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Query: UNIPROT:Q06643 (
non-Hodgkin's lymphoma
)
11,307
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Clonal chromosomal abnormalities were found in tumor tissue of 43 (84%) of 51 patients with
non-Hodgkin's lymphoma
(B-cell, 32; T-cell, 15) from an adult T-cell leukemia/lymphoma-nonendemic area in western mainland Japan. Four tumors were tetraploid, and the other 39 had a chromosome number in the diploid range. Trisomies 3, 5, 7, 18, and X, monosomy 13, and loss of an X in female and a Y in male were found in more than three patients each. Structural abnormalities in arms 1p, 1q, 2q, 3q, 13q, 14q, and 18q were found in eight or more patients each. Clustering of breaks occurred in 3q25-29 (ten patients, nine of whom with a B-cell tumor), 11q13 (five patients), dir dup(12)(q13-15----q21-24) (four patients), 14q32 (12 patients), and 18q21 (seven patients). The 14q32 translocations were all associated with B-cell tumors. t(8;14) was seen in a small noncleaved cell lymphoma, t(11;14)(q13;q32) in one follicular and three intermediately differentiated lymphocytic lymphomas, and t(14;18)(q32;q21) in two follicular lymphomas and one diffuse small cleaved cell tumor. The translocation partner of 14q could not be determined in the other four patients, three of whom had der(18)t(18;?)(q21;?). The seven 18q21 abnormalities, including a novel translocation t(2;18)(
p11
;q21.3), all occurred in B-cell tumors; even in the absence of t(14;18), they were closely associated with lymphomas of follicular center cell origin (six of seven).
...
PMID:Chromosome abnormalities in malignant lymphoma in patients from Kurashiki: histological and immunophenotypic correlations. 232 95
Eleven patients with Burkitt's lymphoma (BL), i.e., small noncleaved
non-Hodgkin's lymphoma
, and 5 patients with Burkitt-type acute lymphocytic leukemia (ALL-L3) were selected for chromosome study. Two of the 16 patients had no B-cell markers, but the erythrocyte marker--glycophorin A--was present on the surface of the leukemic blasts. The critical breakpoint at 8q24 was detected in 14 of the 16 patients, whereas this aberration was not detected in any of the 134 patients belonging to other subgroups of
non-Hodgkin's lymphoma
or ALL that we studied during the same period. In addition to the t(8;14)(q24;q32), the following translocations with the breakpoint at 8q24 were seen: t(2;8)(
p11
;q24), t(8;11)(q24;q13) in BL, and t(2;8;14)(
p11
or p12;q24;q32) in ALL. Additional aberrations seen more than once were trisomy #7 and abnormalities in chromosomes #1, #11, and #13.
...
PMID:Chromosome abnormalities in 16 Finnish patients with Burkitt's lymphoma or L3 acute lymphocytic leukemia. 659 36
In a previous cytogenetic analysis, we showed the recurrence of translocations involving band 3q27 and immunoglobulin gene regions in 20 out of 319 patients with
non-Hodgkin's lymphoma
(
NHL
). We report here the molecular cloning of the translocation breakpoint from tumor cells of a patient (LAR) with t(3;14)(q27;q32) and the isolation of DNA probes which identify a major translocation cluster region (MTC) at band 3q27. A DNA library from LAR tumor cells was screened with a JH probe and several clones were identified corresponding either to a somatic rearrangement of JGH genes (V4-D2-J6-C mu clonal rearrangement) or to the t(3;14). Analysis of the t(3;14) breakpoint showed that chromosome 3 material was translocated to an inverted 14q32 VH-containing fragment which was itself translocated to the J3 gene. Chromosome 3-assigned probes were used to investigate local DNA rearrangements in a series of
NHL
with 3q27 translocations. Rearrangements were detected in 13 of 17 patients including 9 of 11 with t(3;14)(q27;q32), 1 of 2 with t(2;3)(p12;q27), 1 of 2 with t(3;22)(q27;q11), and 2 of 2
NHL
with translocations not involving an IG gene, namely, t(3;4)(q27;
p11
) and t(3;7)(q27;p12). The finding of this MTC should be useful for diagnostic and prognostic studies and for the identification of a novel oncogene at band 3q27 involved in the development of B cell
NHL
.
...
PMID:Cloning of a breakpoint cluster region at band 3q27 involved in human non-Hodgkin's lymphoma. 766 45
Chromosomal breakpoints associated with malignancy are known to cluster at particular regions of the karyotype. Based on a review of the literature we have identified a novel leukaemia syndrome associated with translocations involving 8p11. This syndrome is distinct from the previously described translocation t(8;16)(
p11
;p13) associated with acute monoblastic leukaemia. We have summarized the clinical and cytogenetic features of 13 case reports which describe a myeloproliferative syndrome with eosinophilia, lymphadenopathy and a high incidence of T cell
non-Hodgkin's lymphoma
with progression to acute myeloid leukaemia. The translocations involving 8p11 were: either t(8;13)(
p11
-12;q11-12), t(8;9) (
p11
;q32-34) or t(6;8)(q27;p12). In two cases of t(8;13) molecular studies have mapped the chromosome 13 breakpoint to a 1.5 Mbp region, but a full molecular characterization of these translocations is required. In view of the striking clinicopathological and karyotypic similarities between these cases we propose that they be considered a single nosological entity and termed '8p11 myeloproliferative syndrome'.
...
PMID:A new myeloproliferative disorder associated with chromosomal translocations involving 8p11: a review. 868 12
We report two patients with a distinctive biphenotypic hematologic disorder characterized by lymphoblastic lymphoma (LBL), eosinophilia, and myeloid malignancy and/or hyperplasia associated with a t(8;13)(
p11
;q11) chromosomal translocation in both bone marrow and lymph node specimens. Both patients presented with lymphadenopathy pathologically classified as LBL with a T-cell immunophenotype, myeloid hyperplasia of the bone marrow, and peripheral blood eosinophilia. The first patient achieved clinical complete remission after receiving several regimens of chemotherapy and remains disease-free 16 months after undergoing allogeneic bone marrow transplantation. The second patient developed progressive lymphadenopathy despite several courses of chemotherapy directed against
non-Hodgkin's lymphoma
. Eight months after his initial presentation, he developed acute myelogenous leukemia that was refractory to therapy. Comparison of these patients with four similar cases recently reported in the literature suggests that this constellation of findings constitutes a distinctive clinicopathologic syndrome. Molecular analysis of the t(8;13) translocation breakpoint may identify genes located in this region and provide insight into the pathogenesis of this interesting biphenotypic hematologic malignancy.
...
PMID:A syndrome of lymphoblastic lymphoma, eosinophilia, and myeloid hyperplasia/malignancy associated with t(8;13)(p11;q11): description of a distinctive clinicopathologic entity. 760 17
Fourteen cases of dic(9;12)(
p11
-13;
p11
-12) in early B-lineage acute lymphoblastic leukemia (ALL) and other hematological malignancies are reported with a review of the literature. Altogether 36 cases were collected for analysis: ALL at diagnosis (31 cases) or in relapse (one case), chronic myeloid leukemia in lymphoid blast crisis (two cases), T-cell lymphoblastic lymphoma (one case) and T-cell
non-Hodgkin's lymphoma
(one case). We report the first cases of dic(9;12) with a T-cell phenotype. Dic(9;12) occurs predominantly in B-progenitor ALL of childhood and young adults (age range, 1-47 years, median 12 years) but not of infancy. One or more adverse clinical features, age > 10 years, WBC > 100 x 10(9)/l, pre-B immunophenotype, platelets < 100 x 10(9)/l, were found in over 90% of cases. Additional structural chromosomal changes or trisomy 8 were frequently present. Nevertheless with a median follow-up of 5 years, 29/31 cases (94%) remain in first remission conferring an excellent prognosis to this leukemia. Additional cases are being sought to confirm the prognostic value of this cytogenetic aberration in various hematological malignancies.
...
PMID:Dicentric (9;12) in acute lymphocytic leukemia and other hematological malignancies: report from a dic(9;12) study group. 784 2
Recurrent pleural effusions from a 45-year-old man who was diagnosed as having
non-Hodgkin's lymphoma
of immunoblastic type were studied cytogenetically. The majority of the metaphases were tetraploid, but there were also lymphoma cells observed with pseudodiploid chromosome constitutions. Cytogenetic analysis by G-banding revealed the existence of at least two cell populations. The karyotype of the minor pseudodiploid clone, which exhibited partial trisomy of 1q11qter and monosomy of 6p11pter as sole abnormalities, was 46,XY,der(6)t(1;6)(q11;
p11
). The karyotype of the major clone was 92,XXYY,-1,der(6)t(1;6)(q11;
p11
)x2, +9. The ancestral diploid clone, carrier of the balanced translocation involving chromosomes 1 and 6, was not observed even in the first pleural effusion harvest. The high proportion of tetraploid cells in the recurrent effusions was an indication that these cells were favorably selected in the environment of the somatic cavity. Our cytogenetic findings suggest that partial trisomy of 1q may be a crucial secondary chromosomal abnormality in highly malignant
non-Hodgkin's lymphoma
. This genetic imbalance was predetermined from the primary abnormality and may be responsible for further tumor progression, as suggested from the clonal evolution in this particular case and, therefore, may be associated with the aggressive biologic behavior of malignant cells.
...
PMID:Clonal evolution of an immunoblastic type non-Hodgkin's lymphoma with der(6)t(1;6)(q11;p11) as its primary cytogenetic abnormality. 785 Jul 53
We report a 57-year-old male with
non-Hodgkin's lymphoma
(
NHL
) associated with t(2;3)(p12;q27). The patient showed bone lesions at presentation and brain involvement at relapse in addition to systemic lymph node swelling. Histological diagnosis was malignant lymphoma, diffuse, large cell, immunoblastic, plasmacytoid. Chromosome analysis revealed t(2;3) which is a variant type of t(3;14)(q27;q32). Fluorescence in situ hybridization (FISH) analysis disclosed splits of signals of BCL-6 gene. Among the cases reported in the literature, the common feature of t(2;3)(
p11
or p12;q27) was diffuse, large cell lymphoma of B cell, kappa phenotype and four patients immunosuppressive state before lymphoma.
...
PMID:Bone and brain involvement in a case of diffuse large B cell lymphoma associated with t(2;3)(p12;q27). 858 71
The RhoH/TTF (ARHH) gene encodes a new member of the Ras superfamily of small GTPases. The gene was identified by fusion to the BCL6/LAZ3 oncogene in an initially described t(3;4)(q27;
p11
) translocation in a
non-Hodgkin's lymphoma
cell line. The predicted amino acid sequence of the RhoH/TTF gene product includes Rho-like GTPase structural motifs. The RhoH/TTF gene is restrictively expressed in hematopoietic cells and tissues. Mutations in the human RAS genes have been shown previously to be tumorigenic; in the search for a potential implication of the RhoH/TTF gene in hemopoietic malignancies, we established its genomic structure. The RhoH/TTF gene spans 35 kb and contains two exons, with the second bearing the entire amino-acid-coding region. Chromosomal mapping, by FISH experiments, places the RhoH/TTF gene on the short arm of chromosome 4, band p13.
...
PMID:Genomic structure and assignment of the RhoH/TTF small GTPase gene (ARHH) to 4p13 by in situ hybridization. 922 77
Two distinct leukemia syndromes are associated with abnormalities of chromosome band 8p11. First, a myeloproliferative disorder with features characteristic of both chronic myeloid leukemia and
non-Hodgkin's lymphoma
and second, an acute myeloid leukemia (AML) with French-American-British (FAB) M4/5 morphology and prominent erythrophagocytosis. The two syndromes are exemplified by a t(8;13)(
p11
;q12) and a t(8;16)(
p11
;p13), respectively, but cytogenetic variants of both have been described. Recently, the t(8;16) has been cloned and shown to fuse the MOZ gene at 8p11 to the CBP gene at 16p13. We have used fluorescence in situ hybridization (FISH), Southern blotting, and reverse transcriptase-polymerase chain reaction (RT-PCR) to refine the 8p11 breakpoint in three cases with t(8;13)(
p11
;q12) and in a single case of AML-M5 with a clinical picture apparently identical to that found in patients with a t(8;16), but characterized by an inv(8)(p11q13). FISH analysis was performed with several 8p11 CEPH yeast artificial chromosome (YAC) clones. YAC 782H11 was centromeric to the one case with t(8;13) tested, but was telomeric to the inv(8). YAC 847B12 was telomeric to both the t(8;13) and the inv(8), whereas YAC 829D12 was centromeric to the t(8;13), but split by the inv(8). Southern blotting and PCR of YAC 829D12 showed that it contained the MOZ gene. A 900-bp MOZ fragment encompassing the published t(8;16) breakpoint was amplified by PCR from normal peripheral blood leukocyte cDNA and used to probe Southern blots of patient DNA. A rearrangement was detected in the case with inv(8), but not in any of the three cases with t(8;13). Southern blotting with a CBP probe and RT-PCR with MOZ and CBP primers suggested that the inv(8) does not result in a cryptic MOZ-CBP fusion. It is likely, therefore, that MOZ is fused to a novel gene at 8q13 in this case. We conclude that the t(8;13) breakpoint is flanked by YACs 782H11 and 847B12 and is at least 1 Mb telomeric to MOZ. MOZ is involved, however, in a new variant of the t(8;16).
...
PMID:Abnormalities of chromosome band 8p11 in leukemia: two clinical syndromes can be distinguished on the basis of MOZ involvement. 937 94
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