Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this series of 426 consecutively ascertained, karyotypically abnormal non-Hodgkin's lymphomas (NHLs) derived from 407 patients, a t(9;14)(p13;q32) was encountered in 7 cases; an additional case demonstrated t(9;14)(p1?3;q32). At the time of detection of t(9;14), four cases were small lymphocytic lymphomas with plasmacytoid features; in three of these the t(9;14) was the sole karyotypic abnormality. In two cases of large-cell NHL demonstrating t(9;14), retrospective review of prior lymph node biopsies showed the presence of a small lymphocytic lymphoma of the plasmacytoid subtype. The remaining two cases comprised a large-cell lymphoma of the brain and a follicular NHL. Thus, six of eight cases (75%) had an initial identical low-grade histology. Immunohistochemical analysis of six cases showed no reactivity with CD1, CD2, CD4, CD5, CD8, and CD10 and high reactivity with CD19 and CD20. All four lymphocytic lymphomas and one of the two large-cell NHLs showed cytoplasmic Ig, consistent with plasmacytoid differentiation. Of the eight cases in this series, six presented with or developed stage IV disease; all were characterized by a 6-month to 5-year clinical phase of indolent disease before treatment was instituted. All five patients with low-grade NHL at the time of cytogenetic analysis were alive with recurrent disease at 3-year median follow-up. The remaining three patients with large-cell diffuse histologies relapsed after intensive therapy and expired at a median of 3 years from diagnosis; two of these showed previous or metachronous small lymphocytic tumors. These results suggest a novel biologically distinct subset of NHL; a neoplasm of mature B lymphocytes with plasmacytoid differentiation, characterized by t(9;14); and an indolent presentation followed by gradual clinical progression of disease.
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PMID:t(9;14)(p13;q32) denotes a subset of low-grade non-Hodgkin's lymphoma with plasmacytoid differentiation. 138 92

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

Fresh tumor cells from pleural effusion of a patient with Hodgkin's disease were analyzed cytogenetically, immunologically and enzymocytochemically. They were characterized by the presence of alpha-naphthyl butyrate esterase activity, Fc gamma-receptor, HLA-DR antigen and No. 9 antigen which has been shown to be present in Hodgkin's cells and granulocytes, and the absence of definite T-, B- and myeloid cell markers. The karyotype analysis of these tumor cells revealed chromosome instability, but the clonality was confirmed by the many common abnormalities such as -4, -6, -10, -12, -13, -14, +21, del(X) (q22,q26), del(7) (q32q36), and +der(19)t(19;?). In addition, there were more duplicated tetraploid clones than near-diploid clones. The karyotype of the near-diploid clone was interpreted as: 48, X, del(X) (q22q26), -4, -6, -10, -12, -13, -14, +20, +21, +der(4)t(4;?) (p16;?), del(7) (q32q36), +der(19)t(19;?) (p13;?), +mar1, +mar2, +mar3. The karyotype abnormalities characteristic of lymphomas or leukemias were not found. These results indicate that the tumor cells are not of lymphoid or myeloid lineage. Further studies are needed to determine the cellular origin of the tumor cells of Hodgkin's disease.
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PMID:Karyotype aberrations and surface marker analyses of the tumor cells of Hodgkin's disease: a case report and review of literature. 243 93

The identification of recurring chromosomal translocations has provided clues to the gene regions important in lymphoma development. Among 157 patients with non-Hodgkin lymphoma studied by cytogenetic analysis, four new recurring translocations have been identified--t(8;9) (q24;p13), t(11;18)(q21;q21), t(14,15)(q32;q15), and an unbalanced translocation giving rise to der(22)t(17;22) (q11;p11). Each translocation appeared twice. The t(11;18) was the only karyotypic abnormality in the two patients with it, and the t(14;15) was the sole karyotypic abnormality in one patient. All translocations were found in B-cell malignancies and were associated with both nodal and extranodal disease. Among the regions affected, only the immunoglobulin heavy-chain gene MYC, and BCL2, have thus far been associated with lymphoma. The breakpoint sites identified by these translocations warrant further investigation at the molecular level.
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PMID:Four new recurring translocations in non-Hodgkin lymphoma. 250 53

Simultaneous involvement of bands 8p11 and 16p13 in a primary, even though rare, chromosomal translocation recently described in acute nonlymphocytic leukemia may be of crucial interest in some subtypes of this acute leukemia, particularly in the monocytic form. In the present report we describe this translocation in acute nonlymphoblastic leukemia FAB M4, possibly secondary to Hodgkin's disease, though it is also possible that the leukemia may have developed de novo. The aberration t(8;16)(p11;p13) was present in 100% of direct and cultured bone marrow cell preparations. A very high frequency of cells with nonclonal structural chromosome aberrations was also observed in peripheral blood cultures (more than 53%). Random translocations and deletions constituted most of the observed alterations. These findings are discussed with regard to the relationships between secondary leukemias and intensive polychemotherapeutic treatments of primary neoplasias.
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PMID:Translocation t(8;16)(p11;p13) in acute nonlymphoblastic leukemia (M4) possibly secondary to Hodgkin's disease. 291 27

We have carried out chromosome analysis in a series of 16 non-Hodgkin Lymphoma (NHL) cases in leukemic phase. The diagnoses in these patients based on histology and immunologic markers were as follows: follicular lymphoma (FL), 3 cases; mantle cell lymphoma (Mc), 4 cases; lymphoplasmacytic lymphoma (LPL), 8 cases, and large cell lymphoma, 1 case. We have shown that the t(14;18), t(11;14), and trisomy 12 retained their subtype association with FL, Mc, and LPL, respectively, as in their nonleukemic counterparts with one case of FL showing t(1;19)(q23;p13). Among the four LPL cases without trisomy 12, one case each showed t(12;14)(q13;q32), trisomy 14, t(1;3)(p34;q21), and del(3)(q21). The t(1;19) and t(12;14) may represent rare events in FL and LPL, respectively, and may be uniquely associated with the leukemic phase. The breakpoint 14q32 was the most common single breakpoint involved, sometimes involving both chromosome 14 homologues depicting its association with primary and secondary genetic events in the disease progression. In addition to the main abnormalities, we have shown additional complex abnormalities in 14 of 16 cases. Among these, chromosome 3 was the most commonly involved, affecting the short or long arm or the whole chromosome; 5 of the 16 cases involved breakpoint 3q21. The high incidence of additional abnormalities in these NHL in leukemic phase suggest an association with the development of leukemia and progression of the disease.
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PMID:Cytogenetic abnormalities in the leukemic phase of non-Hodgkin lymphoma. 765 98

We have analyzed the chromosomes of 49 non-Hodgkin lymphoma patients from an area of Japan that is nonendemic for adult T-cell leukemia/lymphoma. Clonal chromosome abnormalities were found in the majority (88%) of the specimens examined. The most characteristic structural abnormalities were: t(14;18)(q32;q21), t(3;22)(q27;q11), t(11;14)(q13;32), idic(18)(p11.2), and the combination del(1)(p13) and del(1)(q11). The t(14;18) were found in four of five follicular lymphomas and in one diffuse lymphoma. The breaks at 3q27 included seven translocations and an inv(3)(q12q27). A t(3;22) was found in three patients, all B-cell type, two of whom had kappa phenotype and one of whom was negative for the surface Ig. Fifteen of 49 cases had deletion of 6q. The common deleted region was found only in the segment distal to 6q21. These findings indicate the high percentage of t(14;18) in follicular lymphomas, which is unusual in Japan, and the high incidence of 3q27 translocations.
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PMID:Correlations of chromosome abnormalities with histologic and immunologic characteristics in 49 patients from Akita, Japan with non-Hodgkin lymphoma. 777 61

MAD and MXI1, two recently described members of the basic helix-loop-helix (bHLH) gene family, encode proteins that dimerize with and modulate the DNA binding of max. In turn, mad-max or mxi1-max heterodimers or max homodimers can compete for DNA binding sites with dimers formed between max and myc oncoproteins and antagonize the transcriptional activities of this latter class of proteins. Using a combination of somatic cell mapping and fluorescence in situ hybridization techniques, we have determined the chromosomal locations of the MAD and MXI1 genes. The MAD gene maps to chromosome 2p12-p13, a region involved in translocations and deletions in acute and chronic lymphocytic leukemias as well as non-lymphocytic leukemias and Hodgkin disease. The MXI1 gene localizes to chromosome 10q24-q25, a region involved in translocations and deletions in acute and chronic lymphocytic leukemias and prostatic carcinomas. The availability of genomic clones of MAD and MXI1 will permit an assessment of their involvement in these diseases at the molecular level.
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PMID:Assignment of the human MAD and MXI1 genes to chromosomes 2p12-p13 and 10q24-q25. 782 91

A new human T-cell non-Hodgkin lymphoma cell line of the T-cell receptor (TCR) gamma/delta lineage has been derived from the peripheral blood of a patient with a subcutaneous T-cell lymphoma in leukemic phase. The cell line (Karpas 384) initially had the same characteristics as malignant cells from the patient. Both the original tumor and the cell line failed to express any T-cell differentiation antigens other than very weak cell-surface expression of CD3 and cytoplasmic CD7; with continued growth in vitro, surface CD3 became undetectable in the presence of maintained strong cytoplasmic expression. The cell line has a complex karyotype with six abnormal chromosomes exhibiting not only t(7;14) (p13;q11.2) but also inv7(p13;q22.1), t(1;2)(q11;q35), t(2;1;14) (q35;q11-q32.1;q22.1), interstitial deletion 12(q24.1q24.3), and an unidentified marker chromosome. DNA blot analysis showed that TCR C beta and TCR J alpha-C alpha DNA sequences were in germline configuration in all restriction endonuclease digests. TCR gamma sequences showed biallelic V gamma 9-J gamma P-C gamma 1 rearrangements, the TCR gamma rearrangement detected in the majority of normal TCR gamma/delta bearing cells. Use of a range of TCR delta probes showed biallelic deletion of both J delta 1 and J delta 2, but three rearranged fragments when probed with a 3' C delta genomic probe. Similar breakpoints at 7p13 have been reported in a wide range of hematologic malignancies. Molecular cloning of the t(7;14)(p13;q11.2) translocation breakpoint in this cell line may define new DNA sequences of oncogenic potential at the 7p13 locus.
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PMID:A new human T-cell lymphoma cell line (Karpas 384) of the T-cell receptor gamma/delta lineage with translocation t(7:14) (p13;q11.2). 839 14

We characterized a t(3;14)(q27;q32) translocation in nine patients with B-cell, non-Hodgkin lymphoma (B-NHL) by fluorescence in situ hybridization (FISH). Fluorescence in situ hybridization with immunoglobulin heavy chain (IgH) and BCL6 gene probes detected t(3;14) rapidly and accurately, including complex t(3;14) in three patients; one with t(3;12;8;14)(q27;p13;q24.1;q32) and two with t(3;?;14)(q27;?;q32). Among these nine patients, seven escaped from cytogenetic detection by our G-banding analysis. Double-color FISH with IgH (Y6) and BCL6 (cosB5-1) showed fusion of BCL6 and IgH genes on der(3)t(3;14) in all nine patients, suggesting that der(3) may play a critical role in the development of lymphoma carrying complex as well as standard t(3;14) translocations. BCL6/IgH fusion gene was also demonstrated in interphase nuclei at a frequency of 23% to 91.5% over the cut-off value in control studies (9.0 +/- 2.76%). The breakpoints assessed by FISH with two cosmid clones containing BCL6 probes, cosB5-1 and cosB5-2, were within the cluster region in seven patients including one with complex type, but were not evaluated in two patients with t(3;?;14), because of the loss of partner chromosome. Using double-color FISH with these two BCL6-specific probes, none of an additional 32 patients in whom mitotic spreads were available showed 3q27 translocations. Fluorescence in situ hybridization with IgH and BCL6 gene probes is a rapid and sensitive method to detect t(3;14) in routine cytogenetic studies.
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PMID:Interphase detection of BCL6/IgH fusion gene in non-Hodgkin lymphoma by fluorescence in situ hybridization. 939 63


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