Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Murine B cell growth factor II (BCGF-II/interleukin 5) was purified from the conditioned media of the helper T cell line D10 . G4 . 1. The purification scheme consisted of sequential batch adsorption onto trimethylsilyl-controlled pore glass beads, high pressure ion exchange chromatography, and reverse phase high pressure liquid chromatography. The purified BCGF-II had a relative molecular weight of 45,000 when analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under nonreducing conditions. Identical analysis of BCGF-II under reducing conditions yielded a m.w. of 22,500, suggesting that native BCGF-II exists as a homodimer. The NH2-terminal amino acid sequence of the purified lymphokine was determined by automated Edman degradation. A single amino acid sequence of 24 residues was obtained that, upon comparison, was contained within the cDNA pSP6K-mTRF23 recently described as encoding murine BCGF-II/T cell-replacing factor. The NH2-terminal methionine in mature BCGF-II is found at position 21 of the amino acid sequence predicted from the cDNA pSP6K-mTRF23. This finding supports the contention of Kinashi et al. (Kinashi, T., N. Harada, E. Severinson, T. Tanabe, P. Sideras, M. Konishi, C. Azuma, A. Tominaga, S. Bergstedt-Lindqvist, M. Takahashi, F. Matsuda, Y. Yaoita, K. Takatsu, and T. Honjo. 1986. Nature 324:70) that amino acids 1-20 serve as the signal sequence for the BCGF-II gene. The ability of BCGF-II to stimulate the proliferation of the B cell lymphoma BCL1 was used to assess the potency of the lymphokine. BCGF-II at 13.5 pM induced 50% of the maximal proliferative response in the BCL1 cells; concentrations as low as 2 pM were still effective in stimulating the growth of the cells. Assuming that the amount of BCGF-II necessary to mount a 50% response in the BCL1 assay is defined as one unit of activity, then the purified BCGF-II has a specific activity of 16.5 U/ng of protein.
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PMID:Purification and partial sequence analysis of murine B cell growth factor II (interleukin 5). 349 67

A 59-year-old Oriental male with chronic uveitis associated with vitiligo, poliosis, tinnitus and sunset glow fundus was diagnosed as having chronic Vogt-Koyanagi-Harada syndrome. He was treated successfully with steroids (systemic and sub-Tenon's) for two years, but then developed intractable vitritis and visual loss that worsened with the addition of azathioprine. A vitreous biopsy showed large B-cell lymphoma; a mass was also apparent in the subretinal space in the operated eye. Evaluation of the central nervous system was negative for lymphoma. Combined radiation treatment and chemotherapy resulted in dramatic resolution of the intraocular tumor. The possible role of immunosuppression in the development and progression of this tumor is discussed.
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PMID:Intraocular lymphoma developing in a patient with Vogt-Koyanagi-Harada syndrome. 806 75

Vogt-Kaganayi-Harada (VKH) syndrome is a rare autoimmune disease characterized by panuveitis, neuropathy and aseptic meningitis. Most patients require long-term treatment with steroids and immunosuppressants. Patients may develop concurrent autoimmune diseases, especially endocrinopathies. Secondary malignancies are rare associations. We report a Chinese man with VKH syndrome presenting with multiple cranial nerve palsy and bilateral pan-uveitis, who developed disseminated high-grade B cell lymphoma after 3-year treatment with azathioprine. This is the first report of systemic non-Hodgkin lymphoma in patients with VKH syndrome. The carcinogenic properties of azathioprine on an abnormally expanded but non-clonal lymphoid system may play a role in the pathogenesis.
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PMID:High-grade lymphoma after azathioprine treatment for Vogt-Kaganayi-Harada syndrome. 1562 16

Vogt-Koyanagi-Harada disease (VKH) is a multisystem autoimmune disorder principally affecting pigmented tissues in the ocular, auditory, integumentary and central nervous systems. Patients are typically 20 to 50 years old and have no history of either surgical or accidental ocular trauma. Pigmented races are more commonly affected. Depending on revised diagnostic criteria, the disease is classified as complete, incomplete or probable based on the presence of extraocular findings (neurological, auditory and integumentary). The clinical course of VKH is divided into four phases: prodromal (mimics a viral infection), uveitic (bilateral diffuse uveitis with papillitis and exudative retinal detachment), convalescent (tissue depigmentation), and chronic recurrent (recurrent uveitis and ocular complications). The pathogenesis of VKH is thought to be related to an aberrant T cell-mediated immune response directed against self-antigens found on melanocytes. VKH has been linked to human leukocyte antigen DR4 (HLA-DR4) and HLA-Dw53, with strongest associated risk for HLA-DRB1*0405 haplotype. The diagnosis of VKH is clinical, and differential includes sympathetic ophthalmia, sarcoidosis, primary intraocular B-cell lymphoma, posterior scleritis, and uveal effusion syndrome. Treatment is typically initiated with high-dose oral corticosteroids, but other immunomondulatory agents (most oftentimes cyclosporine) may be needed for non-responsive patients or when corticosteroid side-effects are not tolerated. Visual prognosis is generally good with prompt diagnosis and aggressive immunomodulatory treatment.
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PMID:Vogt-Koyanagi-Harada disease. 1628 53

Non-Hodgkin's lymphoma is the sixth leading cause of cancer death in the USA. Herein, a patient is presented with primary diffuse large B-cell lymphoma whose initial complaint was blurred vision and who presented with corticosteroid-responsive serous retinal detachments mimicking Vogt-Koynagi-Harada. Extensive clinical examination including imaging and blood testing was negative. Splenectomy led to a diagnosis of splenic lymphoma.
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PMID:Primary diffuse large B-cell lymphoma of the spleen with coincident serous retinal detachments responsive to corticosteroids. 1765 Dec 53