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)

Alternative splicing of ten different variant exons (v1-v10) is responsible for the creation of a large number of different CD44 surface proteins. Some of these proteins play decisive roles in the metastatic spread of rat tumours. Also in human cancers, CD44 splice variants are frequently expressed in advanced states of tumorigenesis. In breast cancer and in non-Hodgkin's lymphomas expression of exon v6 is correlated with poor prognosis of patient survival. In colorectal carcinogenesis, expression of exon v5 is an early tumour marker since it is already detectable on small dysplastic polyps (but not on normal colon epithelium). In contrast, exon v6 expression occurred with increased frequency with tumour progression, and its expression on colorectal tumours indicated reduced survival probability. Most likely, tumours carrying the CD44 v6 epitope acquire selective advantage during tumour progression and metastasis formation. This could be a proliferative advantage since mice transgenic for the CD44 isoform CD44v4-v7 on T lymphocytes show an accelerated T-dependent immune response as compared with non-transgenic siblings.
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PMID:CD44 in colon cancer. 757 2

The protein p27KIP1 belongs to a recently identified family of proteins termed cyclin-dependent kinase inhibitors (CDKIs). These proteins play an important role in regulating cell-cycle progression and loss of their function has been implicated in tumorigenesis. Transforming growth factor beta (TGF-beta) may induce cell growth arrest through p27 activation. TGF-beta often loses its ability to arrest growth of transformed cells; this could potentially occur through a defect in p27. To determine the role of p27 in tumorigenesis, we examined its mutational status in 74 non-Hodgkin's lymphomas (NHLs) (52 of B-cell phenotype, 22 of T-cell phenotype), 5 lymphoma cell lines, and 42 adult T-cell leukemias/lymphomas (ATLs) using polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) and Southern blot analyses. A nonsense mutation (stop codon) that could result in expression of a truncated nonfunctional p27 protein was detected at codon 76 in one case of acute lymphomatous ATL, but not in matched normal tissues. Previously undescribed polymorphisms were also identified at codon 109 in the lymphomas and at codon 55 in the ATLs. Two homozygous deletions of the p27 gene were detected in one case of B-immunoblastic NHL and in one case of acute ATL by Southern blot hybridization. These results indicate that p27 gene alterations are rare events in NHLs and ATLs, but may play an important role in the pathogenesis of some hematologic malignancies.
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PMID:Alterations of the p27KIP1 gene in non-Hodgkin's lymphomas and adult T-cell leukemia/lymphoma. 765 21

The chromosomal translocation t(14;18)(q32;q21), which involves the bcl-2 oncogene, occurs in most follicular lymphomas. Recent evidence suggests that this translocation occurs in Hodgkin's disease, linking its cellular origin and oncogenesis to follicular non-Hodgkin's lymphomas. Using polymerase chain reaction, the authors examined both Hodgkin's disease (n = 60) and reactive lymph nodes (n = 34) for the presence of bcl-2/JH breakpoint fragments, which are indicative of the t(14;18) chromosomal translocation in the major breakpoint region of the bcl-2 gene. The translocation was detected in approximately 10% of both Hodgkin's disease and nonmalignant reactive lymph node cases. These results suggest the possibility that the translocation may occur in the reactive component of Hodgkin's disease and not in the putative malignant cells, the Reed-Sternberg cells. Furthermore, the detection of the translocation in reactive lymph nodes suggests that it may not be the primary factor in the oncogenesis of follicular lymphoma.
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PMID:Bcl-2 rearrangement in Hodgkin's disease and reactive lymph nodes. 820 65

The LAZ3/BCL6 gene on chromosome 3q27 is recurrently disrupted in B-cell non Hodgkin's lymphomas by translocations involving immunoglobulin genes or other chromosome regions. We have studied the t(3; 11) (q27; q23) translocation, present in a B-cell leukemia cell line (Karpas 231). As a consequence of this translocation, a LAZ3 chimeric transcript was created by fusion, 5' to the LAZ3 exon 2, with a transcribed sequence identical to BOB1/OBF1, a B cell-specific coactivator of octamer-binding transcription factors, recently described. Nucleotidic sequence of a nearly full-length cDNA of the BOB1/OBF1 gene revealed particular features in the 3' untranslated region of the gene, including pyrimidine-rich sequence repeats, an Alu motif, and a polymorphic [CCTT] tetranucleotide microsatellite. Two A to G transition mutations were also detected in the coding region of one allele of a lymphoma B-cell line, Raji, leading to 2 amino-acid changes in the C-terminal region. Due to its cell-specificity and role as a coactivating transcription factor, chromosomal translocation and/or perhaps point mutation of BOB1/OBF1 may contribute to B cell tumorigenesis.
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PMID:Fusion of the LAZ3/BCL6 and BOB1/OBF1 genes by t(3; 11) (q27; q23) chromosomal translocation. 857 89

The LAZ3/BCL6 gene on chromosone 3q27 is recurrently disrupted in B cell non-Hodgkin's lymphomas by translocations involving immunoglobulin genes or other chromosone regions. We have cloned the breakpoint region and chromosone derivatives of the t(3;11)(q27;q23.1) translocation, present in a B cell leukemia cell line (Karpas 231), which define a novel 11q23.1 breakpoint site. As a consequence of the translocation, LAZ3 regulatory regions upstream of non-coding exon 2 are replaced by those of BOB1/OBF1, a recently described B cell-specific coactivator of octamer-binding transcription factors. A detailed structural study of the BOB1/OBF1 genomic DNA and of a nearly full-length cDNA revealed particular features in the 3' untranslated region, such as an Alu motif and a polymorphic tetranucleotide microsatellite. Two mutations leading to two potential amino acid changes in the C-terminal region, were also detected in one allele of a lymphoma B cell line, Raji. Due to its cell-specific expression and role as a coactivating transcription factor, chromosomal translocation and/or point mutation of BOB1/OBF1 may contribute to B cell tumorigenesis.
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PMID:The B cell transcriptional coactivator BOB1/OBF1 gene fuses to the LAZ3/BCL6 gene by t(3;11)(q27;q23.1) chromosomal translocation in a B cell leukemia line (Karpas 231). 861 32

Although high-grade non-Hodgkin's lymphoma (NHL) and an unusually aggressive form of Kaposi's sarcoma (KS) remain the most common malignancies seen in AIDS patients, other tumors such as cervical cancer, Hodgkin's disease and others, have been increasingly observed, probably because these patients now live longer. We report the imaging findings of 80 AIDS patients with pathologically confirmed neoplasms from a series of 340 AIDS patients examined 1986-1994. Twenty-four of 80 patients had NHL, 4 Hodgkin's disease, 31 KS, 4 cervical cancer, 2 leukemia, 2 testicular, 1 larynx, 2 lung, 2 breast, 1 esophagus, 1 stomach, 1 liver, 2 kidney and 3 adrenal carcinomas. Twenty of 24 NHLs exhibited extranodal involvement--to the liver (13/24), brain (9/24), lung (7/24) and gastrointestinal tract (6/24). Visceral KS involved the gastrointestinal tract (6/32), lung (4/32) and liver (2/32). The most accredited pathogenetic theories concerning the role of HIV infection in oncogenesis advocate the effect of multiple growth factors produced by HIV-infected lymphocytes (KS) or the disregulation of B-cells caused by T-cell destruction (NHL). The atypical morphostructural features of AIDS-related tumors are discussed--e.g., atypical presentation, occurrence in younger individuals, aggressive clinical course and poor response to conventional therapy--together with the differential diagnostic problems, especially vs. opportunistic infections.
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PMID:[AIDS-related neoplasms: a clinico-radiological study]. 864 55

Substantial evidence indicates that several common viruses are clearly or probable causal factors in the etiology of specific malignancies. These viruses either normally establish latency or can become persistent infections. Oncogenesis is probably linked to an enhanced level of viral activation in the infected host, reflecting heavy viral dose or compromised immune control. The major virus-malignancy systems include hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatocellular carcinoma; human lymphotropic virus-type 1 (HTLV-1) and adult T-cell leukemia/lymphoma (ATL); Epstein-Barr virus (EBV) and endemic Burkitt's lymphoma, nasopharyngeal carcinoma, and Hodgkin's disease; and human papilloma virus (HPV) and cervical cancer. Of these, a vaccine is available only for HBV. These malignancies tend to occur in early to mid-life and account for a substantial amount of morbidity and person-years lost. They are also likely to occur as "opportunistic malignancies" among individuals infected with human immunodeficiency virus type-1, particularly among those who experience prolonged survival.
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PMID:Overview: viral agents and cancer. 874 95

One in 600 children 0-16 years of age develop cancer, and 60% to 70% of them are cured. Projection of the data indicates that by the turn of the century, 1 of every 900 individuals between the ages of 16 and 44 years will be a cancer survivor. In the adult population, carcinogens and irradiation play a major role in oncogenesis. In the pediatric population other factors are probably dominant. Children of low socioeconomic groups, with nutritional deficiencies, are more exposed to viral infections at a very early age and have a greater chance of developing tumors such as Burkitt lymphoma or mixed cellularity Hodgkin disease. Other factors such as hormone-assisted conception or in vitro fertilization may have carcinogenic potential, although this has yet to be determined. Maternal diet during pregnancy, especially low folic acid consumption periconception, may have bearing on the fetus's risk of developing malignancy. The hazards of exposure to electric and magnetic fields from high-voltage transmission lines, home electric appliances, video display terminals, or residence near nuclear plants, although very doubtful, are included in the list of cancer promoters in children. Activated oncogenes, mutated suppressor genes, mismatch repair genes, nucleotide excision genes, and loss of imprinting genes are beginning to evolve as important factors in carcinogenesis. The more in-depth information on genetic and environmental factors should provide new data on the evolution of pediatric tumors and possibly on their prevention.
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PMID:Pediatric cancer: environmental and genetic aspects. 883 38

The Epstein-Barr virus (EBV) latency C promoter drives expression of a family of viral proteins commonly targeted by CD8 cytotoxic T cells. These proteins are not generally expressed in African Burkitt's lymphoma and in EBV-associated Hodgkin's disease. The failure to express these proteins is almost certainly an important factor in the evasion of immunosurveillance by EBV-associated tumors. In a previous study, we have shown that transcriptional activation of the C promoter is inhibited by methylation of a particular CpG site upstream of the promoter that prevents binding of a cellular protein (CBF2), and we have shown that this and adjacent CpG sites are methylated in a Burkitt's lymphoma cell line. In the present study, we show that CpG sites in the CBF2 binding region are predominantly methylated in African Burkitt's lymphoma and in EBV-associated Hodgkin's disease. In addition, we present the first direct evidence that the C promoter is transcriptionally silent in Burkitt's lymphoma. In contrast, we show a complete absence of methylation in the CBF2 binding region in a case of reversible EBV-associated B-cell lymphoma arising in an immunocompromised patient whose tumor shows C promoter transcriptional activity. By inhibiting expression of highly antigenic viral proteins, methylation of transcriptional control sequences may veil the presence of virus in tumor tissue from CD8(+) cytotoxic T-cell immune surveillance and thus facilitate viral tumorigenesis.
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PMID:CpG methylation of the major Epstein-Barr virus latency promoter in Burkitt's lymphoma and Hodgkin's disease. 887 13

As the AIDS epidemic advances, the spectrum of malignancies encountered is expanding. Several non-AIDS-defining cancers are seen in increased incidence in HIV-infected patients. These include basal cell carcinoma of the skin, squamous cell carcinoma of the anus, Hodgkin's disease, seminoma, and pediatric leiomyosarcoma. There appears to be an emerging role for various concurrent viral infections in the HIV-infected host that are likely implicated in the pathogenesis of AIDS-related neoplasms. It will be important to track the epidemiologic and biologic features of non-AIDS cancers in HIV-infected patients. It is likely that further clues about malignant transformation and oncogenesis unraveled in this setting will have broader clinical implications.
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PMID:Non-AIDS-defining cancers. 888 Feb 6


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