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)

We report a case of erythroleukemia (EL;FAB M6), preceded by a myelodysplastic phase, in a 50-year-old male 8 years after treatment for Hodgkin's lymphoma. Cytogenetic analysis of bone marrow at time of diagnosis of EL revealed three cell lines: 1) 28 of 53 cells (53%) were hypodiploid, 43,XY,-5,-7,-12; 2) 23 of 53 cells (43%) were near-triploid, stemline 67-69,XY,+2,del(5)(q11.2),+del(5)(q11.2),+6,-7,+8,-9,-11,-12,+15,-16,der (17)t (17;?) (p11.2;?),-18,-20,-20,+22,+r, + mar (relative to a complete triploid cell); 3) 2 of 53 cells (4%) were normal 46,XY. The relative monosomies of 5, 7, and 12 in both abnormal lines suggest that the near-triploid line evolved from the hypodiploid line. A single hypodiploid cell with both del(5) and der(17) chromosomes that appeared identical to those in the near-triploid line suggests that polyploidization occurred after these structural rearrangements. While EL is not characterized by any well-defined structural abnormality, reported cases are frequently hypodiploid, with occasional cases of polyploidization, as in our patient, EL in adults without previous neoplasia or recognized mutagenic exposure has been shown to have loss or deletion of chromosomes 5 and 7, also characteristic of myelodysplastic syndromes and secondary leukemia. Our patient had a relative lack of chromosomes 5 and 7 in both abnormal clones, as well as a del(5)(q11) in the near-triploid line. This case of EL clearly demonstrates the evolution of a complex near-triploid line from a hypodiploid line, with chromosome abnormalities typical of both EL and secondary leukemia.
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PMID:Evolution of a near-triploid karyotype in a secondary erythroleukemia. 206 5

Cytogenetic studies of 12 patients aged less than 14 years with acute nonlymphoblastic leukemia (ANLL) (M4-M5) showed structural abnormalities on chromosome 11 at band q23-q24 in five cases (41.8%). Four of these 12 patients had ANLL (M4-M5) after treatment with cytostatics for non-Hodgkin lymphoma in one case and for an acute lymphoblastic leukemia (ALL) in the other three. Three of these four cases had 11q23 abnormalities [one [one 46,XY,t(11;17)(q23;25); another 47,XY,+8,-15,del(11)(q23),+der(15)t(15;?)(p11;?); the third 47,XX,+8,t(3;17) (p11;q25),t(4;11)(q21;q23)] and one had a normal karyotype on being diagnosed ANLL (M4-M5). The notable increase of ANLL (M4-M5) in our patients who had received cytostatics as treatment for a previous neoplasia makes evaluation of our results timely in comparison with those of other groups who use these therapeutic protocols.
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PMID:11q23 abnormalities in children with acute nonlymphocytic leukemia (M4-M5). Association with previous chemotherapy. 230 76

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

Cytogenetic studies were performed in four cases of alpha chain disease. Chromosomal abnormalities were found in the lymphoid cells of the mesenteric lymph nodes of three patients, two of whom had not reached the stage of overt malignant lymphoma. In two instances, a rearrangement of 14q32, resulting from a t(9;14)(p11;q32) and a t(2;14)(p12;q32) was observed. One case showed complex rearrangements including t(5;9). No abnormalities were found in the intestinal tumor of the fourth case with immunoblastic lymphoma. It is concluded that alpha chain disease is a clonal proliferation with frequent alteration of chromosome #14 at band q32 resulting from translocations that differ from those observed in the vast majority of other non-Hodgkin lymphomas.
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PMID:Cytogenetic studies in four cases of alpha chain disease. 308 16

Previous work has established the presence of an unbalanced chromosome abnormality [+der(1),t(1;7)(p11;p11)] in some therapy-associated myelodysplastic disorders. Recently the EGF receptor has been found to reside at 7p11. Using a probe specific for erb B oncogene, which encodes a truncated form of the EGF receptor, we examined RNA and DNA derived from bone marrow and peripheral blood mononuclear cells from three patients with myelodysplastic syndromes (MDS) and one with acute lymphocytic leukemia (ALL), all bearing an abnormal clone in their bone marrow with a similar unbalanced 1;7 translocation. DNA-excess slot blot hybridization to 5'-32p-labeled cellular RNA revealed from ten- to thirtyfold enhancement in accumulation of mRNA specific for erb B in both peripheral blood and bone marrow cells of the three MDS patients when compared to normal controls. In addition, enhancement of H-ras mRNA accumulation was detected in some, though expression of other genes such as actin, N-ras, myc, src, B-lym, and 20 other genes was not found to be enhanced. Increased erb B expression was not apparent in mononuclear cells from patients with other hematologic disorders such as chronic lymphocytic leukemia, Hodgkin's disease, or lymphoma. Southern blot analysis of restriction-enzyme-cleaved DNA from three MDS patients with an unbalanced 1;7 translocation revealed that erb B gene was amplified at least twentyfold in peripheral blood white blood cells, while levels of actin hybridization were comparable to those of the controls. No such amplification was evident in the ALL patient. Our data suggest that +der(1),t(1;7)(p11;p11) chromosomal anomalies can be specifically associated with amplification of erb B DNA and RNA sequences.
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PMID:Amplification of RNA and DNA specific for erb B in unbalanced 1;7 chromosomal translocation associated with myelodysplastic syndrome. 346 13

Four patients with chromosome #12 rearrangement at the p11 level are described. One had acute promyelocytic leukemia, one had myelofibrosis evoluting to acute undifferentiated leukemia, one had acute nonlymphoid leukemia (ANLL) secondary to Hodgkin's disease, and another had acute leukemia recurring after allogeneic bone marrow transplantation. This chromosome abnormality was always associated with other karyotypic aberrations, probably as a secondary event. Possible correlations with recent findings in oncogene research are discussed.
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PMID:Chromosome 12 rearrangement with breakage at the p11 level in hematologic disorders: report of four cases. 397 22

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

We have previously shown that the LAZ3/BCL6 gene encoding a potential transcription factor, is disrupted in B-diffuse large cell non-Hodgkin's lymphomas (NHL) with 3q27 chromosomal abnormalities involving the immunoglobulin (IG) genes. However, LAZ3 rearrangement also occurs in NHL bearing 3q27 translocations without involvement of the IG genes: for example the VAl cell line exhibits t(3;4)(q27;p11). In the present work we have used a RT-PCR method to detect and to sequence the LAZ3 mRNA products from the VAL cell line. We report that the consequence of the t(3;4) is the expression of a chimeric transcript of LAZ3 with a new gene encoding a small G-like protein, termed TTF (Translocation Three Four). Nucleotide sequence analysis of a 1.4 kb cDNA predicts that the TTF gene encodes a protein of 191 amino-acids similar to members of the RAS superfamily including HRAS (27% identical), RAB1A (30% identical) and RHO proteins: the human RAC1, RHOB and CDC42Hs proteins (respectively 43, 44 and 45% identical) and the yeast RHO2 protein (44% identical). Unlike most other small G proteins which are expressed ubiquitously, TTF was transcribed only in hemopoietic cells as a 2.2 kb transcript. TTF may define a new subgroup of RHO-like proteins.
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PMID:TTF, a gene encoding a novel small G protein, fuses to the lymphoma-associated LAZ3 gene by t(3;4) chromosomal translocation. 778 61

Although translocations of the BCL2 gene are frequent in B-cell non-Hodgkin's lymphomas (B-NHL) the incidence, nature, and prognostic significance of similar translocations in the phenotypically related chronic leukemias of mature B cells are unknown. Therefore, we examined 170 cases of B-cell chronic lymphocytic leukemia (B-CLL), 7 cases of B-cell prolymphocytic leukemia (B-PLL), 25 cases of hairy cell leukemia (HCL) and 22 cases of splenic lymphoma with villous lymphocytes (SLVL) with defined cytogenetic abnormalities by DNA blot using both 5' and 3' BCL2 probes to search for rearrangement of the BCL2 locus. Translocation t(14;18) (q32.3;q21.3) was detected cytogenetically in 3 cases of B-CLL. All had breakpoints in the 3' region of BCL2, mapping between the major breakpoint region (MBR) and the minor cluster region (mcr), the breakpoint clusters commonly detected in B-NHL. In 2 of the 3 cases, the breakpoint within BCL2 was mapped to a 1.0-kb EcoRI-HindIII fragment indicating a clustering of breakpoints. Two cases of B-CLL had cytogenetically detectable t(2;18)(p11;q21.3) or t(18;22)(q21.3;q11). Both had rearranged the 5' region of the BCL2 gene to the corresponding lg light-chain gene. Molecular cloning of the t(18;22)(q21.3;q11) showed that the translocation disrupted the BCL2 promoter region and the first untranslated BCL2 exon. Nevertheless, high levels of BCL2 protein were seen in this case. Only 2 other cases in whom cytogenetic analysis was not successful showed rearrangement of the 5' region of BCL2, an overall incidence of 2.3%. No cases of B-PLL, HCL, or SLVL showed either 5' or 3' BCL2 rearrangement. These data confirm the cytogenetic observations that translocations involving the BCL2 locus in all forms of leukemia of mature B cells are rare, and limited to a minor subset of B-CLL. BCL2 translocations in B-CLL involve hot spots of recombination of both the 5' and 3' regions of the BCL2 gene, which are distinct from those commonly seen in B-NHL, suggesting distinct pathogenic mechanisms.
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PMID:BCL2 translocations in leukemias of mature B cells. 820 92


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