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

The typical tissue isoferritin pattern varies during neoplastic transformation, usually shifting toward a more acidic profile. To investigate the molecular basis of this phenomenon, we have analyzed the steady-state levels of the H and L mRNAs in several neoplastic tissues. By using specific probes for the two ferritin subunits, we have found, in three different adenocarcinomas and in a case of Hodgkin lymphoma, a two- to four-fold increase of the H and L mRNA levels compared to those found in normal human liver.
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PMID:Ferritin H and L mRNAs in human neoplastic tissues. 338 36

The phenotypic expression of Hodgkin's and Reed-Sternberg (H-RS) cells was determined by analysis with a panel of monoclonal antibodies and peanut agglutinin (PNA) by an immunohistochemical technique. Seven antibodies, including T200, anti-HLA-DR, anti-Leu 10, A1G3, anti-Tac, OKT9, and anti-Leu M1, were found to react with a great majority of H-RS cells. In some cases, H-RS cells also bound PNA. Other antibodies, including those highly specific for T cells (eg, Lyt 3) and B cells (eg, B1, anti-Leu 14) were consistently negative. The results argue against the derivation of H-RS cells from T or B lymphocytes. The H-RS cells were also negatively stained with antibodies which react with monocytes (OKM1, Mo-2, 63D-3), follicular dendritic cells (DRC-1), and natural killer/killer cells (Leu 7, Leu 11a, B73.1). The presence of Leu M1 and Tac in H-RS cells is of interest. Anti-Leu M1 positivity was seen in all 20 of Hodgkin's disease (HD) cases tested and should provide a very useful reagent for differential diagnosis of HD from other reactive and neoplastic conditions. Tac normally is present only on activated T cells. The presence of Tac in H-RS cells may reflect expression of T-cell growth factor receptor or a closely related protein during a stage of neoplastic transformation. Although the nature of the neoplastic cell of HD cannot be determined by these studies, they are consistent with an origin from interdigitating reticulum cells. Both H-RS cells and interdigitating reticulum cells have a similar antigenic phenotype (Leu M1+, T200+, HLA-DR+, Leu 10+, A1G3+, and OKT9+) and a similar pattern of lysosomal enzyme activity.
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PMID:Phenotypic expression of Hodgkin's and Reed-Sternberg cells in Hodgkin's disease. 397 Jan 38

Although supported by a number of experimental models, the assumption assigning a crucial role to the immune system in the antineoplastic defense mechanisms has not been convincingly demonstrated so far for human tumors. Should the theory be correct, severe functional impairment of the immune system would obviously result in the occurrence of tumors with abnormally high frequency. Registry holdings systematically collecting pertinent information on the malignancies developed in patients with primary immunodeficiency diseases or in organ transplant recipients maintained on therapeutically-induced immune depression, as well as the observation of tumors occurring in patients treated with immunosuppressive agents and of second malignancies arising after radio- and/or chemotherapy of the primary tumor consistently indicate that depressed immunity is usually associated with an increased incidence of cancer as compared with that expected in the general control populations. However, not all types of tumors are increased to the same extent, in that lymphoreticular neoplasias (especially non-Hodgkin's lymphomas), acute leukemias as second tumors and, among solid neoplasms, squamous cell carcinomas are those most frequently reported. These observations suggest that even deeply impaired tumoricidal immune mechanisms may facilitate the growth of certain tumors only, especially of those arising from the cells of the immune system itself, in remarkable contrast with their frequency in the general population. Oncogenesis may be favoured in various states of depressed immunity by a number of ways. Their elucidation might have bearing on the comprehension of the more general phenomenon of the neoplastic transformation.
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PMID:[Immunological deficiency syndromes, immunosuppression by drugs and occurrence of neoplasms: a casual association?]. 409 54

A five-step hypothesis on the pathogenesis of Hodgkin's disease (HD) is presented. Weak immune suppressor activity gives a predisposition for the development of the disease, after which a non-specific immune stimulation can initiate a self-perpetuating uncontrolled stimulation between interdigitating cells (IDCs), macrophages and helper T lymphocytes (TH). The disease spreads to other lymph nodes through the secretion of humoral factors and by migration of cells. The response of the suppressor branch of the immune system is delayed, and comes from areas not yet involved in the disease, primarily from the spleen and bone marrow. Treatment will result in the predominance of the suppressor activity and allow calming of the disease. In a terminal phase, a possible neoplastic transformation of the chronically stimulated immune cells may give rise to frequent extranodal localizations and a rapid progression of the disease.
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PMID:Hodgkin's disease: five steps from autoimmunity to cancer. 624 Dec 90

A 74-year-old man developed a locally invasive malignant fibrous histiocytoma of the scalp with multiple facial recurrences and concomitant hematopoietic dysplasia occurring over a 2-year period. One month prior to his death, his hematologic profile evolved into myelomonocytic leukemia. Mixed cellularity Hodgkin's disease involving mediastinal and periportal lymph nodes, which was not suspected antemortem, was discovered at autopsy. In the experience of the authors, this association of neoplasms is unique and raises the possibility in this case of an unidentified stimulus to neoplastic transformation of cells of histiocyte/monocyte origin.
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PMID:Malignant fibrous histiocytoma, myelomonocytic leukemia, and Hodgkin's disease arising in an elderly man. 632 65

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

Epidemiologic studies show that non-Hodgkin's lymphomas tend to develop after prolonged antigenic stimulation, after loss of normal regulation of lymphoid proliferation, or especially after both processes. Study of these tumors in vitro has greatly increased understanding of their pathophysiology and has provided a conceptual framework for their morphologic diversity. Lymphomas are now understood to be expanded clones of their normal counterparts. The anatomic location, phenotypic characteristics, proliferative capacity, and functional capabilities of the neoplasm often reflect those of the equivalent normal cells. If neoplastic transformation can occur at any stage of lymphoid differentiation, then it is theoretically possible that neoplastic lymphocytes may respond, or could be induced, to normal regulatory influences. Further study of selective cytotoxicity may reveal exploitable differences among lymphocytic subpopulations and permit more rational choices of therapy. Of major aid to future clinical trials should be the recent consensus on nomenclature by an international panel of experts.
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PMID:NIH conference. A multidisciplinary approach to non-hodgkin's lymphomas. 700 68

Recent studies have indicated that nodular lymphocyte predominance Hodgkin's disease (nLP-HD) is a B-cell lymphoma. Although molecular events in the neoplastic transformation of B-cells are not well understood, Epstein-Barr virus infection and bcl-2 protein overexpression have been postulated to have etiologic roles in some lymphomas. Epstein-Barr virus has been demonstrated in the Reed-Sternberg cells of Hodgkin's disease cases (other than nLP-HD) as well as in some B-cell lymphomas; bcl-2 overexpression is found in the majority of follicular lymphomas. The biologic role for bcl-2 in HD is controversial. Some reports have indicated the presence of bcl-2 gene rearrangements, associated with the t(14;18) (q32;q21), detected by the polymerase chain reaction in HD; recent studies have failed to confirm this finding. Reports in the literature describe only a few such analyses in the nLP-HD subtype. To address these conflicting issues, we examined 12 cases of nLP-HD to determine whether bcl-2 protein expression (by immunohistochemistry) and Epstein-Barr virus (by in situ hybridization) could be detected in the Reed-Sternberg variants. None of the cases showed expression of bcl-2 protein or Epstein-Barr virus RNA in the neoplastic cells. Epstein-Barr virus does not appear to play an important role in the pathogenesis of nLP-HD. Similarly, we cannot substantiate a role for bcl-2 in the development of this type of Hodgkin's disease.
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PMID:Epstein-Barr virus and bcl-2 protein overexpression are not detected in the neoplastic cells of nodular lymphocyte predominance Hodgkin's disease. 767 75

We recently characterized a novel putative intermediate-filament associated protein which is strongly expressed in the Reed-Sternberg cells of Hodgkin's disease. Therefore we named the protein 'restin', an acronym for Reed-Sternberg cell intermediate filament-associated protein. The protein is also expressed in anaplastic large cell lymphoma or Ki-1 lymphoma, a non-Hodgkin's lymphoma phenotypically related to Hodgkin's disease. Although the functions of restin are not yet fully elucidated, transfection experiments demonstrate that overexpression of the protein increases cell growth by a mechanism which may involve upregulation of the transferrin receptor. Hence, restin may contribute to neoplastic transformation in Hodgkin's disease and anaplastic large cell lymphoma. Study of the mechanisms leading to restin overexpression may provide important data on the etiology of Hodgkin's disease and its relation to anaplastic large cell lymphoma.
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PMID:Restin in Hodgkin's disease and anaplastic large cell lymphoma. 816 33

In view of their reported reciprocal effects on apoptosis, the expression of p53 and bcl-2 proteins was studied in 46 cases of Hodgkin's disease by immunocytochemical labeling. We found p53 protein in Reed-Sternberg cells and their mononuclear variants in 16 of the 46 cases (34.7%) of Hodgkin's disease, mainly in a nuclear pattern. This restricted expression on Reed-Sternberg cells and variants supports their neoplastic nature. This overexpression of p53 protein in one third of Hodgkin's disease cases is similar to that seen in many other human malignancies. bcl-2 protein was present in mantle zone B cells and scattered T cells in all cases, and in 17 cases (37.7%) of Hodgkin's disease in Reed-Sternberg cells and their mononuclear variants. Six cases coexpressed both proteins, whereas in 18 cases neither was identified. There is no apparent relationship between p53 and bcl-2 protein expression, and on the basis of the present results there is no reason to suppose that they have any particular complementary effects on the neoplastic transformation in Hodgkin's disease.
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PMID:An immunocytochemical study of p53 and bcl-2 protein expression in Hodgkin's disease. 832


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