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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anaplastic large-cell Ki-1 lymphoma is defined by its characteristic histological appearance, reactivity with antibodies against CD30, and possibly by a chromosome marker t(2;5)(p23;q35). Because of its pleomorphic appearance, sinus distribution, and frequent reactivity with EMA, this lymphoma is often mistaken for other diseases such as metastatic carcinoma and malignant histiocytosis. The clinical features of this lymphoma are unusual and include a young median age and frequent extranodal disease with skin being a common site. Although remission is easily achieved, relapse is common and combination chemotherapy is suggested. The role of Ki-1 antigen in normal lymphocyte function, the cell of origin of anaplastic large-cell Ki-1 lymphoma, and its relationship to Hodgkin's disease are important questions that hopefully will be answered in the near future.
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PMID:Anaplastic large-cell Ki-1 malignant lymphomas. Recognition, biological and clinical implications. 184 27

Cytogenetic abnormalities in non-Hodgkin's Lymphoma (NHL) provide a model system for the analysis of the role of multiple genomic aberrations in human malignancy. In order to define correlations with histology, tumor evolution, and the effects of genotoxic exposure, cytogenetic analysis was performed on 434 specimens of NHL derived from 423 patients consecutively ascertained over a 5-year period (1984-1989). Six recurring translocations (RT) were observed: t(14;18)(q32;q21), t(8;14)(q24;q32), t(11;14)(q13;q32), t(3;22)(q27;11), t(2;5)(p23;q35), and t(1;6)(q21;q25). No translocation was specific to a single histologic subtype. Other structural chromosome abnormalities were analyzed according to break site; groups of related breaks were considered together for statistical analysis. Recurring other structural and numerical aberrations (ROA) encountered in greater than 10% of specimens included rearrangements with breaks at bands 1p32-36, 1q21-23, 6q21-25, and trisomies of chromosomes 7 and 12. ROA with one of these breaks or numerical abnormalities were the sole abnormalities in at least two cases. Correlations were observed among ROA and between ROA and histologic subtypes. Trisomy 7, breaks at 1q21-23, 1p32-36, 6q21-25, and 7q32 were associated with t(14;18); trisomy 18 was associated with trisomy 3; and structural abnormalities of chromosome 17 were associated with breaks at 1p32-36 and 6q21-25. Trisomy 7 and trisomy 12 were more frequent in t(14;18)-bearing intermediate to high grade tumors compared to low grade tumors. Trisomy 12 and breaks at band 1p22 were associated with large cell diffuse lymphomas. Incidence rates of reciprocal translocations, ROA, and measures of karyotypic complexity, including number of breakpoints and marker chromosomes were compared in pretreatment and posttreatment samples. Karyotypic complexity was greater in the posttreatment samples, reflecting an increased frequency of nonrecurring and low incidence aberrations. These results better define the association of genomic aberrations and tumorigenesis, histologic transformation, and tumor progression.
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PMID:Cytogenetic analysis of 434 consecutively ascertained specimens of non-Hodgkin's lymphoma: correlations between recurrent aberrations, histology, and exposure to cytotoxic treatment. 186 33

Neoplastic cells from patients with a variety of B- or non-B/non-T-lymphoid malignancies, including chronic lymphocytic leukemia, various histologic types of non-Hodgkin lymphoma and acute lymphocytic leukemia, showed strong variation with respect to stimulatory capacity in mixed lymphocyte culture (MLC). MLC stimulatory capacity was either normal or strongly decreased in comparison with that of normal lymphocytes despite the expression of HLA-DR antigens and p23,30 ("Ia-like") determinants on the tumor cells of all patients. Strongly decreased stimulatory capacity of HLA-DR-positive tumor cells could not be ascribed to suppressive activity of the tumor cells. Tumor cells from three patients with a T-cell malignancy failed to stimulate in MLC and did not react with anti-p23,30 serum. The decreased stimulatory capacity of many DR-positive neoplastic cells is ascribed either to altered membrane presentation of DR antigens or to the absence of MLC stimulatory determinants specified by genes closely linked to, but different from, those coding for DR.
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PMID:Variable MLC stimulatory capacity of neoplastic B and non-B/non-T lymphocytes expressing HLA-DR antigens. 621 53

Hodgkin's disease (HD) and Ki-1 positive anaplastic large cell lymphoma (Ki-1 ALCL) appear pathologically and immunohistochemically related, and a common histogenesis has been postulated in at least some cases. The breakpoints of the t(2;5) (p23;q35) [corrected] translocation, which is reported in about 40% of Ki-1 ALCL, have recently been cloned. They involve a novel tyrosine kinase gene, ALK, at 2p23 and the nucleophosmin gene, NPM, at 5q35. Reverse transcriptase polymerase chain reaction (RT-PCR) using NPM and ALK primers consistently detects a fusion product in Ki-1 ALCL cases with the translocation. To determine if this tumor-specific genetic alteration also occurs in HD, we performed NPM-ALK RT-PCR on RNA samples extracted from 40 lymph node biopsies of HD (25 nodular sclerosis, 11 mixed cellularity, 2 lymphocyte depleted, 2 lymphocyte predominant). Using control samples, the sensitivity of the NPM-ALK RT-PCR assay was shown to be at least 1:10(4). Amplifiable template was confirmed in all samples by RT-PCR using beta-actin primers. None of the 40 cases showed the expected 177-bp RT-PCR product indicative of the translocation. We conclude that the most common primary genetic alteration in Ki-1 ALCL, the t(2;5), is absent or very infrequent in typical cases of HD. These results further support the concept that HD and Ki-1 ALCL are pathogenetically distinct entities.
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PMID:Reverse transcriptase polymerase chain reaction for the Ki-1 anaplastic large cell lymphoma-associated t(2;5) translocation in Hodgkin's disease. 752 17

Anaplastic large cell lymphoma (ALCL) and Hodgkin's disease (HD) have some pathologic and immunohistochemical similarities, and a histogenetic relationship between them has been suggested by some investigators. By cytogenetic study, the t(2;5)(p23;q35) translocation appears to be unique for ALCL. The breakpoints of the t(2;5)(p23;q35) have recently been cloned and are reported to involve a novel tyrosine kinase gene, anaplastic lymphoma kinase (alk), on chromosome 2 and the nucleophosmin gene (npm) on chromosome 5. Therefore, we studied the frequency of npm-alk translocation in ALCL using a reverse transcriptase-polymerase chain reaction (RT-PCR) assay. We also studied HD and a variety of reactive lymphoid lesions since there is contradictory information in the literature on the occurrence of the npm-alk rearrangement in HD. We detected npm-alk hybrid mRNA in 8 of 22 cases of ALCL (36%), but none of the 21 cases of HD or the 11 cases with reactive lesions contained amplifiable template. All positive ALCL had the T or indeterminate phenotype and occurred in young adults or children. There was very good correlation between a cytogenetically detectable t(2;5) and a positive signal by RT-PCR. Our results indicate a selective but relatively infrequent association between the t(2;5) and ALCL of T or indeterminate phenotype, not shared with HD or reactive hyperplasia.
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PMID:Transcripts of the npm-alk fusion gene in anaplastic large cell lymphoma, Hodgkin's disease, and reactive lymphoid lesions. 757 58

The translocation t(2;5)(p23;q35), discovered in CD30+ anaplastic large cell (ALC) lymphomas, creates a potentially oncogenic fusion gene, part of which is contributed by a novel tyrosine kinase, ALK. Absence of ALK expression from normal hematolymphoid cells provides a basis for the morphologic assessment of t(2;5). The distribution of the t(2;5) in ALC lymphomas and Hodgkin's disease (HD), as assayed by nonmorphologic methods, is controversial. We used in situ hybridization and/or immunohistology to show ALK gene products in 85 ALC lymphomas, 82 HD cases, 40 other lymphoproliferations, as well as in 6 HD- and 4 ALC lymphoma-derived cell lines. ALK gene products were restricted to t(2;5)-positive ALC lymphoma cell lines and tumor cells of 16 primary non-B cell, common-type ALC lymphomas. These were mainly from young patients with initial lymphonodal disease. ALK expression was not detectable in any other specimen, including all cases of HD and HD-like type ALC lymphoma as well as secondary ALC lymphomas. Full congruence was noted for labeling results obtained with both methods. In agreement with cytogenetic analyses, but at variance with recently published studies, ALK gene expression distinguishes a subset of ALC lymphomas from other CD30+ lymphomas, including HD. The results do not support concepts attributing a significant role to the t(2;5) in the development of HD.
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PMID:ALK gene products in anaplastic large cell lymphomas and Hodgkin's disease. 765 1

The t(2;5)(p23;q35) translocation is associated with a high percentage of anaplastic large-cell lymphomas (ALCL) of T- or null-cell phenotype. This translocation was recently cloned and results in the fusion of the nucleophosmin gene (NPM) on chromosome 5q35 to a novel tyrosine kinase-encoding gene designated anaplastic lymphoma kinase (ALK) on chromosome 2p23. Using a sensitive and specific reverse transcription-polymerase chain reaction (RT-PCR) assay to detect the NPM/ALK fusion transcript, we assessed the involvement of NPM/ALK in a series of histologically and immunohistochemically confirmed ALCL, in non-ALCL aggressive non-Hodgkin's lymphomas of T-cell phenotype, and in Hodgkin's disease (HD) to better define the morphologic spectrum of disease associated with this translocation. Twenty-four cases of ALCL were selected on the basis of CD30 positivity and histologic features. Seventeen cases presented as classical nodal and extranodal disease, four cases presented as primary cutaneous disease, and three were associated with human immunodeficiency virus (HIV) infection. As ALCL may show overlapping histology with both HD and other aggressive non-Hodgkin's lymphomas, particularly of T-cell phenotype (T-NHL), we also studied 34 cases of HD and 19 of T-NHL. NPM/ALK chimeric transcripts of identical size were detected in 11 of the 24 (46%) cases of ALCL. NPM/ALK fusion transcripts were found in 11 of 17 (65%) classical ALCL cases but were not detected in the four primary cutaneous cases of ALCL or in the three HIV-related ALCL cases. In addition, NPM/ALK transcripts were not detected in any of the 34 cases of HD or in the 19 cases of T-NHL. These data indicate that NPM/ALK fusion transcripts occur in a high percentage of classical nodal ALCL (65%). In addition, these data strongly suggest that ALCL, as defined in this study, is not pathogenetically related to either HD disease or the majority of other types of aggressive T-NHL. This is a US government work. There are no restrictions on its use.
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PMID:Analysis of the t(2;5)(p23;q35) translocation by reverse transcription-polymerase chain reaction in CD30+ anaplastic large-cell lymphomas, in other non-Hodgkin's lymphomas of T-cell phenotype, and in Hodgkin's disease. 766 79

Chromosomal aberrations are characteristic and specific events; the detection of chromosomal abnormalities often provides information on diagnosis and prognosis of disease. Some patients with large-cell anaplastic lymphoma (Ki 1 lymphoma) have the translocation t(2;5) (p23; q35), involving a possible growth-regulating tyrosine kinase. We found this translocation in 11 patients with Hodgkin's disease of nodular sclerosis and mixed-cellularity types. This finding has implications for the understanding of the relation between large-cell anaplastic lymphoma and Hodgkin's disease, diseases with morphological and immunophenotypical similarities. Study of this translocation may help understanding of the origins of cancer and cancer growth. It also allows a more precise definition of Hodgkin's disease and may be used as an indicator for clonality--which has long been sought.
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PMID:Large-cell anaplastic lymphoma-specific translocation (t[2;5] [p23;q35]) in Hodgkin's disease: indication of a common pathogenesis? 776 45

In malignant non-Hodgkin lymphomas (NHL), cytogenetic analysis may provide prognostic information including prediction of histologic evolution and responsiveness to therapy. In this study, we correlate clinical data and chromosomal aberrations in 70 adult patients with newly diagnosed NHL followed for a median of 20 months. Clonal aberrations were detected in 68/70 patients (97%). Besides t(2;5)(p23;q35), observed exclusively in three patients with anaplastic large cell lymphoma, Ki-1 positive, none of the characteristic aberrations observed was specific for a given histological subtype. Aberrations of chromosome 7 (n = 21) occurred in all histological subtypes together with aberrations of chromosome 3 and of the short arm of chromosome 17. They were clinically associated with a high serum lactate dehydrogenase level (LDH) and a trend to short survival. Anomalies of the long arm of chromosome 13 (n = 10) were found in patients with high grade B-cell lymphomas and bulky disease. In t(14;18)(q32;q21) bearing lymphomas (n = 27), distinct patterns of additional aberrations were observed in low grade and high grade lymphomas: trisomy 3 and trisomy 18 occurred concomitantly in high grade lymphomas (n = 6, p < 0.001) as well as aberrations of 1q, 5q, 6q and +der (18)(q21). In conclusion, cytogenetic analysis provides information about the complexity of genetic changes in NHL. These changes act not only as indicators of disease activity, but influence clinical outcome as demonstrated by their stringent correlation to the International Index and might reveal more general rules of tumor growth and spreading.
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PMID:Karyotype and prognosis in non-Hodgkin lymphoma. 796 39

The morphology of anaplastic large-cell lymphoma (ALCL) is associated with a clinical syndrome of peripheral lymphadenopathy (> 80%) and frequent extranodal disease (> 40%) in children and young adults (median age < 40 yrs.). Skin lesions occur in more than 20% of patients; other extranodal sites are bone, soft tissue, gastro-intestinal tract, lung, and pleura. Marrow involvement is infrequent (< 10%). Features that distinguish ALCL from Hodgkin's disease (HD) are noncontiguous nodal disease (> 50%), infrequent mediastinal mass (< 20%), and frequent inguinal lymphadenopathy (> 40%). Most patients present with stage III/IV disease. Stage is highly predictive of achieving complete remission, disease-free survival, and overall survival. Localized skin lesions have an excellent prognosis and occasional spontaneous regressions are noted. Distinctive histopathologic features of ALCL are partial lymph node involvement with sinus infiltration, sparing of B-cell regions, and tumor cell pleomorphism. Other features are high mitotic rate, necrosis, fibrosis, and plasma cell infiltrates. Morphologic variants of ALCL resemble carcinoma, syncytial variant of nodular sclerosing HD, true histiocytic lymphoma or interdigitating cell sarcoma, and mycosis fungoides. ALCL can be distinguished from these morphologically similar disorders by immunophenotype (CD30+, CD45+, CD15-, EMA+, BNH9+, keratin-, lysozyme-). A recurrent cytogenetic translocation, t(2;5) (p23; q35), has been observed among morphologic variants, including a small-cell-predominant variant and tumor cell line which contains a spectrum of small cerebriform and large anaplastic CD30+ cells. 70% of ALCL cases are of T-cell lineage, 15% B, 5% T/B, and 10% undefined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Primary Ki-1-positive anaplastic large-cell lymphoma: a distinct clinicopathologic entity. 817 12


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