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lüll mda-7 (IL-24): signaling and functional roles Sarkar D; Su ZZ; Lebedeva IV; Sauane M; Gopalkrishnan RV; Dent P; Fisher PBBiotechniques 2002[Oct]; Suppl (ä): 30-9One hallmark of neoplasia is abnormal differentiation. Induction of differentiation, by chemical or biological methods, provides a possible therapeutic intervention. "Differentiation therapy" is well documented in several model systems. These include melanoma, in which treatment with interferon-beta and the protein kinase C activator mezerein induces irreversible growth arrest and terminal differentiation culminating in programmed cell death. Subtraction hybridization between terminally differentiated and untreated melanoma cells identified melanoma differentiation-associated gene-7 (mda-7), which is selectively induced during the process of melanoma terminal differentiation. Since its identification seven years ago, mda-7 has been the object of intense focus because of its unique biological properties. Firstly, mda-7 is a secreted protein having cytokine-like properties and belonging to the IL-10 cytokine family. Based on this consideration, mda-7 was renamed IL-24. Secondly if delivered by means of an adenoviral vector, mda-7 induces selective apoptosis in cancer cells of diverse origin, while sparing their normal cellular counterparts. As such, mda-7 has become a novel tool for cancer gene therapy and is currently undergoing phase II clinical trials to determine its clinical efficacy in patients. The present review examines the biological properties of mda-7 and the signaling pathways that contribute to its unique cancer-specific apoptosis-inducing properties.|Angiogenesis Inhibitors/therapeutic use[MESH]|Animals[MESH]|Apoptosis[MESH]|Cell Differentiation[MESH]|Chromosomes, Human, Pair 1/genetics[MESH]|Gene Expression Regulation, Neoplastic[MESH]|Genes, Tumor Suppressor[MESH]|Genetic Therapy[MESH]|Humans[MESH]|Interleukins/chemistry/genetics/*physiology/therapeutic use[MESH]|Mammals/genetics[MESH]|Melanoma/genetics/metabolism/pathology[MESH]|Mice[MESH]|Neoplasm Proteins/chemistry/genetics/physiology[MESH]|Neoplasms/drug therapy/therapy[MESH]|Pancreatic Neoplasms/genetics/pathology[MESH]|Rats[MESH]|Recombinant Fusion Proteins/physiology[MESH]|Safety[MESH]|Signal Transduction[MESH]|Tumor Cells, Cultured/pathology[MESH] |