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)

We treated 32 patients with Ph1-negative chronic myeloproliferative disorders (CMD) with excessive thrombocytosis with Interferon alpha-2b (IFN alpha-2b): 26 had essential thrombocythaemia, ET (18 previously untreated, eight pretreated); one thrombocythaemia after treatment for Hodgkin's disease (HD); two thrombocythaemia associated with non-Hodgkin's lymphoma (NHL); three stage II idiopathic myelofibrosis (IM). IFN was given at daily doses of 1-4 x 10(6) IU. Twenty-seven patients (84%) responded, 17 (53%) achieved complete haematologic response after a median time of 12 weeks, and 10 (31%) partial haematologic response. Median platelet levels declined in complete haematologic response patients from 1,190 to 335 x 10(9)/l. Normalization of megakaryocyte (MK) levels was observed in 8/17 complete haematologic response patients treated for 9-12 months, with decreased bone marrow (BM) cellularity. Side effects requiring dose reduction or discontinuation of treatment occurred in 28% of cases with IFN doses of 2 or 4 x 10(6) IU. After 1 year of continuous IFN treatment, responses were maintained with conventional chemotherapy or low-dose IFN. This study demonstrates that IFN has definite therapeutic activity in CMD with excessive thrombocytosis. This biological agent, either alone or in combination with other antineoplastic treatment, may represent a new therapeutic approach for these disorders.
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PMID:Interferon alpha-2b as treatment for Philadelphia-negative chronic myeloproliferative disorders with excessive thrombocytosis. 275 63

Research in oncogenetics has led to the identification of two major classes of tumor-associated genes, oncogenes and tumor suppressor genes. In a wide variety of solid tumor types, mutations of both groups of genes have been implicated in the tumorigenic process. In hematologic neoplasms, on the other hand, most attention has focused on illegitimate activation of oncogenes, e.g., deregulation leading to disturbed transcriptional activity and structural rearrangements resulting in hybrid genes. Whether loss or mutational inactivation of tumor suppressor genes also plays an essential role in the genesis of tumors of the hematopoietic system has received less attention. Because such inactivation can be the result of karyotypically detectable loss of chromosomal material, cytogenetic studies may prove helpful in pinpointing genomic sites that harbor tumor suppressor genes. The present study is based on a total of 12,473 cytogenetically abnormal hematologic neoplasms reported in the literature to date. Among these, we selected the 6,422 cases with sole clonal chromosomal abnormalities in order to include only aberrations of importance in the genesis, rather than in the progression, of these neoplasms. All tumors with monosomies or structural abnormalities resulting in loss of chromosomal material were compiled, and for every such structural aberration, i.e., deletion, unbalanced translocation, isochromosome, and ring chromosome, the chromosome bands lost were ascertained. This cytogenetic deletion mapping revealed that the most commonly lost chromosomes were Y and 7 in acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and chronic myeloproliferative disorders (MPD); X, Y, 7, 20, and 21 in acute lymphocytic leukemia (ALL); X, Y, and 17 in chronic lymphoproliferative disorders (LPD); and X and Y in non-Hodgkin's lymphoma (NHL). Chromosome segments/bands lost due to unbalanced structural abnormalities in at least 5% of the cases were 5q13-33, 7q22-36, 9q13-31, 11q23-25, 12p12-13, 17p11-13, and 20q11-13 in AML; 5q13-35 and 20q11-13 in MDS; 5q22-23, 7q22, 13q12-22, 17p11-13, and 20q11-13 in MPD; 6q15-27, 9p11-24, 12p12-13, and 19p13 in ALL; 6q16-27, 11q21-25, 13q13-14, and 14q32 in LPD; and 6q21-27, 11q13-25, and 14q24-32 in NHL. Based on these findings, three conclusions can be drawn. First, there is no good correspondence between total and partial monosomies, the only exception being -7 and 7q-, both of which are common in myeloid neoplasms. This indicates different pathogenetic effects of total and partial losses.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cytogenetic deletion maps of hematologic neoplasms: circumstantial evidence for tumor suppressor loci. 751 63

In order to ascertain the frequency and distribution of isochromosomes in neoplasia, we surveyed the cytogenetic data from 20,007 tumors with clonal chromosome aberrations reported in the literature. Tumor types for which at least 50 cases with acquired aberrations and 10 cases with isochromosomes had been reported were selected, yielding a total of 18,160 neoplasms. Of these, 1,792 cases (9.9%) displayed a total of 2,014 isochromosomes. The 9 most common isochromosomes (detected in at least 50 cases) were, in decreasing order of frequency, i(17q), i(8q), i(1q), i(12p), i(6p), i(7q), i(9q), i(5p), and i(21q). The frequency of isochromosomes varied among the different tumor types, with the highest incidence in germ cell neoplasms (60%) and the lowest in chronic myeloproliferative disorders (2.3%). Also, the spectrum of isochromosomes differed among the neoplasms. The most common isochromosomes in the different tumor types were i(11q), i(17q), and i(21q) in acute myeloid leukemia; i(9q), i(17q), and i(22q) in chronic myeloid leukemia; i(17q) in chronic myeloproliferative disorders; i(X)(q13), i(17q), and i(21q) in myelodysplastic syndromes; i(7q), i(9q), and i(17q) in acute lymphoblastic leukemia; i(1q), i(7q), i(8q), and i(17q) in chronic lymphoproliferative disorders; i(1q), i(6p), i(9p), i(17q), and i(21q) in Hodgkin's disease; i(1q), i(6p), and i(17q) in non-Hodgkin's lymphoma; i(1q), i(8q), and i(17q) in adenocarcinoma; i(1q), i(3q), i(5p), and i(8q) in squamous cell carcinoma; i(5p), i(8q), and i(11q) in transitional cell carcinoma; i(1q), i(7q), and i(17q) in Wilms' tumor; i(1q), i(12p), and i(17q) in germ cell neoplasms; i(1p), i(1q), i(6p), and i(17q) in sarcoma; i(5p), i(6p), i(7p), and i(21q) in mesothelioma; i(1q), i(6p), and i(17q) in malignant neurogenic neoplasms; i(1q), i(6p), and i(17q) in retinoblastoma; and i(1q), i(6p), and i(8q) in malignant melanoma.
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PMID:Isochromosomes in neoplasia. 752 35

Serum levels of hepatocyte growth factor (HGF), a potent angiogenic factor, increase during various haematological malignancies. In this study, we examined serum HGF in 59 patients with non-Hodgkin's lymphoma (NHL). Serum HGF levels in NHL patients were increased, as were levels in patients with multiple myeloma, chronic myeloproliferative disorders, and myelodysplastic syndrome. Some 29 patients with T-cell lymphoma, including 20 with adult T-cell leukemia/lymphoma, exhibited a significant increase in serum HGF, as did 23 with B-cell lymphoma. The levels of serum HGF correlated with increased neutrophil counts (r=0.487, p<0.0001), and also paralleled a neutrophil increase in NHL patients who received granulocyte-colony stimulating factor (G-CSF) at the nadir of neutrophil count following chemotherapy. Additionally, in in vitro experiments, HGF secretion from polymorphonuclear neutrophils and its expression in bone marrow myeloid cells were stimulated by G-CSF. Although HGF has been thought to be involved in the pathogenesis of NHL through its angiogenic activities, these results suggest that HGF production by neutrophils and myeloid lineage cells may also contribute to an increase in serum HGF in NHL patients.
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PMID:Possible involvement of neutrophils in a serum level increase of hepatocyte growth factor in non-Hodgkin's lymphoma. 1570 13

Myelofibrosis is often observed in chronic myeloproliferative disorders (CMPD), but non-Hodgkin's lymphoma with diffuse myelofibrosis is rare. We describe an elderly case with peripheral T-cell lymphoma-unspecified (PTCL) presenting as diffuse myelofibrosis. Bone marrow biopsy revealed infiltration of atypical lymphocytes and diffuse myelofibrosis without any increase in megakaryocytes. To discuss the pathogenesis of fibrosis, we examined cytokines relative to fibrosis using immunostaining. The expression of basic fibroblast growth factor (bFGF) was diffusely detected in the area of extracellular matrix of bone marrow. In addition, in situ hybridization revealed that infiltrating lymphoma cells expressed bFGF mRNA. Basic FGF, originally identified based on its mitogenicity for fibroblasts, has multiple potential, influencing neoangiogenesis, bone marrow fibrosis and the proliferation of tumor cells. Basic FGF might play an important role in the pathogenesis of myelofibrosis in the present case.
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PMID:Peripheral T-cell lymphoma presenting as myelofibrosis with the expression of basic fibroblast growth factor. 2000 60