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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 karyotypes of cells from 10 Burkitt lymphoma (BL) biopsies, eight cell lines established from BL and nine cell lines from non-BL sources were studied by chromosome banding techniques. With the exception of the BL-derived cell lines BJAB, GC-BJAB, Maku and U-8691 all biopsies and lines of Burkitt origin contained an extra band at the distal region of the long arm of one chromosome 14. An extra band on chromosome 14 was also found in cells of one non-BL biopsy, in cells from a lymphosarcoma-derived cell line and in a long-established cell line derived from the pleural exudate of a patient with Hodgkin's disease. A distal region at the long arm of one chromosome 8 was missing in all metaphase figures of good technical quality in the same material. The size, morphology and stain-ability of the missing region corresponded fairly well to the extra region at chromosome 14. We therefore suggest that the chromosome 14 marker represents a translocation between chromosomes 8 and 14,t (8q-; 14q+). The translocation was present neither in lymphocytes of the peripheral blood of five Burkitt patients nor in five lymphoblastoid cell lines of non-BL origin. Trisomy 7 was found in two of the 10 BL biopsies, in two BL-derived cell lines, in one non-BL biopsy, in two lymphosarcoma-derived cell lines and in one cell line derived from a patient with Hodgkin's disease.
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PMID:Characteristic chromosomal abnormalities in biopsies and lymphoid-cell lines from patients with Burkitt and non-Burkitt lymphomas. 94 70

Two t(14;18)-negative follicular B-non-Hodgkin's lymphomas with the same chromosomal abnormality, dup(12)(q13----qter), are presented. The absence of a BCL2 gene rearrangement was confirmed by molecular studies in both cases. Instead, duplication of a 12q segment was found. Further evidence for the presence of the dup(12)(q13----qter) was found using fluorescence in situ hybridization. dup(12q) may be equivalent to the trisomy 12 originally described in B-chronic lymphocytic leukemia. This chromosome anomaly has also been reported in B-non-Hodgkin's lymphomas, usually in association with other chromosome anomalies and a more aggressive tumor phenotype. Occurrence of dup(12q) in two histologically similar cases of follicular small cleaved-cell lymphoma without a typical t(14;18), suggests that this karyotypic change may play a critical role in some cases of follicle center-cell lymphomas.
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PMID:dup(12)(q13----qter) in two t(14;18)-negative follicular B-non-Hodgkin's lymphomas. 137 36

Chromosome studies carried out using lymph nodes of 47 patients with Hodgkin's disease gave analyzable metaphases in 22 patients of which 16 (72.7%) showed chromosome abnormalities. The modal chromosome number ranged from near-diploidy to near-tetraploidy. Chromosomes 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 18, 21 and 22 were involved in trisomy and tetrasomy whereas chromosome 17 was involved in monosomy. Structural abnormalities like deletions of chromosomes 1(p13), 6(q24) and addition of chromatin material to chromosomes 11(q13) and 14(q32) were also detected. The involvement of chromosomes 2, 5, 12, 18 and 21 in numerical abnormalities, and chromosome 14(14q+) in structural aberrations was found to be more frequent in Hodgkin's disease. No clinical correlation could be defined between the various chromosome abnormalities and prognosis of these patients.
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PMID:Chromosomes in Hodgkin's disease--analysis of involved lymph nodes. 143 37

Recent advances in immunology, cytogenetics and molecular genetics has allowed for a better understanding of the origin and evolution of non Hodgkin lymphoma (NHL). Over the last decade a number of recurrent chromosome aberrations has been disclosed and some correlations with well defined histologic subsets of B-cell NHL has been established. Five important cytogenetic-histologic associations has been documented, well defined by combined cytologic, immunologic and genetic investigations: t(14;18) (q32;q21) and NHL of follicle centre cell origin, frequently with follicular histologic pattern; t(8;14) (q24;q32) and Burkitt's lymphoma, Burkitt-like lymphoma or the equivalent small non-cleaved cell category of the "working formulation system"; t(3;22) (q27;q11) and diffuse large cell lymphoma; t(11;14) (q13;q32) and mantle zone lymphoma; trisomy 12 and chronic lymphocytic leukemia and well-differentiated small lymphocytic lymphoma. Molecular genetic studies elucidated some mechanisms operating during the normal lymphocyte differentiation which may be held responsible for the illegitimate recombination between the immunoglobulin genes and some oncogenes normally located on other chromosome regions. It has thus been demonstrated that the early events leading to neoplastic transformation in B-cell neoplasias occur in immature lymphocyte precursors in the bone marrow during the assembly of the immunoglobulin heavy chain gene. According to some recent studies chromosome changes may have prognostic value in B-cell NHL and chronic lymphocytic leukemia and may be employed in clinical practice in the construction of proportional hazard models in several histologic subsets of NHL.
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PMID:[Current view on non-Hodgkin lymphomas. Origin and evolution in relation to cytogenetic-histologic correlations]. 158 38

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

Chromosome studies were carried out by G-banding technique on the bone marrow cells of 24 newly diagnosed, untreated Hodgkin's disease patients and 25 treated patients. Seven of these treated patients had also been studied at diagnosis. In the untreated group of patients, cytogenetic studies were carried out on stimulated peripheral blood lymphocytes in 11 patients and on skin fibroblasts in five. Of the 24 untreated patients, 14 showed normal diploid pattern, while 10 were seen with 8-30 per cent chromosomally aberrant cells in the bone marrow. The frequent anomalies were trisomy C/8 and trisomy 22 seen in 5 and 4 patients respectively. The cytogenetic picture of peripheral blood lymphocytes revealed normal diploid pattern in 7 patients; while 4 other patients showed abnormal clones with trisomy 21. The cultured skin fibroblasts represented normal diploid karyotypes. An altered karyotypic pattern was seen in the bone marrow of treated patients. In patients with abnormal karyotypes, the common anomalies were monosomy C, monosomy D/15 and trisomy 21. In patients which showed no involvement of the bone marrow by haematological parameters, chromosomally abnormal karyotypes were seen in the marrow. Thus, marrow involvement can be detected earlier cytogenetically.
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PMID:Cytogenetic studies in Hodgkin's disease. 227 68

ATL-cell lines producing C-type retroviruses were established by culture of the peripheral blood mononuclear cells from a patient with chronic ATL. These cell lines had the surface feature of inducer/helper T-cells with electron microscopic finding of C-type retrovirus on the cell surface. Chromosome analysis revealed the presence of a marker chromosome, but did not identify 7 trisomy nor 14q+. Of the cell lines, the line established by culture with TCGF was named "Yana-I" and the line established by culture of Yana-I without adding TCGF was named "Yana-II". Serum ATLA-antibody was positive in 1.5% of the healty individuals examined (4/257). Among malignant lymphoma patients, ATLA antibody was positive in none of the patients with B-cell type lymphoma (0/10) and Hodgkin's disease (0/2). In contrast, ATLA antibody was found in half of the patients with T-cell type lymphoma (3/6) and all with ATL (4/4). This suggested that C-type retrovirus in closely associated with ATLL.
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PMID:Establishment and characterization of T-cell lines (Yana-I and Yana-II) derived from a patient with chronic adult T-cell leukemia (ATL). 282 81

In 1968 a special variant of Hodgkin's disease, epithelioid cellular lymphogranulomatosis--later on termed lymphoepithelioid cell lymphoma/Lennert's lymphoma--was defined. There are increasing indicators that Lennert's lymphoma is of T-cell origin. Seven cases of Lennert's lymphoma are studied with cytogenetic as well as immunohistochemical techniques. Six of them have cytogenetic abnormal clones always including aberrations of chromosome No. 3 (+3, break in q22, dup q22----q24). In all cases band 3q22 is either broken or duplicated. Immunohistochemically it is clearly demonstrated that the proliferating cells are of T-cell nature (Ki67+, Leu4+, Leu1+). Under consideration in the literature it can be stated in conclusion that (1) lymphoepithelioid cell lymphoma (Lennert's lymphoma) with aberrations has to be designated as malignant lymphoma, (2) immunohistochemical double labeling proved the T-cell nature of this lymphoma, (3) there are remarkable similarities between the chromosomal patterns of lymphoepithelioid cell lymphoma, lymphogranulomatosis X/angioimmunoblastic lymphadenopathy and probably Hodgkin's disease: many normal mitoses and abnormalities of chromosome No. 3, especially trisomy. It is discussed that abnormalities of chromosome No. 3 involving band q22 are an indicator of a common genetic background of these lymphomas.
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PMID:Cytogenetic and immunohistochemical analysis of lymphoepithelioid cell lymphoma (Lennert's lymphoma): further substantiation of its T-cell nature. 308 66

The results of a longterm study on 55 children are presented whose parents were treated by radiotherapy. Five or ten years after a first examination, these children were submitted to a check-up investigation of their physical and intellectual development. The group of twenty irradiated fathers received an average dose to the gonads of 0.55 Gy (0.01 to 6.4 Gy), the group of twenty irradiated mothers 0.72 Gy (0.01 to 8.0 Gy). In all parents the most frequent finding was Hodgkin's disease, which was diagnosed as a neoplasm in 23 cases. Chemotherapy was applied in two out of 40 patients. The proof of paternity was made with a 86% accuracy for ten out of twenty fathers by determination of HLA types. A conception was demonstrated beyond all doubt after a dose to the testicles of 1.2 Gy in the irradiated fathers and after a dose to the ovaries of 3.0 Gy in the irradiated mothers. The offspring of the F1 generation showed no modification in the sex ratio. In the primary examination, a rate of 5.5% of severe malformations was found (trisomy E, bradyacousia of the inner ear, cleft hands and feet). 24% of the children had malformations which needed a treatment (hernias, torticollis, hip dysplasia). 18 out of 55 children (33%) presented abnormalities in the widest sense of the word. Three children (5.5%) were premature infants, and there is a general tendency towards shortened pregnancy (-3.6 days). Hernias (7/55) are a frequent finding. In children of both sexes, carporadiography shows a delayed development which is not compensated in the check-up examinations at five or ten years, but does not cause an underdevelopment in body height as compared to great normal collectives. The results suggest a slightly increased malformation rate among children whose parents were treated by radiotherapy. Above all the connective and supporting tissue seems involved. Some proposals are made how to give a radiogenetic advice to tumor patients who want to have children.
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PMID:[Children of parents irradiated prior to conception--a longitudinal study (results, 1986)]. 320 81

Clonal chromosome abnormalities were found in 89 (97%) of 92 patients with non-Hodgkin's malignant lymphoma including immunologically determined 34 B- and 25 T-lymphomas; only 3 of 19 T-lymphoma patients examined had serum adult T-cell leukemia/lymphoma-associated antigen antibody. Association of 8q24 translocations with small non-cleaved cell (P less than 0.01) and that of t(14;18) (q32;q21) with follicular histology (P = 0.03) were significant. Several other abnormalities were also found to be correlated with histological or immunological phenotypes: trisomy 5 with diffuse, mixed cell lymphoma (P = 0.03); a break at 3q21 with diffuse, large cell lymphoma (P = 0.04); gain of chromosome 18 or X and rearrangements of 13q with immunoblastic lymphoma (P = 0.02, 0.03, and 0.03, respectively); and rearrangements of 7q with diffuse large cell histology (P = 0.02) and T-cell phenotype (P = 0.02). Multiple clones were more frequently seen in T-cell lymphoma than in B-cell lymphoma (P = 0.01). Structural changes of the long arm of chromosome 4 or 15 and a break in 6p21 were also associated with T-lymphoma (P = 0.03, respectively). Since the frequency of T-lymphoma is significantly higher and that of t(14;18) is significantly lower in the adult T-cell leukemia/lymphoma nonendemic area of Saitama in Japan than in Minnesota in the United States (P less than 0.01), factors affecting the lymphoma-genesis may be different or operating in different intensities in different areas.
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PMID:Chromosome abnormalities in malignant lymphoma in patients from Saitama. 331 91


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