Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty consecutive evaluable specimens from patients with non-Hodgkin's lymphoma (NHL) were studied for the incidence of polysomy of chromosome 12 by fluorescence in situ hybridization (FISH) with probes for the repetitive DNA sequence in the centromeric region of chromosome 12. Thirty-six samples were from follicular lymphomas (FLs), and twenty-four were from diffuse large cell lymphomas (DLCLs). Fifty-two specimens (86%) were obtained by fine-needle aspiration of a diseased node, seven (11.6%) were from involved bone marrows, and one specimen was from a pleural effusion. Twelve of the thirty-six (33%) cases with FL had trisomy 12 in 3-41% of the cells (median, 10%) (normal controls had three signals in 1.4 +/- 0.7% of cells). Trisomy 12 was found in 62% of the patients who had had FL for more than 5 years. Nine of the twenty-four cases (37%) with DLCL had more than two copies of chromosome 12 in 4-92% of the cells (median, 78%), and all nine cases were of B-cell phenotype. Unlike FL cells, some DLCL cells had 4-6 copies of chromosome 12. In previously untreated patients, 54% of DLCLs and 26% of FLs had subpopulations of cells containing more than two copies of chromosome 12 (P = 0.04). Only 2/7 cases of DLCL with polysomy 12 had rearrangement of the BCL2 gene, indicating that the majority of DLCL cases with polysomy 12 did not result from histologic transformation of low grade follicular lymphomas. These data demonstrate that FISH of interphase cells is a sensitive method for detecting numerical abnormalities of chromosome 12 in NHL.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Polysomy of chromosome 12 in 60 patients with non-Hodgkin's lymphoma assessed by fluorescence in situ hybridization: differences between follicular and diffuse large cell lymphoma. 751 57

In a study of abnormal chromosomes in non-Hodgkin's lymphoma (NHL) cells we have identified one case which contained extrachromosomal chromatin bodies that, on the basis of their morphology and negative C-banding, appeared to be double minute chromosomes (dmin). However, fluorescence in-situ hybridization (FISH) analysis using an X-specific centromeric alphoid repeat probe and a pan-centromere probe, clearly demonstrated the presence of centromere-associated DNA in these dmin. FISH analysis with the pan-centromere probe of the dmin in neuroblastoma and sarcoma cells failed to reveal the presence of centromere-associated DNA, but analysis of two cases of acute myeloid leukemia cells revealed centromere-associated DNA in 25% of their dmin. These data indicate the existence of dmin that contain centromere-associated DNA and suggest that such dmin might represent a new class of extrachromosomal chromatin bodies.
 ...
PMID:Identification of a subclass of double minute chromosomes containing centromere-associated DNA. 752 Feb 68

Chromosome X numerical abnormalities are frequently observed in non-Hodgkin's lymphoma (NHL), with an incidence of 3% to 14% for chromosomal loss and 7% to 33% for chromosomal gain. Because sex chromosome numerical abnormalities are thought to be due to aging, little information is known about their relation to gender, therapy, and prognosis. Therefore, to determine the incidence and clinical relevance of this abnormality in NHL, we studied specimens from 59 NHL patients (31 men and 28 women) by fluorescence in situ hybridization (FISH) using a directly conjugated centromeric probe for chromosome X. The median age for the entire group was 52 years (range, 31-88 years). All specimens were obtained by fine-needle aspiration of diseased lymph nodes. Sex-matched lymphocytes from benign hyperplastic lymph nodes were used as controls. The overall incidence of chromosome X numerical abnormalities was 49.2%. Female patients had a higher overall incidence than males (76% vs. 24%; p < 0.001). The median percentage of cells involved in this abnormality in each specimen was 5.2%. There was no statistically significant difference in the incidence in previously treated than untreated patients (53.1% vs. 44.4%; p < 0.75) and in intermediate-grade NHL than low-grade NHL (61.1% vs. 50%; p < 0.75). There was a trend towards a higher incidence of chromosome X loss in older patients. While the difference in the incidence of chromosome X abnormalities observed between women and men may be due to the difference in the normal copy numbers of this chromosome in each sex group, this abnormality remained higher than any other autosomal chromosome abnormality in NHL previously evaluated by FISH. We conclude that, although FISH detected a high incidence of chromosome X numerical abnormalities and that females had a higher incidence than males, only a small percentage of the cells were involved, suggesting that this abnormality is most likely a secondary genetic defect that is not important in the pathogenesis of NHL.
 ...
PMID:Chromosome X numerical abnormalities in patients with non-Hodgkin's lymphoma. A study of 59 patients using fluorescence in situ hybridization. 762 30

Monosomy 17 and structural abnormalities of the short arm of chromosome 17 have been reported to influence prognosis and treatment outcome in patients with non-Hodgkin's lymphoma (NHL). In diffuse large cell lymphoma, these abnormalities were associated with refractoriness to chemotherapy, higher proliferative rate and poor prognosis. We studied the incidence of chromosome 17 abnormalities in 55 patients with NHL by using fluorescence in situ hybridization with a directly conjugated centromeric probe for chromosome 17. Twenty-three patients (42%) were previously untreated. Thirty-four patients (62%) had diffuse large cell lymphoma, 18 (33%) had follicular low-grade lymphoma, one had small lymphocytic lymphoma, one had diffuse mixed cell lymphoma, and one had mantle cell lymphoma. Cells from benign lymphoid hyperplasia were used as controls. Eight patients (15%) had trisomy 17 in 1.2-40.7% of cells and one patient (1.8%) had monosomy 17 in 68.8% of cells. We conclude that monosomy 17 is not common in NHL. Chromosome 17 deletions should be investigated with region-specific probes to determine their clinical relevance in NHL.
 ...
PMID:Chromosome 17 numerical abnormalities in 55 patients with non-Hodgkin's lymphoma: a fluorescence in situ hybridization study. 763 Jan 87

Translocation of the BCL2 gene in B-cell malignancies carrying t(14;18) and amplification of the BCL2 gene in a cell line (HBL-2) derived from a non-Hodgkin's lymphoma (NHL) were detected specifically in both metaphase spreads and interphase nuclei by fluorescence in situ hybridization (FISH) using yeast artificial chromosomes (YACs). A YAC clone containing the BCL2 gene yA153A6, a 360-kb clone spanning from approximately 60 kb upstream of BCL2 exon 1 to approximately 60 kb 3' of the minor breakpoint cluster region, was used for single-color FISH analysis. Seven patients with NHL and one patient with acute lymphoblastic leukemia were analyzed for BCL2 translocations. Interphase nuclei of NHL patients showed three signals when hybridized with the yA153A6 probe. This was expected because the YAC clone spans the BCL2 breakpoint regions on 18q21.3. In a patient with acute lymphoblastic leukemia, a positive signal for BCL2 was detected on der(14) at band 14q32.33 by single-color FISH with the yA153A6 probe, whereas no signals were detected on der(18). The amplification of BCL2 in the HBL-2 cell line was observed on a characteristic abnormal chromosome 18, add(18)(q23); the periodic pattern of the fluorescent signal of this region was suggestive of an amplicon. Using double-color FISH with YAC clones containing the more centromeric 18q21.3 gene gastrin-releasing peptide (y302F10) and the 14q32.33 gene (IgH; Y6), we detected t(14;18) by showing the juxtaposition of the 18q21.3 and 14q32.33 bands on the derivative chromosome 18. Interphase FISH with these YAC clones provided a rapid procedure for the diagnosis of B-cell malignancies carrying t(14;18). In addition, we showed that translocations and amplification of the BCL2 gene can be detected at the single-cell level.
 ...
PMID:Translocations and amplification of the BCL2 gene are detected in interphase nuclei of non-Hodgkin's lymphoma by in situ hybridization with yeast artificial chromosome clones. 763 55

Unbalanced translocations as well as interstitial deletions of the short arm of chromosome 12 [del(12p)] are found as recurring chromosomal changes in a broad spectrum of hematopoietic malignancies. These changes result in the hemizygous deletion of genetic material from 12p. We mapped a yeast artificial chromosome containing the TEL gene, a cosmid contig containing part of TEL and a P1 contig containing the KIP1 gene to 12p13. These probes were used for fluorescence in situ hybridization to analyze samples from 47 patients with various hematologic malignancies who had unbalanced translocations (25 patients) leading to loss of 12p or deletions (22 patients) involving 12p13. The patients had acute lymphoblastic leukemia (8 cases), myelodysplastic syndrome (MDS; 11 cases), acute myeloid leukemia (AML; 10 cases), myeloproliferative disorders (4 cases), therapy-related MDS or AML (7 cases), non-Hodgkin's lymphoma (2 cases), and other hematopoietic malignancies (5 cases). All three probes were hemizygously detected in 26 cases and were completely retained in only 9 cases. In 12 cases probes for one of the two genes were deleted, allowing us to map the smallest region of overlap of these deletions to a small genomic region that is bordered on the telomeric side by the TEL gene and on the centromeric side by KIP1. The genomic distance between TEL and KIP1 is estimated to be about 1 to 2 Mbp.
 ...
PMID:TEL and KIP1 define the smallest region of deletions on 12p13 in hematopoietic malignancies. 763 60

Previous studies have indicated that a candidate tumor suppressor gene resides telomeric of the RB1 gene at 13q14, a region that is commonly deleted in B-cell chronic lymphocytic leukemia (B-CLL). In this study, we have evaluated the frequency and minimal region of overlap for 13q deletions in malignant cells from various lymphoid neoplasms. We observed losses at 13q14 in 33/75 (44%) B-CLL cases, four of 16 (25%) non-Hodgkin's lymphoma (NHL) cases, eight of 29 (28%) patients with acute lymphocytic leukemia (ALL), and one of 15 T-cell lines. In some ALL cases, inactivation of the RB1 gene is suggested as the important event in the 13q deletions. The most commonly deleted marker in CLL and NHL was D13S319, between RBkpt and the D13S25 loci. Homozygous deletions of this marker were observed in 10 of 75 B-CLL cases, in six of which the homozygous deletions included only the D13S319 locus. Our data suggest that 13q deletions are common in lymphoid neoplasms, and that deletion of a candidate tumor suppressor gene(s) in the vicinity of the D13S319 marker is a tumorigenic event in these diseases.
 ...
PMID:13q deletions in lymphoid malignancies. 765 20

The breakpoint of 14q32 translocations found in B-cell malignancies was delineated specifically in both metaphase spreads and interphase nuclei by double-color fluorescence in situ hybridization (FISH) using bacteriophage clones containing the human immunoglobulin gamma chain gene locus (Ig gamma) and a cosmid clone, CY24-68, containing VH segments. CY24-68 is more telomeric than Ig gamma, separated by approximately 1 megabase (Mb). FISH studies were performed on four patients with non-Hodgkin's lymphoma (NHL), one with acute lymphoblastic leukemia (ALL), one with plasma cell leukemia (PCL), and three cell lines. In each patient with t(8;14), t(14;18), and t(3;14), the signal of Ig gamma gene was observed on der(14) and that of CY24-68 at respective partner sites of these translocations, 8q24.1, 18q21.3, and 3q27. Interphase nuclei with a signal of Ig gamma clearly separated from that of CY24-68 were more frequently encountered in all of the patients (45% to 74%) than those in normal controls (4% to 5%). Even in cases where only interphase nuclei were available for FISH studies, 14q32 translocations are detected as shown in two patients each with NHL and t(11;14)-carrying PCL. In two cell lines, HS-1 derived from ALL carrying t(8;14) and FR4 derived from a plasmacytoma carrying a complex form of t(8;14), the signal of Ig gamma was observed at the breakpoint region 8q24.1 of the der(8) in addition to the der(14), indicating that translocation event occurred within the Ig gamma locus. Intense Ig gamma signal was found at the breakpoint region on the der(14)t(11;14) in HBL-2 derived from NHL, indicating amplification of the Ig gamma gene, and presumably the resultant chimeric DNA between Ig gamma and DNA sequences at 11q13. The present approach allowed us to unequivocally detect tumor-specific breakpoints of 14q32 translocations. Furthermore, interphase FISH provides a rapid diagnostic procedure to detect 14q32 translocations in B-cell malignancies.
 ...
PMID:Interphase and metaphase detection of the breakpoint of 14q32 translocations in B-cell malignancies by double-color fluorescence in situ hybridization. 775 53

We studied the incidence of numerical chromosome 18 abnormalities in 107 patients with lymphoid malignancies by fluorescence in situ hybridization (FISH) using a directly conjugated centromeric probe for chromosome 18. Samples were obtained by fine needle aspiration of diseased nodes, bone marrows or peripheral blood. Monosomy 18 was more common in chronic lymphocytic leukemia (43%), small lymphocytic lymphoma (28%), and follicular lymphomas (12.5%) than in diffuse lymphomas (5.3%; p < 0.01). Monosomy 18 was detected in 9.7-17.1% of the cells in non-Hodgkin's lymphoma (NHL) (background, 5.4%; 99% CI, 4.2%-6.6%) and in 8%-16.7% (median, 10%) of the cells in (CLL) (background, 3.4%; 99% CI, 2.5%-4.3%). All patients with monosomy 18 were found to have bone marrow involvement. Of all untreated patients who had disease involving the bone marrow, 32% were found to have monosomy 18. Trisomy 18 was detected in 3.6%-48.2% of the cells in NHL (background, 0.9%; 99% CI, 0.2%-1.6%) and was most common in diffuse large-cell lymphoma (34%) and follicular lymphomas (31%). None of the patients with small lymphocytic lymphoma or chronic lymphocytic leukemia had trisomy 18. There was no correlation between trisomy 18 and response to treatment or clinical presentation. In this study, monosomy 18 was observed frequently in patients with lymphoid malignancies that involve the bone marrow and peripheral blood. Our data suggest that important gene(s) located on chromosome 18 may be involved in homing of the malignant lymphocytes to the bone marrow and peripheral blood.
 ...
PMID:High incidence of monosomy 18 in lymphoid malignancies that have bone marrow and peripheral blood involvement. 792 81

In somatic cells, each DNA replication round gives a shortening of the telomere ends as a consequence of incomplete lagging strand synthesis. Telomeres are essential for chromosomal integrity and extensive telomere length reduction is associated with increased instability of the genome. In germ line cells and in established cell lines, telomerase activity maintains the length of the telomeres by de novo synthesis of telomeric repeats, in humans (T2AG3)n. Recently, it was for the first time shown the existence of telomerase activity in human ovarian carcinomas. In the present study we show that telomerase activation can also occur in human hematopoietic tumor cells in vivo. Cell extracts from 19 cases with leukemia, lymphoma and myeloma were tested for telomerase activity using an in vitro assay with (T2AG3)3 or permutations of this sequence as primers. Eight cases demonstrated an RNAse A sensitive ability to add new nucleotides to the human telomere sequence. Nine acute leukemias were tested telomerase negative. Our data demonstrate that telomerase activation in vivo seems to be a common event in B cell neoplasias with a mature immunophenotype like non-Hodgkin's lymphoma and myeloma, in contrast to acute leukemias of B, T or myeloid cell origin. Telomere length evaluation indicated no marked differences between samples with or without telomerase activity which could argue for a telomere length independent mechanism for telomerase activation in at least some cases.
 ...
PMID:Telomerase activity in vivo in human malignant hematopoietic cells. 808 12


1 2 3 Next >>