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

An increasing frequency of malignant lymphomas occurs among patients infected by human immunodeficiency virus. Because of the close similarities to human malignancies, we used a nonhuman primate model to study the pathogenesis of simian immunodeficiency virus (SIV)-associated malignancies. Specifically, we investigated (1) the presence of the SIV genome in tumor cells, (2) the presence of coinfecting viruses, and (3) the presence of a rearrangement of the immunoglobulin and c-myc genes. We observed 5 cases of non-Hodgkin's lymphomas (4 of B- and 1 of T-cell origin) among 14 SIV-infected cynomolgus monkeys. No c-myc translocation was observed in the tumors, whereas B-cell lymphomas were characterized either by a monoclonal (in 2 of 4) or by an oligoclonal (in 2 of 4) VDJ rearrangements of the immunoglobulin heavy chain gene. Molecular, biological, and immunological analyses did show the presence of infectious SIV in the tumor cells of 1 T-cell and 2 oligoclonal B-cell lymphomas. Neither Simian T-lymphotropic nor Epstein-Barr viruses were detectable, whereas Simian herpes virus Macaca fascicularis-1 was detectable at a very low copy number in 3 of 4 B-cell lymphomas; however, only 1 of these also harbored the SIV genome. These results support the possibility that SIV may be directly involved in the process of B or T lymphomagenesis occurring in simian acquired immunodeficiency syndrome.
 ...
PMID:Detection of infectious simian immunodeficiency virus in B- and T-cell lymphomas of experimentally infected macaques. 955 63

cdc25A, cdc25B, and cdc25C are a family of human phosphatases that activate the cyclin-dependent kinases at different points of the cell cycle. cdc25A and cdc25B have been shown to have oncogenic potential, and they have been identified as transcriptional targets of c-myc. To determine the role of cdc25 genes in the pathogenesis of human lymphomas and their possible correlation with c-myc deregulation, we have analyzed the expression of cdc25A, cdc25B, and cdc25C and c-myc genes in a series of 63 non-Hodgkin's lymphomas and 8 nonneoplastic lymphoid tissues. The mRNA levels of the three phosphatases in the nonneoplastic tissues were negative or negligible. cdc25B overexpression was detected in 35 tumors (56%). This overexpression was more frequently found in aggressive (81%) than in indolent lymphomas (36%; P < 0.01). cdc25B overexpression was also significantly associated with a higher proliferative activity of the tumors. No cdc25B gene amplification or rearrangements were detected by Southern blot analysis. A biallelic EcoRI polymorphism of cdc25B gene was identified with a similar distribution in patients with lymphoma and in a normal population. cdc25A was overexpressed in three aggressive lymphomas. No detectable cdc25C mRNA levels were seen in any of the tumors. c-myc was overexpressed in 43% of tumors, and it correlated significantly with the presence of cdc25B up-regulation. Twenty-six of 35 (74%) lymphomas with high levels of cdc25B mRNA also showed c-myc overexpression, whereas 27 of 28 (96%) tumors without detectable or with very low cdc25B expression also had undetectable c-myc levels (P < 0.0001). In addition, a significant linear correlation was found between the cdc25B and c-myc mRNA levels (r = 0.575, P < 0.001). These findings suggest that cdc25B overexpression in non-Hodkin's lymphoma may participate in the pathogenesis of aggressive variants, and it may cooperate with c-myc oncogene in the development of these tumors.
 ...
PMID:cdc25 cell cycle-activating phosphatases and c-myc expression in human non-Hodgkin's lymphomas. 956 96

The role of oncogene or tumor supressor gene in Epstein-Barr virus (EBV) associated malignant lymphomas (MLs) is poorly understood. We examined 36 MLs (21 EBV positive and 15 EBV negative) and 6 reactive hyperplasias for the presence of myc gene amplification. Polymerase chain reaction (PCR) technology was used to examine the state of amplification of the proto-oncogene c-myc in formalin-fixed paraffin-embedded tissues. Variable degrees of myc gene amplification were detected in reactive hyperplasias and MLs. However, significant increase of c-myc copy numbers above 3 times were only found in 12 out of 31 non-Hodgkin's MLs (38.7%), in which 6 cases were EBV positive and 6 cases were EBV negative. In conclusion, myc gene amplification appears to play a part in MLs but no correlation was found between EBV infection and myc gene amplification.
 ...
PMID:Detection of MYC gene amplification in malignant lymphomas. 961 Jun 16

Epstein-Barr virus (EBV) has been associated with several malignant processes in man, most notably Burkitt lymphoma in previously healthy individuals and lesions resembling large cell non-Hodgkin lymphomas in organ transplant recipients. Mice with the severe combined immunodeficiency phenotype (SCID mice) are exquisitely susceptible to the development of EBV-associated lymphoproliferative lesions following the intraperitoneal (ip) inoculation of EBV-infected human lymphocytes. Recently, we reported that EBV-infected marmoset lymphocytes do not form lymphomas in SCID mice following ip injection, while human lymphocytes infected with the same EBV strains do. On the assumption that the EBV-infected marmoset cells were lacking a factor necessary for tumor formation, we transfected a plasmid containing c-myc into EBV-infected marmoset cells (B95-8, FF41, and W91 cells). Despite expression of the c-myc protein as determined by immunoblot and flow cytometry when probed with a monoclonal antibody, no increase over baseline lesion development was seen in SCID mice inoculated with 5 x 10(6) c-myc-expressing marmoset lymphoblastoid cells. Thus, cells that express c-myc and harbor EBV are not sufficient to form lymphomas in certain immunocompromised hosts.
 ...
PMID:Epstein-Barr virus-infected marmoset cells transfected with c-myc do not form lymphomas in mice with severe combined immunodeficiency. 971 30

Alterations of onco/tumour suppressor genes are involved in the formation of human hematological malignancies. Previously, in animal models, we demonstrated the applicability of in vivo gene expression investigations to monitor the effects of certain carcinogenic chemicals. In our present study we determined the expression of onco/suppressor genes from isolated peripheral white blood cells of patients with chronic myeloid leukaemia (CLL) and non-Hodgkin lymphoma (NHL). Gene expressions were determined by isolation of total RNA and slot blot hybridization with chemiluminescently labeled gene probes (Ha-ras, c-myc and p53) Expression levels were compared before and after treatment with a combined cytostatic protocol, containing cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP). Both the CLL and NHL group of patients exhibited significantly higher expression of the investigated genes than healthy controls. One month after the cytostatic treatment, we found considerably fewer individuals with overexpressed oncogenes than before the treatment. Our study proved that onco/tumour suppressor gene expressions could be used as biomarkers of certain hematological malignancies, and to monitor the therapeutical effect of cytostatic drugs.
 ...
PMID:The usefulness of in vivo gene expression investigations from peripheral white blood cells: a preliminary study. 1049 9

Burkitt-lymphoma is a rare disease, that belongs to the aggressive Non-Hodgkin-lymphomas. Next to histology, that shows a characteristic pattern, and immunophenotyping additional cytogenetic and molecular biology techniques are used to demonstrate in most cases a translocation of the oncogen c-myc on chromosome 8 to any of the immunoglobulin genes on chromosome 14, 2 or 22. With short term intensive chemotherapies a cure rate of 85-95% of patients with Burkitt-lymphoma can be obtained today.
 ...
PMID:[Burkitt's lymphoma--a case report]. 1050 Apr 20

Primary mediastinal B-cell lymphoma (PMBL) shows chromosome 9p anomalies in 50% of cases. Based on reports that p16INK4A gene, located on this chromosomal arm, is frequently altered in aggressive lymphomas, we analysed for alterations of this gene in 27 cases of PMBL, which were part of a series of 32 PMBL cases that have been characterized for alterations in c-myc, p53, N-ras, bcl-1, bcl-2, bcl-6 and for Epstein-Barr virus (EBV) infection. Four cases showed p16INK4A gene anomalies, including three with promoter methylation and one homozygous deletion. Eight PMBLs showed c-myc rearrangements. Three additional cases showed sequence variations in the c-myc P2 promoter, two of which consisted of the same germline variation involving a novel polymorphic XhoI site. Four tumours contained p53 gene mutations and three had clonal EBV infection. One case had a bcl-6 rearrangement. In conclusion, our study shows that p16INK4, c-myc and p53 alterations occur in 15%, 25% and 13% of PMBLs, respectively. EBV monoclonality was found in 9% of cases, whereas no abnormality was detected in bcl-1, bcl-2 and N-ras. Thus, none of the common genetic aberrations seen in other types of non-Hodgkin's lymphomas appears to be stringently involved in the pathogenesis of this unique lymphoma type.
 ...
PMID:Molecular features of primary mediastinal B-cell lymphoma: involvement of p16INK4A, p53 and c-myc. 1052 30

Cyclin D1 is a weak oncogene that cooperates with c-myc activation in the development of B cell lymphomas in transgenic animals. Cyclin D1 is constantly overexpressed in human mantle cell lymphomas (MCL). However, the status of c-myc gene in these tumors is not known. We have examined the c-myc mRNA expression and genomic alterations, including mutational analysis of exon 1, intron 1, and exon 2 regulatory elements, in a series of 33 MCL, 22 typical and 11 blastoid variants. In addition, c-myc alterations were also examined in 56 nodal non-Hodgkin's lymphomas (NHL). c-myc mRNA overexpression was found in 38% (11/29) of MCL with a slightly higher frequency in blastoid variants (5/10, 50%) than in typical cases (6/19, 31%). Genetic alterations were only found in one blastoid MCL showing a three-fold c-myc gene amplification. In other nodal NHL, c-myc overexpression was found in 24% (7/29) of indolent tumors but in 70% (19/27) of aggressive variants. c-myc Genetic alterations detected in these cases were gene rearrangement and hypermutations in one Burkitt's lymphoma, and individual point mutations in intron 1 or exon 2 in 1/19 (5%) indolent and 7/16 (44%) aggressive variants. These results indicate that c-myc is overexpressed in a subset of MCL, but structural gene alterations are less frequent than in other nodal NHL.
 ...
PMID:c-myc mRNA expression and genomic alterations in mantle cell lymphomas and other nodal non-Hodgkin's lymphomas. 1060 33

Of 84 renal transplants performed in our center since 1986, six recipients (7.1%) developed posttransplant lymphoproliferative disorder (PTLD). All received quadruple immunosuppression with Minnesota anti-lymphoblastic globulin or anti-thymocyte globulin, methylprednisolone, cyclosporine, and azathioprine or mycophenolate mofetil. Five were seronegative for Epstein-Barr virus (EBV) when they received their renal transplant. All patients received prophylactic acyclovir treatment postrenal transplant and none developed a cytomegalovirus (CMV) infection. All patients were positive for EBV by serology and polymerase chain reaction at the time of diagnosis of PTLD. Clinical features at presentation included fever (6/6), adenopathy (4/6), hypertrophied adenoids (4/6), liver involvement (2/6), and allograft involvement (2/6), 2-78 months (4/6<6 months) postrenal transplant. Histopathology of PTLD tissue revealed T cell rich/ Hodgkin disease-like B cell PTLD in one patient, polymorphic PTLD in four, and monomorphic (large B cell lymphoma) PTLD in one. Immunophenotyping of the PTLD biopsy specimen revealed predominant T cells in three, mixed B and T cells in two patients, and B cell in one. No aneuploid populations were identified by flow cytometric DNA ploidy assay. DNA from the PTLD tissue revealed weak to moderate IgH gene rearrangement in four of six patients but no T cell receptor beta-chain or c-myc gene rearrangement on Southern blot analysis. The child with monomorphic (large B cell lymphoma) PTLD was clonal with lambda light chain restriction on immunophenotyping. Treatment consisted of reduced immunosuppression and ganciclovir/ acyclovir in all patients. CMV hyperimmune globulin was used as an adjunctive therapy in two patients. Chemotherapy was needed in only one patient. A single rejection episode occurred in two children following reduction in immunosuppression, which reversed following intravenous methylprednisolone therapy. PTLD resolved in all patients and at present all patients are alive with functional grafts 2-54 months post diagnosis. Our experience suggests that reduced immunosuppression and anti-viral treatment is adequate in most cases of PTLD, but chemotherapy and hyperimmune globulin therapy may be beneficial in cases resistant to first-line therapy. Since all but one of our patients were EBV seronegative at the time of transplant, vigilance is especially important for early detection of PTLD in this group of the pediatric renal transplant population.
 ...
PMID:Posttransplant lymphoproliferative disorder in pediatric renal transplantation. 1060 13

Primary cutaneous B-cell lymphomas (CBCLs) should be clearly separated from non-Hodgkin's B-cell lymphomas with secondary cutaneous involvement and from cutaneous B-cell pseudolymphomas. The majority of CBCLs are characterized by a homogeneous clinical presentation and behavior, with good response to local radiotherapy, low tendency to extracutaneous spread, and excellent prognosis. According to the European Organization for Research on the Treatment of Cancer classification of primary cutaneous lymphomas, CBCLs with an indolent behavior are divided into 2 subgroups: follicular center cell lymphoma and immunocytoma/marginal zone lymphoma, due to putative histologic similarities with their purported nodal counterparts. In addition, a third subgroup with intermediate prognosis (large B-cell lymphoma of the leg) is identified. Conversely, the identification of distinct subgroups is disputable from a strictly histologic, immunophenotypic, and genotypic point of view, and has neither correlation with the clinical course nor the prognosis of the disease. Moreover, the majority of CBCLs show a uniform immunophenotype (CD5-, CD10-) and genotype (lack of bcl-1/bcl-2 and c-myc gene rearrangement) of neoplastic cells. Therefore, we favor the use of the term Skin-Associated Lymphoid Tissue (SALT)-related B-cell lymphomas, due to the close similarities between CBCLs and mucosa-associated lymphoid tissue (MALT) lymphomas, and the evidence for an acquired B-cell arm of SALT.
 ...
PMID:The skin-associated lymphoid tissue-related B-cell lymphomas. 1089 14


<< Previous 1 2 3 4 5 6 7 8 Next >>