Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nodular lesion in renal glomeruli develops as a localized accentuation of mesangial volume augmentation. First described by Kimmelstiel and Wilson in 1936, it was soon accepted as the characteristic form of glomerular sclerosis in patients with long-term diabetes mellitus. It has for a long time been recognized that lesions very similar to nodular glomerulosclerosis may rarely occur in patients without diabetes. Clinical and pathological investigations of such cases have shown that glomerular nodules can also develop, 1. as a sequal to light chain deposit disease associated with plasma cell dyscrasia (e.g. myelomatosis), 2. in mesangioproliferative and membranoproliferative glomerulonephritis ("lobular" GN) and 3. in some cases of glomerular amyloid deposition. A survey is given of the characteristic light microscopy, ultrastructure and immunopathology of the glomerular nodules in these diseases. The differential diagnosis and pathogenesis is discussed.
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PMID:[Clinical pathology of the glomerulus--from phenomenon to entity. The nodular-lobular lesion]. 248 39

Using the human liver cancer DNA transfected NIH/3T3 cell line, the human N-ras oncogene and the over expression of the oncoprotein P21ras was demonstrated, BALB/C mice were immunized. The spleen cells from the immunized mice were fused with SP2/0 myeloma cells. After the HAT medium selection and screening, two hybridoma cell lines, SCI-Oncogema 1 and 2, were established. In the immunoprecipitation test, the molecular weight of the protein reacting to Oncogema 1 was 21,000. This M.W 21,000 protein possessed the capability to bind with GTP, i.e. the character of P21ras. These data indicate that the Oncogema 1 is the monoclonal antibody against P21ras. Using Oncogema 1, specimens from 6 liver cancer patients were studied by immunopathology. With ABC stain, it was observed that the malignant cells in all the samples showed dark staining; the P21ras revealed over expression. Although the staining was heterogeneous, it implied that the ras oncogene was involved in the carcinogenesis of these six samples. No over expression was seen in the normal liver cells even in those around the cancerous lesion. However, dysplastic cells were moderately stained which means that the ras oncogene was activated and P21ras over expressed in these cells. The results suggest that the ras oncogene and P21ras play an important role in the early stage of liver cancer carcinogenesis.
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PMID:[Localization of oncoprotein P21ras in the human liver cancer]. 330 83

To determine the effects of anti-T cell monoclonal antibody-induced systemic T cell depletion in neuro-autoimmune disease, we studied the in vivo effects of 8BE6, a mouse anti-guinea pig (GP) pan-T cell monoclonal antibody, on the course and immunopathology of the disease model experimental allergic encephalomyelitis (EAE) in adult Strain 13 GP. Central nervous system (CNS) tissues were studied by routine histology and by an immunoperoxidase staining technique using monoclonal antibodies to T cells, IgM, and macrophages. From 3 days before to 10 days after sensitization with GP spinal cord and complete Freund's adjuvant, the GP were given one or two i.p. doses of 3.4 mg 8BE6 or MOPC 21, the parent mouse myeloma ascites, or normal saline. Eighteen of 18 control-treated GP developed typical acute, paralytic EAE 11 to 21 days after sensitization, whereas acute EAE was prevented in 33 of 49 8BE6-treated GP (67%), and the onset was delayed and disease progression was slowed in the others. Five GP treated with 8BE6 from days 11 to 14 after sensitization, at the onset of neurologic signs, rapidly deteriorated within hours after treatment and had loss of T cell staining, and lymphocytolysis in the CNS. 8BE6-treated GP which did not develop acute EAE were observed daily for up to 700 days (mean = 213 days). Twenty-nine of 39 (74%) had from one to six relapses or fixed neurologic deficits. GP in relapse were additionally treated with 8BE6 (22), MOPC-21 (5), or saline (6) in a cross-over protocol. Clinical scores were improved from days 2 to 12 after treatment (p less than 0.05), and complete recovery within 30 days occurred more frequently (p = 0.046) and more rapidly (p less than 0.01), after 8BE6 as compared with control treatments. Recoveries occurred more often if 8BE6 was given early in the relapse. Multiple treatments led to dose-dependent levels of serum antibodies to mouse immunoglobulin detected by an ELISA. There were no differences between acute and chronic EAE in numbers of inflammatory foci or numbers of macrophages and T cells in CNS infiltrates, but GP with chronic EAE had more extensive demyelination and vascular fibrosis and more numerous IgM+ B cells in parenchymal and meningeal infiltrates than in acute EAE (p less than 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Anti-T cell monoclonal antibodies in vivo. II. Modulation of acute and chronic experimental allergic encephalomyelitis (EAE) in guinea pigs. 349 72

Avoiding immune destruction is a hallmark of cancer. Over the past few years, significant advances have been made in understanding immune dysfunction and immunosuppression in multiple myeloma (MM), and various immunotherapeutic approaches have delivered improved clinical responses. However, it is still challenging to completely eliminate malignant plasma cells (PCs) and achieve complete cure. The interplay between the immune system and malignant PCs is implicated throughout all stages of plasma cell dyscrasias including asymptomatic states called monoclonal gammopathy of undetermined significance and smoldering myeloma. While the immune system effectively eliminates malignant PCs or at least induces functional dormancy at early stages, malignant PCs eventually evade immune elimination, leading to progression into active MM, in which dysfunctional effector lymphocytes, tumor-educated immunosuppressive cells, and soluble mediators coordinately act as a barrier for anti-myeloma immunity. An in depth understanding of this dynamic process, called cancer immunoediting, will provide important insights into the immunopathology of plasma cell dyscrasias and MM immunotherapy. Moreover, a growing body of evidence suggests that together with non-hematopoietic stromal cells, BM immune cells with unique functions support the survival of normal and malignant PCs in the BM niche, highlighting the diverse roles of immune cells beyond anti-myeloma immunity. Together, the immune system critically acts as a rheostat that fine-tunes the balance between dormancy and disease progression in plasma cell dyscrasias.
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PMID:Cancer immunoediting and immune dysregulation in multiple myeloma. 3264 35