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)

Congenital dyserythropoietic anaemia type III (CDA III) is a rare disease inherited in an autosomal dominant way and characterized by mild to moderate haemolytic anaemia. Most patients are adapted to their disease and have no or few complaints. Bone marrow examination shows a characteristic picture with erythroid hyperplasia and multinucleate erythroblasts. 20% of patients in a Swedish family affected with the CDA III condition have monoclonal gammopathy or multiple myeloma. By linkage and recombination analysis in the same family, the gene linked to the CDA III condition (CDAN3) has been located to chromosome 15q22. In this paper we report the observation of visual disturbances with macular degeneration and angioid streaks in six patients with CDA III and discuss the apparent association between CDA III, angioid streaks and monoclonal gammopathy. We suggest that this triad forms a previously unreported syndrome.
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PMID:Angioid streaks are part of a familial syndrome of dyserythropoietic anaemia (CDA III). 932 76

Thalidomide has demonstrated a broad spectrum of pharmacological and immunological effects, with potential therapeutic applications that span a wide spectrum of diseases: cancer and related conditions; infectious diseases; autoimmune diseases; dermatological diseases; and other disorders such as sarcoidosis, macular degeneration and diabetic retinopathy. Immunomodulatory derivative lenalidomide has more potent antitumour and anti-inflammatory effects. The molecular mechanisms of antitumour activity of lenalidomide have been extensively studied in multiple myeloma (MM). It directly induces growth arrest and/or apoptosis of even drug-resistant MM cells; inhibits binding of MM cells to bone marrow extracellular matrix proteins and stromal cells; modulates cytokine secretion and inhibits angiogenesis in the bone marrow milieu; and augments host antitumour immunity. Importantly, lenalidomide induces significant clinical responses even in patients with relapsed/refractory MM. Therefore, lenalidomide represents a new class of antitumour agents that is useful in the treatment of MM. Lenalidomide has received fast track designation from the FDA for the treatment of MM and myelodysplastic syndromes.
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PMID:Current therapeutic uses of lenalidomide in multiple myeloma. 1643 96

The idea of antiangiogenesis as a therapeutic strategy has been around for several decades (1). Vigorously pursued as a novel anticancer strategy (reviewed in (2-6), it is now widely considered to be a promising approach to the treatment of a range of pathologies of which uncontrolled vascular proliferation is a component (see Table 1). To date, therapeutic benefit has been achieved with antiangiogenic therapy in the treatment of life-threatening infantile hemangioma, pulmonary hemangiomatosis, and in the treatment of some vascular tumors (7,8). Table 1 Table 1 Pathologies Likely to Benefit from Therapeutic Intervention in Angiogenesis Excess angiogenesis Insufficient angiogenesis Arthritis Angiology Inflammatory, Vascular malformation Rheumatoid, Hemifacial micromia Kaposi's sarcoma Bone fracture nonunion Leukemia, lymphoma, and myeloma Chronic wounds Macular degeneration Ischemia/infarction Paget's disease Cerebral Psoriasis Intestinal Retinopathy (and its vascular complications) Myocardial Proliferative Peripheral Of prematurity Pyrogenic granuloma Solid carcinomas Ulcer Primary Duodenal Secondary (metastasis) Gastric Vascular tumors Hemangioma Capillary Juvenile (infantile) Hemangiomatosis Hemagioblastoma Other benign vascular proliferations.
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PMID:Therapeutic inhibition of angiogenesis. 2134 Sep 8

Neurodegenerative diseases are often associated with both normal and premature aging. Resumption of the cell cycle by neurons induced by DNA damage may lead to their apoptosis, which contributes to the degeneration of neuronal tissue. Cell cycle and DNA replication proteins are frequently found in patients with neurodegenerative diseases. Oxidative stress, which is considered to play an important role in aging and pathogenesis of many neurodegenerative diseases, can induce DNA damage and stimulate cell cycle re-entry by neuronal cells. DNA damage activates ataxia telangiectasia mutated (ATM), ataxia telangiectasia and Rad3-related (ATR), breast cancer 1 (BRCA1), E2F transcription factor 1 (E2F1), and other proteins that regulate the cell cycle, DNA damage repair, and apoptosis. Because the E2F complexes associate with histone-modifying enzymes, histone modifications, including histone acetylation and methylation, are required for cell cycle re-entry and may play a regulatory role in DNA repair or apoptosis. Aberrant cell cycle regulation has been shown to play a role in age-related macular degeneration (AMD) in which retinal cells are affected and in inclusion body myositis, which is characterized by muscle cell dysfunction. There is also evidence to suggest that cytostatic chemotherapy could decrease dementia in Alzheimer's disease and multiple myeloma, supporting the use of cell cycle inhibitors in the therapy of degenerative diseases.
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PMID:Role of the Cell Cycle Re-Initiation in DNA Damage Response of Post-Mitotic Cells and Its Implication in the Pathogenesis of Neurodegenerative Diseases. 2621 10