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)

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

Between January 1978 and December 1982 successful sequential chromosome analyses were carried out on bone marrow cells of five patients previously treated for Hodgkin's lymphoma (HL) presenting unexplained cytopenia or pancytopenia during follow-up. All patients had concurrent morphological examination of bone marrow specimens showing signs of dysplasia and/or hypoplasia, without leukaemic infiltrate. Six other patients treated for HL who had normal haematological parameters served as controls. All the patients with unexplained cytopenias had clonal chromosome abnormalities; monosomy for chromosome No. 5 was the most frequent. No abnormalities were detected in the control group. Two patients have evolved to resistant leukaemia, one died of sepsis before leukaemic conversion while severely neutropenic, and two are in full marrow and cytogenetic recovery after aggressive anti-leukaemic treatment in the pre-leukaemic phase. Our data suggest that cytogenetic studies may be of crucial value in detecting therapy-induced preleukaemia (t-PL) at an early stage of its evolution and in planning appropriate therapy before the establishment of overt leukaemia.
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PMID:Therapy-induced preleukaemia in patients treated for Hodgkin's lymphoma: clinical and therapeutic relevance of sequential chromosome banding studies. 646 72

Normal cross-reacting antigen, a glycoprotein that shares some antigenic determinants with carcinoembryonic antigen, was consistently demonstrated by tissue immunoperoxidase staining in the cytoplasm of both non-neoplastic and neoplastic neutrophilic granulocytes. It was absent in lymphoid cells, but occasional cells of the macrophage/histiocyte series showed variable staining. Malignant cells from patients who had non-Hodgkin or Hodgkin lymphomas were negative for normal cross-reacting antigen. These findings were in contrast to the findings of specific normal cross-reacting antigen positivity in neoplastic granulocytes from three patients who had acute granulocytic leukemia, three who had chronic granulocytic leukemia, and one who had a granulocytic sarcoma. Similar normal cross-reacting antigen positivity was also seen in granulocytes from two patients who had granulocyte dysplasia. It is suggested that direct tissue visualization of normal cross-reacting antigen using immunoperoxidase technics may be of value in the classification and diagnosis of hematologic malignancies, and may provide an additional marker for cells of the granulocytic series.
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PMID:Direct tissue visualization of normal cross-reacting antigen in neoplastic granulocytes. 698 61

A recently described splice variant of CD44 has been shown to confer metastatic potential to non-metastasizing rat pancreatic carcinoma and sarcoma cell lines. Using antibodies raised against a bacterial fusion protein encoded by variant CD44 sequences, we have explored the expression of variant CD44 glycoproteins in human lymphoid cells and tissues, in non-Hodgkin's lymphomas, and in colorectal neoplasia. Normal lymphohematopoietic cells express barely detectable low levels of variant CD44 glycoproteins, while T lymphocytes, upon activation by mitogen or antigen, transiently upregulate expression of specific CD44 variant glycoproteins. The reaction pattern of various antibodies indicates that these CD44 variants contain the domain encoded by exon v6, which is part of the variant that in the rat confers metastatic capability. Interestingly, overexpression of v6 was also found in several aggressive, but not in low-grade, non-Hodgkin's lymphomas (NHL). In human colorectal neoplasia we also observed strong overexpression of CD44 splice variants in all invasive carcinomas and carcinoma metastasis. Interestingly, focal expression was already observed in adenomatous polyps, expression being related to areas of dysplasia. The findings establish CD44 variants as tumor progression markers in colorectal cancer.
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PMID:CD44 splice variants: expression during lymphocyte activation and tumor progression. 750 54

We describe a family in which two sisters with the autosomal dominant skeletal dysplasia, Leri-Weill dyschondrosteosis (LWD), developed Hodgkin's disease (HD) in late adolescence. In a preliminary attempt to identify HD susceptibility gene(s), HLA-typing and linkage analysis were carried out in the family. Using HLA molecular typing, both sisters were found to have inherited a variant of the HD-susceptibility allele, DPB1*0301, known as DPB1*2001. Following a previous report of a constitutional chromosome translocation (t(2q;8p)) in a family with LWD, preliminary linkage studies were carried out using chromosome 2q and 8p molecular markers. Regions covered by 7/10 chromosome 2 markers and 4/8 chromosome 8 markers were excluded as the location of a candidate LWD gene. Given the rarity of LWD and HD, their simultaneous occurrence is unlikely to have been due to chance. We suggest that a mutation in the LWD gene itself, or a gene closely linked to it, perhaps acting with increased susceptibility to infection conferred by DPB1*2001, resulted in HD in the two sisters.
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PMID:Molecular genetic analysis of a family with a history of Hodgkin's disease and dyschondrosteosis. 776 45

Autopsy findings for two patients with the Nijmegen breakage syndrome (NBS) are presented. This syndrome has the same type of immunologic and cytogenetic abnormalities as ataxia telangiectasia (AT). In NBS, however, microcephaly is found and progressive cerebellar ataxia and oculocutaneous telangiectasia are lacking. We demonstrate a clear neuropathologic difference between these two syndromes, as the diffuse cortical cerebellar degeneration characteristic of AT was absent in NBS. In the thymus the histologic picture was suggestive of simple dysplasia. Lymphoid tissues were slightly atrophic but otherwise structurally normal. In one of the two presented cases an extranodal diffuse large cell malignant non-Hodgkin lymphoma of B cell immunoblastic type was found in Waldeyer's ring, in the small and large intestines, and in the brain, whose sequelae had caused death. Six of the 19 patients known with certainty to have this syndrome have developed lymphoid malignancy, which indicates that these patients are prone to develop malignancies.
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PMID:Postmortem findings in the Nijmegen breakage syndrome. 780 77

Antigen receptor gene rearrangement studies are a sensitive means of determining lineage and clonality in lymphoproliferative disorders (LPDs) which remain difficult to classify after assessment of morphology and immunohistochemistry (IHC). This study investigates the utility of genotyping LPDs in a surgical pathology laboratory servicing a large teaching hospital. Ninety-eight specimens with detailed frozen (FS) and/or paraffin section IHC were studied, including 65 B-cell lymphomas, 14 T-cell lymphomas, 2 biopsies of T-zone dysplasia, one unclassifiable lymphoma, 8 Hodgkin's disease (HD) and 8 reactive nodes. Southern blotting (SB) was performed on tumor and control DNA cleaved with restriction enzymes EcoR1, Hind III and BamH1, using radiolabelled probes for the immunoglobulin heavy chain joining region, constant regions of kappa and lambda light chains, and the constant region of the T-cell receptor beta chain. All reactive nodes and those harbouring HD and DNA in the germline configuration, apart from JH rearrangement in one case each of HD and florid reactive hyperplasia. Of the non-Hodgkin's lymphomas (NHL), 17% did not reveal clonal rearrangements (11% B-NHL; 44% T-NHL). Most of the negative results could be explained by sampling error in partially involved nodes, highly polymorphous infiltrates where the neoplastic population may have been below the 1% threshold detectable by SB, and instances of anaplastic large cell lymphoma. After accounting for these cases, a 5% negative rate of genoclonality remained (3% B-NHL; 13% T-NHL). In the majority of NHL (95%), the diagnosis could be established on the basis of morphology and/or IHC alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Southern blot analysis of lymphoproliferative disorders: use and limitations in routine surgical pathology. 799 Dec 81

Anorectal lesions in patients carrying the HIV virus are uncommon (13%, in our personal life, 1 women/15 men). The following raise the possibility of AIDS: Kaposi sarcoma, non Hodgkin's lymphoma and also with the young patients, intraepithelial dysplasia, in situ carcinoma or squamous carcinoma of the anus. Other anorectal lesions encountered in proctology, should lead to suspicion of HIV infection: anal involvement in STD, florid papillomatosis, the most frequent lesion in his serious form which recur on a interminable bases, extensive and chronic herpes, lesions refractory to standard treatment, megalovirus and ulcers. Date by history indicating sexual habits, toxicomania as well as the existence of chronic diarrhea and full physical examination scoking enlarged lymph nodes are all factors to be taken into consideration in support of the diagnosis. Apart from painful emergencies justifying immediate surgery, indications for surgery should be weighed in terms of the patient's general condition, the stage of advancement of the disease and expected benefit in terms of patient comfort.
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PMID:[Update of anal-perineal and rectal lesions observed in AIDS]. 801 11

Infection with human immunodeficiency virus type 1 (HIV-1) primarily involves a subgroup of T-lymphocytic cells, but other cell types are also invaded by the virus, including cell lines within the haematopoietic system. Together with infectious, inflammatory and neoplasic processes, invasion of haematopoietic tissue explains the haematological alterations which are seen during the course of infection with HIV-1. Anaemia develops in the large proportion of patients. Thrombocytopenia frequently occurs during the course of the disease, but may be seen in some patients already at the time of diagnosis, where the condition may be misdiagnosed as "idiopathic" thrombocytopenic purpura. Neutropenia is seen in all disease stages, but is most severe in patients with advanced disease. Bone marrow changes include varying degrees of dysplasia in one or more cell lines, which in some patients may mimic a myelodysplastic syndrome. The number of plasma cells is always increased. In many patients the bone marrow stroma exhibits an increased amount of reticular fibres. HIV-1 infection is associated with an increased risk of non-Hodgkin malignant lymphoma. Acute myelogenous leukaemia and myelomatosis have been described in patients with advanced disease. Treatment of the above mentioned haematological abnormalities aims primarily at reducing replication of HIV-1, thereby diminishing suppression of haematopoiesis by the virus infection, and at controlling the opportunistic infections during the course of the disease. Specific antiviral therapy (AZT) is most successful in correcting thrombocytopenia. The possibility of bone marrow suppression mediated by a toxic drug effect should always be considered in this patient group.
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PMID:[Hematological changes associated with human immunodeficiency virus (HIV-1) infection]. 831 70

The messenger RNA level of several MAGE genes, some of which have been proven to encode tumor rejection antigens recognized by cytotoxic T lymphocytes, were examined in 41 benign and malignant lesions of the head and neck region. By a reverse transcription-polymerase chain reaction assay and Southern blot hybridization, MAGE-1, -2, -3, -4, and -6 genes were expressed in 25%, 41.7%, 33.3%, 8.3% and 33.3% of 12 non-squamous cell carcinomas, respectively. These tumors consisted of 6 papillary adenocarcinomas, 3 adenoid cystic carcinomas, 2 adenocarcinomas, and 1 mucoepidermoid tumor. Of 7 non-Hodgkin's lymphomas, one case from the oropharynx and 2 from the nasopharynx expressed for the MAGE-1 and MAGE-2 genes, respectively. In contrast, none of 12 benign tumors expressed any of these MAGE genes. Interestingly, of 10 other lesions including hyperplasia, keratosis, and ulcer, one histologically diagnosed as dysplasia expressed the MAGE-2, -3, -4, and -6 genes. These results suggest that the MAGE genes may be expressed in malignant tumors and precancerous lesions but not in benign tumors. In addition, non-squamous cell carcinomas may be suitable targets for specific immunotherapy against MAGE gene products.
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PMID:Expression of the MAGE-1, -2, -3, -4, and -6 genes in non-squamous cell carcinoma lesions of the head and neck. 883 54


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