similarly, we cannot substantiate a role for bcl-2 in the development of this type of Hodgkin's disease.

Base Sequence↗

PubMed1995

Peripheral T-cell non-Hodgkin's lymphoma following treatment of nodular lymphocyte predominance Hodgkin's disease.

Previous reports have suggested that nodular lymphocyte predominance Hodgkin's disease (NLPHD) is a germinal center-derived B-cell lymphoma that is distinct from other types of Hodgkin's Disease. A relationship between NLPHD and simultaneous or subsequent development of large-cell (LC) non-Hodgkin's lymphoma (NHL) has been established. Both Reed-Sternberg cell variants in NLPHD and NHL cells in these cases express B-cell-associated antigens, and in some cases the B-cell lineage of the NHL has been confirmed by immunoglobulin gene rearrangement studies. The B-cell phenotype and the indolent course of both lymphomas suggest histologic progression of NLPHD to B-cell NHL, rather than a de novo LCNHL unrelated to Hodgkin's Disease. We report a unique case of T-large-cell lymphoma (TLCL) following successful chemotherapy of NLPHD. A 54-year-old male was treated with seven cycles of mechlorethamine, vincristine, procarbazine, prednisone chemotherapy for NLPHD and 4 years later developed recurrent adenopathy. Lymph node biopsy showed a diffuse LCNHL. Frozen section immunotyping and gene rearrangement studies confirmed the diagnosis of TLCL. To our knowledge, this case represents only the second report of TLCL associated with NLPHD and is of significance in that: (1) it demonstrates that T-cell neoplasia can occur in the setting of NLPHD; (2) this case does not appear to represent histologic progression of NLPHD and most likely represents de novo disease that may be secondary to chemotherapy; and (3) the clinical course may differ from the favorable prognosis seen in NLPHD associated with B-cell NHL.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1995

Development of extrasalivary gland lymphoma in myoepithelial sialadenitis.

Myoepithelial sialadenitis of the salivary gland is associated with an increased risk of lymphoma, but criteria that predict its development have not been clearly defined. We attempted to identify morphologic and immunologic features that correlated with the presence of extrasalivary lymphoma in patients with myoepithelial sialadenitis. Twenty-five patients (20 women, 5 men; median age, 56 yr) were studied with clinical follow-up in 22 patients; 19 were followed for 3 or more yr (median, 8.0 yr overall). Immunostains were done on paraffin sections in 28 of 31 specimens (22 of 25 patients) using antibodies to immunoglobulin light chains, CD20, CD45RO, CD3, and CD43. Morphologic features studied included density of infiltrate, lymphoepithelial lesions, follicle atypia, and pattern of monocytoid B-cells. Twenty-four of 25 patients had dense lymphoid infiltrates expanding and effacing salivary gland architecture with lymphoepithelial lesions and epimyoepithelial islands; all but one of these cases showed monocytoid B-cells in and around ducts, whereas six also had interconnecting broad strands of these cells. One case showed predominantly follicular hyperplasia. Two cases contained follicles with large atypical cells. Plasma cells were monotypic in four patients (18%) and polytypic in 18 (82%); in 18 of 28 specimens (64%) from 15 of 22 patients (68%), monocytoid B-cells coexpressed CD20 and CD43. Seven patients developed extrasalivary lymphoma, one before and six after the diagnosis of myoepithelial sialadenitis (median, 30.5 mo). Monotypic immunoglobulin in plasma cells correlated with past or subsequent extrasalivary lymphoma (P < 0.005); broad strands of monocytoid B-cells correlated with both monotypic plasma cells (P < 0.005) and extrasalivary lymphoma (P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1994

Gamma/delta T-cell posttransplantation lymphoproliferative disorder primarily in the spleen.

A 31-year-old renal transplant recipient developed an unusual T-cell lymphoproliferative disorder 3 years after transplantation. The neoplasm involved the spleen, without concomitant hepatomegaly, lymphadenopathy, or obvious bone marrow involvement. Peripheral blood involvement developed after splenectomy. Immunophenotypically, the neoplastic cells expressed CD2, CD3, CD7, CD16, CD45, CD56, and the gamma/delta T-cell receptor on the surface membrane. The neoplastic cells were negative for surface membrane CD4, CD5, and CD8. Serologic and/or DNA analyses for viruses, including Epstein-Barr virus, human T-cell lymphotropic virus-1, human immunodeficiency virus, and human herpesvirus-6, were negative. Cytogenetic findings included a translocation breakpoint at chromosome 7p15, consistent with involvement of the T-cell receptor gamma-chain locus. Although gamma/delta T-cell lymphomas have been reported to have a predilection for hepatosplenic localization, this is the first well-documented case to be described in the setting of posttransplantation immunosuppression.

Adult↗

PubMed1993

Acute biphenotypic leukaemia: immunophenotypic and cytogenetic analysis.

The incidence of acute biphenotypic leukaemia has ranged from less than 1% to almost 50% in various reports in the literature. This wide variability may be attributed to a number of reasons including lack of consistent diagnostic criteria, use of various panels of antibodies, and the failure to recognize the lack of lineage specificity of some of the antibodies used. The morphology, cytochemistry, immunophenotype and cytogenetics of acute biphenotypic leukaemias from our institution were studied. The diagnostic criteria took into consideration the morphology of the analysed cells, light scatter characteristics, and evaluation of antibody fluorescence histograms in determining whether the aberrant marker expression was arising from leukaemic blasts or differentiated bone marrow elements. Fifty-two of 746 cases (7%) fulfilled our criteria for acute biphenotypic leukaemias. These included 30 cases of acute lymphoblastic leukaemia (ALL) expressing myeloid antigens, 21 cases of acute myelogenous leukaemia (AML) expressing lymphoid markers, and one case of ALL expressing both B- and T-cell associated antigens. The acute biphenotypic leukaemia cases consisted of four major immunophenotypic subgroups: CD2+ AML (11), CD19+ AML (8), CD13 and/or CD33+ ALL (24), CD11b+ ALL (5) and others (4). Chromosomal analysis was carried out in 42/52 of the acute biphenotypic leukaemia cases; a clonal abnormality was found in 31 of these 42 cases. This study highlights the problems encountered in the diagnosis of acute biphenotypic leukaemia, some of which may be responsible for the wide variation in the reported incidence of this leukaemia. We suggest that the use of strict, uniform diagnostic criteria may help in establishing a more consistent approach towards diagnosis of this leukaemic entity. We also suggest that biphenotypic leukaemia is comprised of biologically different groups of leukaemia based on immunophenotypic and cytogenetic findings.

Adolescent↗

PubMed1992

CD30 (Ki-1)-positive, anaplastic large cell lymphoma mimicking gastrointestinal carcinoma.

BACKGROUND: There is great diversity in the clinical presentation of CD30 (Ki-1)-positive, anaplastic large cell lymphoma (ALCL). The authors report two patients in whom the clinical and morphologic features mimicked gastrointestinal carcinoma. METHODS: Surgical pathology specimens were examined using standard histologic techniques. Paraffin- and frozen-section immunohistochemistry was performed by an avidin-biotin-peroxidase method. RESULTS: The first patient is a 58-year-old man who presented with a constricting mass of the sigmoid colon. Immunohistochemical staining for CD45 (LCA) was negative in formalin-fixed paraffin sections. However, CD45 and CD74 (LN2) were detectable in B5 postfixed material. The second patient is a 44-year-old woman who presented with dysphagia and back pain. Endoscopic examination revealed an ulcerated luminal mass in the proximal esophagus and a gastric ulcer. Mucosal biopsy specimens of the esophagus and stomach contained ALCL, which was CD45 positive. Retroperitoneal lymph nodes contained ALCL infiltrating the sinuses, interfollicular areas, and blood vessel lumina. In addition to CD45 and pan-T-cell antigens, the neoplastic cells expressed CD68 (KP1) and epithelial membrane antigen (EMA). Monoclonal antikeratins were negative, but a polyclonal antikeratin stain was positive. CONCLUSIONS: These findings indicate that clinical, morphologic, and some immunologic features of ALCL may mimic gastrointestinal carcinoma.

Adult↗

PubMed1992

Anti-CD34 immunoperoxidase staining in paraffin sections of acute leukemia: comparison with flow cytometric immunophenotyping.

Anti-CD34 is a monoclonal antibody that reacts with bone marrow progenitor cells and leukemic blasts, and is expressed on 30% to 50% of all acute leukemias. Detection of CD34 has previously been restricted to flow cytometric studies. To expand the utility of CD34, we immunostained 46 paraffin-embedded bone marrow specimens with acute leukemia; results were compared with flow cytometric studies. CD34 reactivity was also evaluated in nine chronic leukemia cases, 27 malignant lymphoma cases (Hodgkin's disease and non-Hodgkin's lymphoma), six normal bone marrow specimens, and three benign, hyperplastic lymph node specimens. All cases that were CD34 positive by flow cytometry (11 of 19 B-cell precursor acute lymphoblastic leukemia cases, one of six T-cell acute lymphoblastic leukemia cases, and seven of 21 acute myeloblastic leukemia cases) were also CD34 positive in paraffin sections. Both cell membrane and cytoplasmic staining was seen. The positivity percentage and fluorescence intensity by flow cytometry correlated with the estimated number of stained cells and the intensity of immunoperoxidase staining in 18 of 19 CD34-positive cases. The remaining bone marrow and lymph node cases studied were CD34 negative; prominent endothelial cell staining, however, was noted. This is the first report of anti-CD34 staining of acute leukemia in paraffin-embedded sections. In contrast to other monoclonal antibodies reactive in bone marrow paraffin sections with leukemia, anti-CD34 immunoperoxidase staining is limited to leukemic blasts and may provide useful diagnostic information when flow cytometric studies are not available.

Acute Disease↗

PubMed1992

A clinicopathologic study of familial chronic lymphocytic leukemia.

The familial occurrence of chronic lymphocytic leukemia was studied using morphologic, immunophenotypic, cytogenetic, and immunoglobulin gene rearrangement analyses. Three of six siblings developed chronic lymphocytic leukemia. One (patient 1) died 9 years after the diagnosis of chronic lymphocytic leukemia at age 67 years. The other two patients, ages 64 and 68 years (patients 2 and 3, respectively), are alive after chronic lymphocytic leukemia was diagnosed 11 and 4 years ago, respectively. Using the Rye classification, patient 2 and patient 3 had Stage I and Stage O disease, respectively. In contrast, patient 1 had Stage IV disease. The bone marrow of patient 2 was 90% cellular, with sheets of mature lymphocytes, and that of patient 3 was 70% cellular, with a nodular pattern of similar cells. Both patients 2 and 3 had normal karyotypes. Immunophenotyping studies revealed that patient 3 had an expanded population of B cells with minimal to no detectable expression of surface immunoglobulins and membrane-bound light chains. In contrast, the B-cell population of patient 2 expressed immunoglobulins M, D, and Kappa light chains. Gene rearrangement studies performed on these two patients revealed different but distinct patterns of heavy chain rearrangement. This may represent an evolution of two different clones of chronic lymphocytic leukemia in this family.

Aged↗

PubMed1992

Ki-1 large cell lymphoma with regressing lesions in a child.

An 8-year-old boy was seen with a cutaneous Ki-1 anaplastic, large cell lymphoma with multiple lesions. Some of the lesions showed spontaneous regression. During more than seven years of disease no systemic involvement was observed, but recurrent, self-healing lesions did appear. Histopathologic examination of five lesions revealed a variety of findings, from an inflammatory infiltrate to a highly anaplastic pattern. The neoplastic cells expressed Ki-1 and leukocyte common antigens. Ultrastructurally, those cells showed ruffled indentations. The differential diagnosis includes microvillous malignant lymphoma. The patient has had a four-year follow-up without relapses.

Abdominal Neoplasms↗

PubMed1992

Detection of Epstein-Barr virus genome in Ki-1 (CD30)-positive, large-cell anaplastic lymphomas using the polymerase chain reaction.

Ki-1 (CD30)-positive, large-cell anaplastic lymphoma (LCAL) is a distinctive subset of non-Hodgkin's lymphoma; morphologically, the neoplastic cells of LCAL may closely resemble Reed-Sternberg cell variants of Hodgkin's disease. The neoplastic cells in Hodgkin's disease are often CD30-positive, as are some of the transformed lymphocytes in infectious mononucleosis. Recent evidence suggests an etiologic role for the Epstein-Barr virus (EBV) in Hodgkin's disease. Because of the phenotypic similarities between Hodgkin's disease and LCAL, we used the polymerase chain reaction (PCR) to analyze eight specimens of LCAL for EBV genome. Diagnoses were established by paraffin section morphology and immunohistochemistry. For comparison, we also analyzed nine non-Hodgkin's lymphomas other than the LCAL type, three Hodgkin's disease specimens, and nine non-neoplastic lymph nodes. PCR was performed using DNA extracted from frozen tissue; DNA was amplified using two sets of oligonucleotide primers corresponding to the BamH1 W-fragment of the EBV genome. Amplified EBV genome was obtained from all specimens except for one mantle zone lymphoma, one diffuse mixed-cell lymphoma, and six non-neoplastic lymph nodes. EBV terminus region probing and in situ hybridization techniques, each less sensitive than PCR, were performed in selected cases in an attempt to corroborate our PCR results. Only 2 of 13 specimens contained EBV detectable by these other techniques, and neither specimen was a LCAL. In view of the high incidence of latent EBV infections in humans, the biologic significance of our PCR results is uncertain. Despite the detection of EBV genome by PCR in a high percentage of lymphomas, we were unable to substantiate an etiologic role for EBV in LCAL. The PCR technique may be too sensitive to provide meaningful data on the possible role of EBV in lymphomagenesis.

Antigens, CD↗

PubMed1992

CD30-positive, anaplastic large-cell lymphomas that express CD15 but lack CD45. A possible diagnostic pitfall.

We report the immunohistochemical and clinical features of two cases of morphologically typical anaplastic large-cell lymphoma. One patient had lymph node and focal visceral involvement, and the other patient had multiple-organ involvement by lymphoma. In both cases, the lymphoma cells were CD30 (Ber-H2) and CD15 (Leu-M1) positive and CD45 (common leukocyte antigen) negative--a phenotype that is commonly seen in Hodgkin's disease. This unusual phenotype in large-cell anaplastic lymphoma led to an initial misinterpretation in one of the cases. Large-cell anaplastic lymphomas are highly variable, both in immunophenotype and clinical presentation. Because of this variability, a broad immunophenotypic panel, in conjunction with morphological features, should be used to establish the correct diagnosis.

Adult↗