Author
Michael B. Sporn
Other affiliations: Cornell University, Reata Pharmaceuticals, University of Texas MD Anderson Cancer Center ...read more
Bio: Michael B. Sporn is an academic researcher from Dartmouth College. The author has contributed to research in topics: Transforming growth factor & Transforming growth factor beta. The author has an hindex of 157, co-authored 559 publications receiving 94605 citations. Previous affiliations of Michael B. Sporn include Cornell University & Reata Pharmaceuticals.
Papers published on a yearly basis
Papers
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TL;DR: Although TGF-/3 was initially discovered and named in the context of a transformation assay, the ubiquitous distribution of the molecule suggests that it must play a fundamental regulatory role in normal cell physiology.
Abstract: Transforming growth factor-/3 (TGF-/3) is the founder member of a growing family of structurally related peptides that are involved in the regulation of cell growth and development in organisms as phylogenetically distant as flies and man. TGF-/3 itself is a multifunctional molecule whose biological effects are highly context-dependent. Thus, depending on the cell type and the cell environment, TGF-/3 in vitro can stimulate or inhibit proliferation, promote or block differentiation, and modulate cellular function.’.’ Two closely related forms of TGF-/3 have been identified. Type 1 and type 2 TGF-/3 share 70% sequence identity and are indistinguishable in most biological assay systems. However, activities unique to cach type are emerging2 and it can be anticipated that the two types may be differentially regulated. Structurally, the active form is a disulfide-linked homodimer of 25 kDa and the monomeric unit is encoded as the C-terminal 112 amino acids of a 390-residue p r e c ~ r s o r . ~ With 2 mg extractable TGF-p/kg, platelets are the most concentrated source of TGF-/3 1 in the body, probably reflecting an important role for the molecule in wound healing4 Bone is also a major source (0.1 mg/kg), and all other tissues examined have detectable, though lower (0.01-0.03 mg/kg) TGF-/3 levels. Thus, although TGF-/3 was initially discovered and named in the context of a transformation assay, the ubiquitous distribution of the molecule suggests that it must play a fundamental regulatory role in normal cell physiology.
27 citations
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TL;DR: Observations support the experimental use of synthetic triterpenoids in the treatment of ovarian cancer as studies on primary ovarian cancer cells have shown that these cells are sensitive to the pro-apoptotic effects of CDDO-Im.
27 citations
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TL;DR: Further in vitro metabolism of [3H]retinyl acetate paralleled the metabolism of [/14C]retinoic acid suggesting that these two compounds are being metabolized through similar pathways.
26 citations
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TL;DR: The paper chromatographic method can be applied to either in vivo or in vitro studies of RNA metabolism, for the purpose of differentiating between sugar-methylation and base- methylation of RNA.
26 citations
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TL;DR: The number of rats with colon carcinoma and the number of tumors per rat were dose related and "blind" histopathologic evaluation of four predesignate colon locations revealed a dose-related incidence of microscopic preinvasive and invasive colon carcinomas.
Abstract: Male F344 rats, 8 weeks of age, were given 16 intrarectal administrations of N-methyl-N-nitrosourea (NMU) at one of three dose levels over a period of 8 weeks. Five days after the final NMU instillation, rats were placed on one of three diets: chow with gelatin beadlets, chow with beadlets containing 0.024% 13-cis-retinoic acid, or chow and beadlets with 0.006% of the trimethylmethoxy phenyl analog of retinoic acid ethylamide. Groups of 20-40 rats were killed at 22-26 weeks after the first carcinogen treatment. The number of rats with colon carcinoma and the number of tumors per rat were dose related. In addition, "blind" histopathologic evaluation of four predesignate colon locations revealed a dose-related incidence of microscopic preinvasive and invasive colon carcinomas. The feeding of diets containing these two retinoids did not significantly alter the incidence of these parameters of carcinogenesis or the mean histopathologic score at predesignated colon locations for preinvasive or invasive neoplastic lesions. Over 90% of the colon neoplasms induced were invasive tubulopapillary adenocarcinomas. The diameters of the tumors correlated significantly with degrees of invasion of the colons. Only 1 tumor (a signet ring carcinoma) metastasized to the peritoneal cavity. Only 2 of 300 rats treated with NMU had tumors at sites other than the colon.
25 citations
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TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
28,811 citations
28 Jul 2005
TL;DR: PfPMP1)与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1(PfPMP1)与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员,通过启动转录不同的var基因变异体为抗原变异提供了分子基础。
18,940 citations
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TL;DR: The ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation.
Abstract: Atherosclerosis, the principal cause of heart attack, stroke and gangrene of the extremities, is responsible for 50% of all mortality in the USA, Europe and Japan. The lesions result from an excessive, inflammatory-fibroproliferative response to various forms of insult to the endothelium and smooth muscle of the artery wall. A large number of growth factors, cytokines and vasoregulatory molecules participate in this process. Our ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation.
10,861 citations
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TL;DR: The principal mechanisms that govern the effects of inflammation and immunity on tumor development are outlined and attractive new targets for cancer therapy and prevention are discussed.
8,664 citations
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TL;DR: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms and mutations in these pathways are the cause of various forms of human cancer and developmental disorders.
Abstract: The transforming growth factor beta (TGF-beta) family of growth factors control the development and homeostasis of most tissues in metazoan organisms. Work over the past few years has led to the elucidation of a TGF-beta signal transduction network. This network involves receptor serine/threonine kinases at the cell surface and their substrates, the SMAD proteins, which move into the nucleus, where they activate target gene transcription in association with DNA-binding partners. Distinct repertoires of receptors, SMAD proteins, and DNA-binding partners seemingly underlie, in a cell-specific manner, the multifunctional nature of TGF-beta and related factors. Mutations in these pathways are the cause of various forms of human cancer and developmental disorders.
7,710 citations