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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-random chromosome abnormalities have been found in all types of malignant lymphomas. It is obvious that some cytogenetic abnormalities are associated with certain morphological types. Thus, among the Burkitt's lymphomas the 2;8-, 8;14- and 8;22-translocations are found in the great majority of cases; t(14;18) is associated with follicular lymphomas; +12 and t(11;14) with well differentiated lymphomas; and rearrangements of 14q11 and trisomy 3 with T-cell lymphomas. The molecular changes involving the c-myc oncogene and the immunoglobulin loci in Burkitt's lymphoma have been intensively studied. Among other non-Hodgkin's lymphomas the molecular mechanisms behind t(11;14) and t(14;18) in B-cell lymphomas and 14q11 rearrangements in T-cell lymphomas are starting to be unravelled. A number of other aberrations, such as +3, 6q-, and +12, have been associated with non-Hodgkin's lymphoma although the molecular mechanisms behind these rearrangements are still unknown. Very little is known about clinicocytogenetic correlations, but some observations clearly indicate that the karyotypic pattern is an important prognostic factor in non-Hodgkin's lymphoma. Contrary to non-Hodgkin's lymphoma, very little is known about the cytogenetic findings in Hodgkin's disease. The sparse results, however, indicate that there are similarities to those in non-Hodgkin's lymphoma.
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PMID:What's new in lymphoma cytogenetics? 336 47

We have shown that the human cellular oncogene c-myc is composed of three exons and is transcribed from two initiation sites separated by 175-base-pair DNA in HeLa cells. For both resulting mRNA species, exon 1 composes the 5' untranslated region and the initiator methionine is located 16 base pairs down-stream from the 5' splice acceptor of exon 2. In a non-Hodgkin lymphoma, Manca, harboring a t(8; 14) translocation, c-myc gene is broken within intron 1, and its exons 2 and 3 are translocated to a site between the heavy chain joining region cluster and C mu-coding DNA segment of the immunoglobulin heavy chain locus. The translocated c-myc gene is transcribed from points within intron 1 but is apparently still translated from the same methionine codon as the mRNA from the unrearranged c-myc gene. The nucleotide sequence of the c-myc gene shows that a region of exon 1 is highly complementary to a region of exon 2. Thus the mRNA from the untranslocated c-myc gene, as opposed to that of the translocated c-myc gene, could form a stable stem-loop structure (delta Go = -90 kcal/mol; 1 cal = 4.184 J) where the initiator AUG would be located within the loop. In view of the bind-and-scan model for the initiation of eukaryotic translation, we propose that such a secondary structure will severely hinder the translation. We further propose that the c-myc gene is often activated by translocation through the escape from such a translational suppression.
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PMID:Activation of the c-myc gene by translocation: a model for translational control. 632 75

c-myc is the cellular gene homologous to the transforming sequence of MC29, an acute avian retrovirus. The human c-myc gene was cloned and used to study the structure and expression of c-myc in a variety of human hematopoietic malignancies. In a careful study of 106 patients, c-myc RNA was found to be expressed at elevated levels in tumor cells of 17 leukemia patients and five lymphoma patients. The c-myc gene was found to be rearranged in two lymphomas, an African Burkitt's lymphoma and a non-Hodgkins lymphoma in leukemic phase. The Burkitt's rearrangement involved the insertion of new DNA sequences upstream from the c-myc 5' coding region, presumably replacing the normal c-myc transcriptional promoter. None of the other 104 patients, including 20 with elevated myc expression, exhibited any evidence of a genetic rearrangement involving the c-myc gene. Our results show that there is a subset of hematopoietic malignancies characterized by elevated expression of c-myc. This elevated expression in most cases is not due to obvious genetic changes (rearrangement, amplification) at the c-myc locus nor to chromosomal translocations in the vicinity of this gene.
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PMID:Structure and expression of the oncogene c-myc in fresh tumor material from patients with hematopoietic malignancies. 633 May 29

We have used in situ chromosome hybridization techniques to map the human cellular counterparts (c-onc genes) of the transforming genes of two RNA tumor viruses on human meiotic pachytene and somatic metaphase chromosomes. We find that the human c-mos gene is located on chromosome 8 at a position corresponding to band 8q22 on the somatic map. The human c-myc gene is found on chromosome 8 at position 8q24. These regions on the long arm of chromosome 8 have been previously reported to be involved in specific translocations found in the M-2 subset of acute nonlymphoblastic leukemias. Burkitt lymphoma, and other forms of non-Hodgkin lymphoma, and a familial abnormality that predisposes to renal cell carcinoma. These results suggest that translocations of the human c-mos or c-myc genes may be causally related to neoplastic transformation.
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PMID:Two human c-onc genes are located on the long arm of chromosome 8. 696 56

Diffuse large B cell lymphomas (DLBLs) represent a heterogeneous collection of aggressive non-Hodgkin's lymphomas that can arise either de novo or as a result of transformation from chronic lymphocytic leukemia, small lymphocytic lymphoma, follicular lymphomas, or lymphomas of mucosa-associated lymphoid tissue. A small percentage of DLBLs express the CD5 antigen. The majority of these cases have evolved from a pre-existing low grade non-Hodgkin's lymphoma (Richter's syndrome). However, we identified and characterized nine CD5-positive DLBLs in which the patients did not have a previous history or concomitant evidence of chronic lymphocytic leukemia, small lymphocytic lymphoma, follicular lymphoma, or mucosa-associated lymphoid tissue-associated non-Hodgkin's lymphoma, suggesting that they arose de novo. All nine cases expressed CD20 and monotypic immunoglobulin, all eight cases examined expressed CD19, CD22 and CD43, eight of the nine cases expressed HLA-DR, and two of eight cases expressed CD11c. None of the cases expressed CD3, CD10, CD11b, CD21, CD23 or CD30. CD5 expression by these cells was found to be identical to that of CD5-positive B cell chronic lymphocytic leukemia by quantitative polymerase chain reaction analysis of CD5 mRNA. These nine de novo CD5-positive DLBLs exhibited clonal immunoglobulin heavy and light chain gene rearrangements but lacked integration of the Epstein-Barr virus genome and structural alterations of the bcl-1, bcl-2, c-myc, H-ras, K-ras, and N-ras proto-oncogenes and the p53 tumor suppressor gene. However, bcl-6 proto-oncogene rearrangement, which is involved in chromosome band 3q27 aberrations, was found in four cases (44.4%). This is comparable with the frequency of bcl-6 gene rearrangement in CD5-negative DLBL. In contrast, bcl-6 gene rearrangement was absent in six cases of DLBL associated with Richter's syndrome. These findings suggest that de novo CD5-positive DLBLs are genotypically similar to CD5-negative DLBLs and may be pathogenetically distinct from the DLBLs associated with Richter's syndrome.
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PMID:De novo CD5-positive and Richter's syndrome-associated diffuse large B cell lymphomas are genotypically distinct. 754 11

Among extranodal non-Hodgkin's lymphomas, primary cutaneous lymphomas (CLs) represent a consistent group of B- and T-cell malignancies. We investigated the arrangement of Ig and T-cell receptor (TCR) genes, together with the involvement of several oncogenes and the tumor-suppressor gene p53, in a panel of primary cutaneous B- and T-cell lymphomas (CBCLs and CTCLs). Southern blot analysis was performed to detect rearrangements of the Ig, c-myc, bcl-1, bcl-2, bcl-3, bcl-6, and the NFKB2/lyt-10 genes in 52 cases of CBCLs and of the TCR, bcl-3, and NFKB2/lyt-10 genes in 38 cases of CTCLs. tal-1 gene deletions were analyzed in CTCLs by means of polymerase chain reaction (PCR). p53 gene mutations were assayed using PCR, single-strand conformation polymorphism analysis, and direct DNA sequencing in CBCL and CTCL cases. Clonal rearrangements of Ig genes or oncogenes were found in 25 of the 52 CBCLs. In particular, we detected rearrangements of the bcl-1 locus (2 cases), the bcl-2 gene (2 cases), the NFKB2/lyt-10 gene (2 cases), and the bcl-6 gene (1 case); interestingly, 4 of these cases showed a germline arrangement of the Ig genes. Clonal rearrangements of TCR genes were detected in 37 of the 38 CTCLs. Rearrangements of the NFKB2/lyt-10 gene were present in 2 cases and tal-1 gene deletions in 3 CTCL cases; p53 gene mutations were detected in 1 CTCL case. Overall, our data indicate that (1) clonal rearrangement of Ig genes is frequently undetectable by means of Southern blot in CBCLs (60%); (2) genetic lesions are involved in a limited but significant fraction of primary CLs showing a molecular marker of clonality (13/62; 20%); and (3) rearrangements of the bcl-1, bcl-2, or bcl-6 loci, associated with specific subsets of nodal lymphoid neoplasias, are rarely observed in CBCLs. Moreover, our results suggest that tal-1 gene deletions may play a pathogenetic role in non-acute T-cell malignancies and that, in the context of lymphoid malignancies, CLs may represent a favorable target for the possible oncogenic potential of the NFKB2/lyt-10 gene.
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PMID:Molecular analysis of cutaneous B- and T-cell lymphomas. 757 11

Epstein-Barr virus (EBV) encodes genes that permit its persistence in human B lymphocytes and genes that ensure its replication in epithelial cells. Immune restraints on the virus are usually so effective that most EBV infections are limited to a minute fraction of B lymphocytes and of epithelial cells. As a result, most EBV infections are never symptomatic. Occasionally, the virus causes disease, often with the cooperation of the immune system or other less characterized cofactors. Infectious mononucleosis, a generally self-limited lymphoproliferative illness common in adolescents and young adults, is due to primary EBV infection and to the brisk cellular immune response it elicits. Lymphoproliferative disorders of EBV-infected B cells arise almost exclusively when cellular immunity is grossly compromised. EBV-positive Burkitt's lymphoma contain a translocated and deregulated c-myc oncogene and EBV-positive non-Hodgkin's lymphomas are characterized by the presence of Reed-Sternberg's and Hodgkin's cells, features that have not been directly linked to EBV. Many recent observations, however, including evidence that virus infection precedes malignant transformation and is often associated with a characteristic pattern of viral gene expression, provide continued interest in the relationship between the virus and these haematological malignancies.
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PMID:Epstein-Barr virus as an agent of haematological disease. 766 46

The oncogenes c-myc and c-ras are known to elicit a cooperative tumorigenicity. In this study we investigated their role in the pathogenesis of Hodgkin's disease. The expression of these oncogenes was determined in Hodgkin's disease patients by avidin-biotin peroxidase complex immunohistochemical staining and was compared to their expression in patients with non-Hodgkin's lymphomas and inflammatory reactive lymph nodes. Of 29 examined patients with different histological types of Hodgkin's disease, 21 (72.4%) showed an elevated expression of c-myc and 28 (96.5%) of c-ras. Although this expression was marked especially in the neoplastic Reed-Sternberg cells, it was also noted in the numerous reactive cells present in the involved lymph nodes. By contrast, a much lower frequency of increased expression of these oncogenes was recorded in 19 patients with different grades of non-Hodgkin's lymphoma and in 29 patients with inflammatory reactive lymph nodes. The elevated expression of c-myc and c-ras in the neoplastic Reed-Sternberg cells may reflect an oncogenic event that directly activates these genes. However, their increased expression in the surrounding non-neoplastic cells probably results from signal transduction induced by certain growth-promoting factors possibly released by the Reed-Sternberg cells and that act paracrinally to stimulate the proliferation of the neighboring cells. Furthermore, the continuous c-ras elevation may impair the normal cell cycle control and thereby promote mutagenesis and overt malignancy.
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PMID:Expression of c-myc and c-ras oncogenes in the neoplastic and non-neoplastic cells of Hodgkin's disease. 767 90

Proliferating cell nuclear antigen (PCNA) and c-myc p62 oncoprotein are two nuclear proteins expressed in proliferating and transformed cells. They can be recognized immunohistochemically in paraffin sections by the monoclonal antibodies PC-10 and c-myc 1-9E10, respectively. On the other hand, nucleolar organizer regions (NORs) are loops of DNA that carry the r-RNA genes and can be visualized in paraffin sections as black dots (AgNORs) using a silver impregnation method. It has been suggested that the mean number of AgNORs may reflect the cellular kinetics of a tumor. We independently examined 200 cases of non-Hodgkin's lymphomas using the monoclonal antibodies PC-10 and c-myc 1-9E10, as well as the AgNOR method. Our study shows a very significant correlation between PCNA, c-myc expression, and AgNOR count on the one hand and histologic grade on the other (P < .001), although a significant overlap among the three grades exists. PC-10, c-myc 1-9E10, and AgNOR scores are all shown to be linearly related, even though significant discrepancies were observed, and the correlation is stronger between PCNA and AgNORs (PCNA v c-myc p62, r = .551; PCNA v AgNORs, r = .746; c-myc p62 v AgNORs, r = .529; P < .001). A remarkable finding is that the intermediate group of lymphomas is heterogeneous as far as the proliferative rate is concerned: diffuse large cell cleaved/non-cleaved lymphomas (category G of the Working Formulation) are characterized by a significantly higher proliferative index, as evidenced by the elevated PCNA, c-myc p62, and AgNOR scores, in comparison with the other types of intermediate-grade lymphomas (P < .001). However, the proliferative rate is lower than that of the high-grade lymphomas (PCNA, P < .05; c-myc p62, P < .001; AgNORs, P < .005). No significant difference exists between B-cell and T-cell lymphomas except for the higher expression of c-myc p62 in intermediate-grade B-cell lymphomas, obviously due to the higher proliferative rate of diffuse large cell lymphomas. Based on our findings, it appears that the combination of PCNA, c-myc p62, and AgNORs provides an accurate estimate of the proliferative rate of non-Hodgkin's lymphomas in paraffin sections. Clinical studies may show whether this information has prognostic value independent of histologic classification. In addition, our results suggest that category G (diffuse large cell) lymphomas may belong to a malignancy grade higher than the intermediate grade, a suggestion consistent with their more aggressive biologic behavior.
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PMID:A comparative assessment of proliferating cell nuclear antigen, c-myc p62, and nucleolar organizer region staining in non-Hodgkin's lymphomas: a histochemical and immunohistochemical study of 200 cases. 768 20

The occurrence of HIV associated non-Hodgkin's lymphoma (NHL) is a well recognized event. HIV associated Hodgkin's disease (HD) has also been observed. A unique patient with both entities is described. The patient was a 29 year old homosexual male who developed clinical IIA nodular sclerosis HD in 1985. He was HIV + with CD4/CD8 = 0.2 and his sister had HD 20 years earlier. He received MOPP and had a complete response. In October 1988 he developed weight loss with an abdominal mass and biopsy revealed diffuse small non-cleaved NHL, with bone marrow involvement. This was his first AIDS associated illness. Probes identified clonally rearranged DNA fragments in the J region of IgH chains and clonal rearrangements in the c-myc gene were also observed but EBV sequences could not be demonstrated. He was treated with m-BACOD but died in March 1989. His course was not complicated by opportunistic infection. Possible etiologies for the HD include his HIV status or shared sibling environment. The development of the NHL may have resulted from HIV infection and/or secondary to his treatment for HD. The relationship between the two lymphomas is uncertain and factors other than HIV exposure and its immune dysfunction may have been causal.
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PMID:Hodgkin's disease and non-Hodgkin's lymphoma in an HIV positive patient. 768 28


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