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

The immunophenotypic properties of 25 cutaneous non-Hodgkin lymphomas other than mycosis fungoides or Sezary syndrome were investigated and correlated with clinical and histopathological data. The 11 low grade lymphomas were all of B cell origin, whereas the 14 high grade lymphomas comprised B and T cell tumours, true histiocytic proliferations, and one "nul" cell lymphoid neoplasm. For the high grade lymphomas correct prediction of the immunological phenotype based on morphological criteria was only possible in three cases. In contrast, all of the low grade lymphomas showed the non-epidermotropic infiltration pattern considered to be characteristic of cutaneous B cell tumours. For these conditions, however, immunophenotypic investigations provided a convenient means of improving discrimination between benign (polyclonal) and malignant (monoclonal) lesions, and also showed similarities with nodal lymphomas in terms of expression of lymphoid subset markers and composition of the non-neoplastic white cell infiltrate. No differences were identified between primary and secondary or concurrent cutaneous and extracutaneous lymphomas. Cutaneous non-Hodgkin lymphomas other than mycosis fungoides or Sezary syndrome constitute a heterogeneous group of neoplasms and most of these disorders are likely to represent cutaneous equivalents of nodal malignancies. Immunophenotypic investigations form a useful supplement to their histogenetic characterisation and may provide a common conceptual basis for their classification.
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PMID:Immunocytochemical characterisation of cutaneous lymphomas other than mycosis fungoides. 352 33

Persons infected with human immunodeficiency virus have an increased risk for development of high-grade, non-Hodgkin's lymphomas. Anaplastic large-cell Ki-1 lymphoma is a recently described lymphoid neoplasm characterized by cellular pleomorphism, a sinusoidal growth pattern, and Ki-1 epitope reactivity. This type of lymphoma is often mistaken for metastatic carcinoma, melanoma, or malignant histiocytosis. Although persons with acquired immunodeficiency syndrome frequently have non-Hodgkin's lymphoma at extranodal sites, the oral cavity and mandible, in particular, are unusual locations. We report two cases of anaplastic large-cell Ki-1 lymphoma that occurred in persons with the human immunodeficiency virus and with initial presentation as soft tissue masses of the posterior mandible. Immunocytochemical studies were positive for Ki-1 (CD30) in both cases. In situ hybridization for Epstein-Barr virus-deoxyribonucleic acid was positive with tumor cells in both cases. Flow cytometry on paraffin, formalin-fixed tissue revealed tetraploidy and high proliferative fractions that are characteristic of high-grade lymphomas. Intraoral presentation of rapidly enlarging, soft tissue masses may represent a high-grade non-Hodgkin's lymphoma in persons with the human immunodeficiency virus. Although rare, anaplastic large-cell Ki-1 lymphoma should be considered and requires immunocytochemical study to eliminate the possibility of other malignant conditions associated with the acquired immunodeficiency syndrome.
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PMID:Intraoral presentation of anaplastic large-cell Ki-1 lymphoma in association with HIV infection. 839 61

Recently, a new classification system for lymphoid neoplasms, known as the REAL classification, has been proposed. Our aim is to know the distribution of lymphoid neoplasms according to this schema and compare it with the Updated Kiel classification. We also estimate incidence rates of lymphoid neoplasms in our area. From January 1993 to November 1996, 940 patients were diagnosed of lymphoid neoplasm in our center. Histologic material was prospectively classified according to both the REAL and the Updated Kiel classifications. According to the REAL classification, distribution of all cases of lymphoid neoplasms was as follows: 73.6% B-cell neoplasm, 9.4% T-cell neoplasms, 9.6% Hodgkin's disease and 7.4% unclassifiable. Considering only non-Hodgkin's lymphomas (NHL), 87.2% of cases could be categorized according to the REAL and 77.7% with the Updated Kiel classification. These figures differed due to unrecognized categories in the Kiel schema. Annual incidence rate per 100,000 inhabitants was 20.1 for lymphoid neoplasms, and NHL alone was 9.0. In conclusion, the REAL classification allowed us to categorize more cases of NHL than did the Updated Kiel classification, fundamentally because of the inclusion of some recently described entities.
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PMID:Distribution and incidence rates of lymphoid neoplasms according to the REAL classification in a single institution. A prospective study of 940 cases. 933 21

This report describes two cases of Philadelphia chromosome-negative (Ph(-)) non-Hodgkin's lymphomas (NHLs) recognized in patients with chronic phase Ph-positive (Ph(+)) chronic myelogenous leukemia (CML). Lymph node biopsy of patient 1 was initially diagnosed as diffuse large B cell non-Hodgkin's lymphoma (NHL, T cell rich variant), but at relapse showed immunoblastic features with a marked decrease of admixed lymphocyte components. Patient 2 presented with thickened parietal pleura which revealed a CD30-positive anaplastic large cell lymphoma showing null cell phenotype and genotype with abundant admixed neutrophils and lymphocytes. At the time of lymphoma diagnosis, the patients had CML for 33 and 10 months, respectively. DNA obtained from bone marrow cells at the time of lymphoma diagnosis showed BCR/ABL gene rearrangements by both Southern blot analysis and reverse transcription polymerase chain reaction (RT-PCR), but lacked both immunoglobulin and T cell receptor gene rearrangements. BCR gene rearrangement and BCR/ABL fusion gene were also identified in lymph node and pleural biopsies by Southern blot and RT-PCR analysis, respectively. However, both biopsy specimens also contained reactive lymphocytes and neutrophils, and no fusion signals between BCR and ABL genes were identified in the hyperdiploid lymphoma cells of either case by fluorescence in situ hybridization (FISH). These data suggest the lymphoma cells in both cases were not genetically associated with BCR/ABL. Therefore, these cases were not diagnosed as an extramedullary localized blast crisis in CML, but as Ph(-) NHLs. This represents the first definitive demonstration of peripheral B cell lymphoma occurring by a separate genetic pathway, lacking BCR/ABL, in patients with Ph(+) CML. A review of the literature identified two different subtypes of malignant lymphomas arising in patients with an antecedent or concurrent diagnosis of CML. The most common are T cell lymphomas displaying an immature thymic phenotype, while peripheral B cell lymphomas are more rare. Our study shows, however, that 'Ph(+) NHL' occurring in CML or acute lymphocytic leukemia (ALL) may represent an unrelated neoplasm, even if standard cytogenetic analysis reveals a Ph(+) chromosome, and that FISH is required to confirm whether a localized lymphoid neoplasm is either a true extramedullary localized blast crisis or genetically distinct neoplasm. Leukemia(2000) 14, 169-182.
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PMID:Ph-negative non-Hodgkin's lymphoma occurring in chronic phase of Ph-positive chronic myelogenous leukemia is defined as a genetically different neoplasm from extramedullary localized blast crisis: report of two cases and review of the literature. 1063 93

The revised European-American classification of lymphoid neoplasms has been reported as reproducible among expert pathologists and feasible in a community setting. We evaluated the reproducibility of lymphoid neoplasm diagnoses between a community and an academic center. We subtyped 188 lymphoid neoplasms using revised European-American classification criteria. Clinical findings, histologic or cytologic preparations, paraffin-section immunostains, and flow cytometry data were reviewed as appropriate. Diagnoses were compared only after completion of the study. Lymphoma subtype was concordant for 167 (88.8%) of 188 cases. Discordant cases included 15 B-cell, 2 T-cell, and 4 Hodgkin lymphomas. For B-cell neoplasms, discordance was most often due to classifying diffuse large cell lymphoma as another aggressive subtype of lymphoma (n = 6), marginal zone lymphoma as another subtype (n = 4), or follicle center lymphoma grade II as grade III (n = 3). For Hodgkin disease, discordance was most often due to classifying nodular sclerosis as mixed cellularity type (n = 3). Comparison of community and academic center diagnoses demonstrated high concordance for most revised European-American classification subtypes. Some sources of discordance have been addressed in the new World Health Organization classification of neoplastic diseases of the hematopoietic and lymphoid tissues.
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PMID:Comparison of lymphoid neoplasm classification. A blinded study between a community and an academic setting. 1134 27

Castleman's disease is a benign lymphoid neoplasm first reported as hyperplasia of mediastinal lymph nodes. Some authors referred to the lesions as isolated tumors, described as a variant of Hodgkin's disease with a possibility of a malignant potential and others proposed that the lymphoid masses were of a hamartomatous nature. Three histologic variants and two clinical types of the disease have been described. The disease may occur in almost any area in which lymph nodes are normally found. The most common locations are thorax (63%), abdomen (11%) and axilla (4%). We report two separate histologic types of Castleman's disease which were rare in the literature, mimicking sigmoid colon tumor and Hodgkin lymphoma. The diagnostic and therapeutic aspects of this rare entity is discussed.
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PMID:Castleman's disease masquerading as sigmoid colon tumor and Hodgkin lymphoma. 1188 46

Hodgkin's disease (HD) is a lymphoid neoplasm characterized by a low frequency of malignant giant tumor cells, known as Hodgkin's and Reed-Sternberg (HRS) cells. Sequence analysis of the immunoglobulin heavy chain hypervariable region (IgH V) genes of HRS cells revealed multiple nucleotide substitutions, indicating somatic mutations, and suggested that HRS cells originate from germinal center B cells or their progeny. We previously reported that CD99-antisense transfected B cell lines led to the generation of cells with a HRS phenotype. Because it is considered that HRS cells in HD carry somatic mutations of the IgH genes, we assume that somatic mutation may take place in the IgH genes of HRS-like cells which do not express CD99. Here we report that CD99 downregulated BJAB cell line has several mutations in IgH V genes. The frequency of mutation was 5.2 x 10(-4) mut.bp(-1) out of total sequenced cell clones. On the contrary, control vector transfected BJAB cell line or CD99 downregulated IM9 cell line did not show any mutations on single strand conformational polymorphism (SSCP) and sequence analysis. We expect that the analysis of the mutation pattern of the CD99-deficient BJAB cell line might be the basis for the understanding of the molecular and cellular mechanism that regulate somatic mutation and B cell selection.
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PMID:Mutations of the immunoglobulin heavy chain variable region gene in CD99-deficient BJAB cell line. 1201 45

Hodgkin's lymphoma (HL) is a lymphoid neoplasm with a low frequency of malignant tumor cells, known as Hodgkin and Reed-Sternberg (H-RS) cells, in a background of mixed cellular infiltrates. Despite extensive studies on H-RS cells, the molecular mechanisms of their growth and regulation have remained uncertain for a long period. Recently, constitutively activated nuclear factor-kappaB (NF-kappaB) was reported to be a unique and common characteristic of H-RS cells that prevents the cells from undergoing apoptosis. NF-kappaB triggers proliferation and provides a molecular basis for these cells' aberrant growth and cytokine gene expression. In HL pathogenesis associated with Epstein-Barr virus infection, the activation of NF-kappaB is induced by viral latent membrane protein 1 (LMP1). Coupled with recent insights into the molecular mechanisms of activation of NF-kappaB signaling in H-RS cells, this review discusses a linkage between LMP1 and HL via CD99, which has recently been reported to be down-regulated by LMP1 through the NF-kappaB signaling pathway. This down-regulation leads to the generation of cells with H-RS phenotypes related to the clinical and histologic characteristics of HL.
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PMID:The molecular basis for the generation of Hodgkin and Reed-Sternberg cells in Hodgkin's lymphoma. 1277 19

The centrofacial angiocentric lymphoma is a rare lymphoid neoplasm, with an often-difficult diagnosis due to the non-specific clinical picture. On many occasions it is necessary to perform various biopsies to reach the correct diagnosis. This lymphoma is an aggressive Non-Hodgkin's (NHL) type, which is normally found in the upper respiratory tract (predominantly in the nasal cavity), and has an ominous prognosis, as the average survival rate is between 12 and 18 months (1). It is predominantly found in subjects of oriental and South American extraction, who are between the ages of 50 and 60 years and with a slight tendency towards males (2:1). This is the case study of a female Ecuadorian patient who was referred to our department with a hemifacial edema, chocolate- like rhinorrhea and nasal respiratory obstruction, which had been treated with antibiotics and anti-inflammatories for a month without success. After performing a number of diagnostic tests, it was found histologically that the patient had an extranodal T-cell lymphoma of the nasal type (also known as T-cell angiocentric lymphoma).
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PMID:Centrofacial angiocentric lymphoma. 1562 13

Because the causes of most lymphoid neoplasms remain unknown, comparison of incidence patterns by disease subtype may provide critical clues for future etiologic investigations. We therefore conducted a comprehensive assessment of 114,548 lymphoid neoplasms diagnosed during 1992-2001 in 12 Surveillance, Epidemiology, and End Results (SEER) registries according to the internationally recognized World Health Organization (WHO) lymphoma classification introduced in 2001. Cases coded in International Classification of Diseases for Oncology, Second Edition (ICD-O-2), were converted to ICD-O-3 for WHO subtype assignment. Age-specific and age-adjusted rates were compared by sex and race (white, black, Asian). Age-adjusted trends in incidence were estimated by sex and race using weighted least squares log-linear regression. Diverse incidence patterns and trends were observed by lymphoid neoplasm subtype and population. In the elderly (75 years or older), rates of diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma increased 1.4% and 1.8% per year, respectively, whereas rates of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) declined 2.1% per year. Although whites bear the highest incidence burden for most lymphoid neoplasm subtypes, most notably for hairy cell leukemia and follicular lymphoma, black predominance was observed for plasma cell and T-cell neoplasms. Asians have considerably lower rates than whites and blacks for CLL/SLL and Hodgkin lymphoma. We conclude that the striking differences in incidence patterns by histologic subtype strongly suggest that there is etiologic heterogeneity among lymphoid neoplasms and support the pursuit of epidemiologic analysis by subtype.
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PMID:Lymphoma incidence patterns by WHO subtype in the United States, 1992-2001. 1615 Sep 40


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