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)

Among annually 1000 consultation cases of soft tissue tumors, minimally 1.2% to maximally 2% malignant lymphomas could be identified, which presented as (primary) soft tissues tumor. Thus malignant lymphoma as soft tissue tumor is rare, however, it has to be considered in differential diagnosis not only of cellular round cell sarcoma, but also with undifferentiated carcinomas (large cell Ki-1 lymphomas) and various myxoid spindle cell sarcomas (sarcomatoid lymphoma). Decisive in differential diagnosis were decorations with pan-leucocyte antibody, as well as, B- and T-cell markers. All cases turned out to be non-Hodgkin lymphomas, the majority of B-cell type, with large cells which qualified as centroblasts (according to Kiel classification). Similar findings, predominance of B-cell non-Hodgkin lymphomas with large cells, were reported in the few series published of malignant lymphomas as soft tissue tumors. Remarkable were relatively good prognosis with "highly malignant" morphology and preference for involvement of soft tissue even after dissemination. Future studies are requested to shed light on possible specific cellular findings as to phenotype and genotype in malignant lymphoma presenting as soft tissue tumors, as already had been done with subcutaneous T-cell lymphoma and primary lymphoma of the bone.
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PMID:[Malignant lymphomas of soft tissues]. 128 46

The Ki-1 antibody not only detects a Hodgkin-associated membrane molecule of 120 kd (Ki-1/120 = CD30), but also reacts with an independently synthesized molecule of 57 kd (Ki-1/57) that only occurs intracellularly. Hodgkin's disease-derived cell lines L428 and L540 contain both Ki-1-reactive antigens, whereas others, e.g., U266/Bl myeloma cells, only express the intracellular Ki-1/57. The present immunoelectronmicroscopic analysis detected the Ki-1/57 antigen of U266/Bl cells not only in the cytoplasm, but also in association with the nuclear envelope, chromatin structures, and nucleoli. This Ki-1/57-specific type of labeling also was observed in L428 and L540 cells that, in contrast to U266/Bl cells, showed an additional staining of cell membranes and cytoplasmic vesicles. These results were confirmed by two independent methods: 1) cytocentrifuge preparations of isolated nuclei of L540 cells showed a spotted Ki-1-specific labeling, 2) immunoprecipitations demonstrated that the Ki-1/57, but not the Ki-1/120 antigen, was transferred into the nuclei of L540 and U266/Bl cells, whereas the Ki-1/120 antigen with its 90-kd precursor remained in the non-nuclei fraction of L540 cells.
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PMID:Cellular localizations and processing of the two molecular forms of the Hodgkin-associated Ki-1 (CD30) antigen. The protein kinase Ki-1/57 occurs in the nucleus. 131 Aug 32

In man, Hodgkin's disease (HD) represents the most frequent lymphoma entity whose pathogenesis is still unknown. In order to contribute to the characterization of the molecular mechanisms of this disease, cDNAs coding for the HD characteristic antigen CD30 were cloned from expression libraries of the human HUT-102 cell line using the monoclonal antibodies Ki-1 and Ber-H2. The open reading frame of the cDNA that can be translated from two mRNA species of 2.6 kb, and 3.8 kb, respectively, predicts a 595 amino acid protein with leader, extracellular, single transmembrane, and intracellular domains. When expressed in COS-1 cells, the cDNA presented properties comparable to native CD30 antigen. The CD30 extracellular domain proved to be homologous to members of the nerve growth factor receptor superfamily. Six cysteine-rich motifs could be recognized within the putative ligand-binding domain.
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PMID:Molecular cloning and expression of a new member of the nerve growth factor receptor family that is characteristic for Hodgkin's disease. 131 Aug 94

Activated lymphocytes and malignant lymphoma cells derived from them (Ki-1 positive lymphoma cells) share similar mechanisms of proliferation. To further examine the inhibitory role of endogenous transforming growth factor beta (TGF beta) in Ki-1 positive lymphoma cells, the authors studied anti-TGF beta antibodies and measured their effect on proliferation. A monoclonal antibody (T1A5) prepared against a unique antigenic epitope of high molecular weight Hodgkin's TGF beta and a polyclonal rabbit antibody prepared against highly purified 25,000 D porcine platelet TGF beta 1 were used. Both antibodies are shown here to inhibit the biological activity of Hodgkin's TGF beta and to crossreact with their respective antigens in immunoblotting. DNA synthesis by Ki-1 lymphoma cells was increased 138-fold by anti-TGF beta 1 antibody and 262-fold by anti-Hodgkin's TGF beta. Exogenous TGF beta 1 suppression was completely reversed by anti-TGF beta 1 antibody and IL-2-induced proliferation was markedly potentiated (41 fold). L-428 Reed-Sternberg cells secrete physiologically active TGF beta but have fewer than 500 TGF beta receptor sites per cell; no significant proliferative response was measured for either anti-TGF beta 1 or anti-Hodgkin's TGF beta. These results show the suppressive effect of exogenous TGF beta 1 on indolent Ki-1 lymphoma cells and suggest that the endogenous secretion of high molecular weight physiologically active TGF beta is important in maintaining the indolent nature of this low-grade Ki-1 positive lymphoma.
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PMID:Neutralizing antibodies against transforming growth factor beta potentiate the proliferation of Ki-1 positive lymphoma cells. Further evidence for negative autocrine regulation by transforming growth factor beta. 131 8

We describe the clinical course of a 20-year-old man who suffered generalized convulsive seizures with postictal aphasia and hemiparesis of the right side. Computed tomography (CT) displayed a left postcentral lesion with prominent perifocal edema and only a little contrast medium enhancement. The completely removed tumor proved to be a primary cerebral non-Hodgkin lymphoma consisting of T-cells. Only ten days after the operation the patient once more presented a clinical deterioration. A nuclear magnetic resonance imaging (MRI) displayed an annular structure in the area previously operated upon, suspected to be an abscess. The second operation disclosed a large recurrence of the primary T-cell lymphoma extending diffusely into the white matter. On account of the rapid recurrence, a whole brain irradiation was started twelve days after the second operation. Four cycles of chemotherapy followed. Immunohistochemical studies of the anaplastic large lymphoma cells showed staining with the pan T-cell markers (UCHL1, CD3) and with the CD30 (Ki-1) antibody. The B-cell markers (L26, LN1) were negative. The EMA (epithelial membrane antigen) was only partially expressed. Further investigation excluded the presence of systemic lymphoma manifestation. 24 months after the last operation the patient remained free of symptoms. The last MRI displayed no evidence for the recurrence of a lymphoma. In reference to this unusual clinical course the few previously reported cases of the extremely rare primary cerebral T-cell lymphoma are reviewed.
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PMID:Primary cerebral anaplastic T-cell-lymphoma (type Ki-1): review and case report. 131 14

Ki-1 (CD30)-positive, large-cell anaplastic lymphoma (LCAL) is a distinctive subset of non-Hodgkin's lymphoma; morphologically, the neoplastic cells of LCAL may closely resemble Reed-Sternberg cell variants of Hodgkin's disease. The neoplastic cells in Hodgkin's disease are often CD30-positive, as are some of the transformed lymphocytes in infectious mononucleosis. Recent evidence suggests an etiologic role for the Epstein-Barr virus (EBV) in Hodgkin's disease. Because of the phenotypic similarities between Hodgkin's disease and LCAL, we used the polymerase chain reaction (PCR) to analyze eight specimens of LCAL for EBV genome. Diagnoses were established by paraffin section morphology and immunohistochemistry. For comparison, we also analyzed nine non-Hodgkin's lymphomas other than the LCAL type, three Hodgkin's disease specimens, and nine non-neoplastic lymph nodes. PCR was performed using DNA extracted from frozen tissue; DNA was amplified using two sets of oligonucleotide primers corresponding to the BamH1 W-fragment of the EBV genome. Amplified EBV genome was obtained from all specimens except for one mantle zone lymphoma, one diffuse mixed-cell lymphoma, and six non-neoplastic lymph nodes. EBV terminus region probing and in situ hybridization techniques, each less sensitive than PCR, were performed in selected cases in an attempt to corroborate our PCR results. Only 2 of 13 specimens contained EBV detectable by these other techniques, and neither specimen was a LCAL. In view of the high incidence of latent EBV infections in humans, the biologic significance of our PCR results is uncertain. Despite the detection of EBV genome by PCR in a high percentage of lymphomas, we were unable to substantiate an etiologic role for EBV in LCAL. The PCR technique may be too sensitive to provide meaningful data on the possible role of EBV in lymphomagenesis.
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PMID:Detection of Epstein-Barr virus genome in Ki-1 (CD30)-positive, large-cell anaplastic lymphomas using the polymerase chain reaction. 132 22

A 59-year-old man was initially diagnosed as having Hodgkin's disease, nodular sclerosis type, and complete remission was achieved after combination chemotherapy. One year later, he developed a high fever and recurrence of the Hodgkin's disease was diagnosed. Salvage chemotherapy was ineffective, and the patient died. Autopsy specimens showed infiltration of lymphoma cells into multiple organs. Lymph nodes showed characteristics of non-Hodgkin's lymphoma, with expansion of anaplastic large cells; this differed from the histological features at initial diagnosis. Immunohistochemical staining was positive for CD30/Ki-1, but negative for CD15 (LeuM1). These findings were compatible with Ki-1 lymphoma, suggesting that this may be a case of CD30/Ki-1 lymphoma preceded by Hodgkin's disease and that a certain proportion of Ki-1 lymphomas and Hodgkin's disease may share the same cellular origin.
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PMID:CD30/Ki-1-positive anaplastic large cell lymphoma preceded by Hodgkin's disease. 132 72

The "large cell anaplastic lymphoma, Ki-1 positive" is a recently described lymphoma subtype (about 1-8% of all NHL). Distinction from Hodgkin's disease and true histiocytic lymphoma/malignant histiocytosis is not always possible, even by experienced pathologists. It was recently incorporated in the updated Kiel Classification of lymphomas. Classical histologic appearance is a sinusoidal growth pattern in lymph nodes and presence of large bizarre anaplastic cells. Use of cell markers LCA, EMA and Ki-1 or Ber-H2 is essential for diagnosis. The mean age of patients is 50 years. Approximately 50% of patients have an advanced stage (III-IV). Prognosis depends on age and tumor localisations. Cutaneous involvement only is usually associated with a good prognosis. Median survival for patients with extra-cutaneous disease is 13 months. Treatment with intensive chemotherapy is usually needed. Long term remissions are more frequently seen in children and adolescents.
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PMID:Large cell anaplastic lymphoma (Ki-1 lymphoma). 133 47

Two hundred Hodgkin's and non-Hodgkin's lymphomas were immunohistochemically studied for the presence of the CD30 (Ki-1) activation antigen using a monoclonal antibody BerH2 on paraffin-embedded, formaldehyde-fixed tissue. Immunohistochemistry was performed by using the avidin-biotin complex technique and was preceded by enzymatic digestion with pepsin (0.05% for 20 minutes). Ninety percent (56/64) of cases of Hodgkin's disease, other than lymphocyte predominance type, showed positive tumor cells, although the positivity was often focal. In contrast, lymphocyte predominance type showed CD30 in only two of nine cases. CD30 was commonly seen in non-Hodgkin's lymphomas. Five of 37 large-cell lymphomas showed extensive CD30 positivity and morphologically represented large-cell anaplastic lymphomas ("Ki-1 lymphomas"). Apart from this, occasional CD30-positive cells were seen in nine of 32 large-cell non-Hodgkin's lymphomas. About half of the nodular small cleaved-cell lymphomas contained CD30-positive cells, two of them showing large numbers of positive cells both within and outside the nodules. Lymphocytic lymphoma sometimes (6/17) showed a few CD30-positive cells. Peripheral T-cell lymphomas showed positive cells in three of eight cases. The positive cases were one lymphoma with small groups of epithelioid cells (Lennert's lymphoma) and two immunoblastic lymphadenopathylike peripheral T-cell lymphomas. The results show that CD30 is more widespread than originally thought in non-Hodgkin's lymphomas and that especially nodular small cleaved-cell lymphomas often contain positive cells. These findings have to be considered in the immunohistochemical differential diagnosis of lymphomas. Obviously, CD30 alone cannot be used to differentiate between Hodgkin's and non-Hodgkin's lymphomas. The CD30-positive cells in non-Hodgkin's lymphoma may represent a link between Hodgkin's and non-Hodgkin's lymphomas.
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PMID:CD30 distribution. Immunohistochemical study on formaldehyde-fixed, paraffin-embedded Hodgkin's and non-Hodgkin's lymphomas. 133 42

Ki-1 positive (anaplastic, large cell) lymphoma is a subgroup of non-Hodgkin lymphomas identified recently by Ki-1 (or BER-H2) (CD 30) monoclonal antibody. The clinicopathological features of two such pediatric cases of lymph node origin described here, and also the available literature emphasize the heterogenous nature of Ki-1 positive lymphomas, in almost every respect. Nevertheless, the Ki-1 antibody serves as an important diagnostic tool to differentiate lymphomas from other anaplastic, large malignancies.
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PMID:Ki-1 positive (anaplastic, large cell) lymphoma (case reports and review). 133 39


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