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
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TL;DR: From a contemporary perspective in 2016, it is difficult to realize that not very long ago, the prevailing primary screen for testing new anticancer drugs was the lung cancer screening test.
Abstract: See related article by Eagle and Foley, [Cancer Res 1958;18:1017–25][1] .
Visit the Cancer Research 75th Anniversary [timeline][2].
From a contemporary perspective in 2016, it is difficult to realize that not very long ago, the prevailing primary screen for testing new anticancer drugs was the
1 citations
TL;DR: Treatment with bardoxolone for 24 weeks in patients with Stage 3b/4 chronic kidney disease and type 2 diabetes resulted in a large increase in eGFR, relative to no change in the placebo group, and significant improvements were also noted in other measured of kidney function, including blood urea nitrogen, serum phosphorus, and serum uric acid relative to placebo.
1 citations
Book•
01 Jan 1992
TL;DR: Concepts of Preneoplasia for the Goal of Cancer Prevention and Prospects for the Chemoprevention of Breast Cancer are presented.
Abstract: Concepts of Preneoplasia for the Goal of Cancer Prevention- Steroids, Retinoids, and their Mode of Action- Epidermal Growth Factor, Glucocorticoid Hormones and Prolactin Act Sequentially in the Induction of Milk Protein Gene Expression- Interactions of Retinoids and Transforming Growth Factor-Beta in the Chemoprevention of Cancer- Growth Regulatory Networks in the Prostate- Prospects for the Chemoprevention of Breast Cancer
1 citations
TL;DR: Olaparib and veliparib are evaluated as effective PARP inhibitors for cancer prevention in a BRCA1-deficient mouse model and significantly delayed tumor development.
Abstract: An inherited mutation in the BRCA1 gene leads to genomic instability and those with this mutation have a 50-80% risk for developing breast cancer by age 70. Though bilateral prophylactic mastectomy and surveillance are viable options for this high-risk population, chemoprevention may serve as a good alternative strategy. BRCA1 functions to repair double stranded DNA breaks via homologous recombination and as such, BRCA1 mutations force the cells to rely on other DNA repair mechanisms such as base excision repair, a process which requires Poly ADP ribose polymerase (PARP). Thus, PARP inhibition in BRCA1-deficient cells may induce apoptosis in these cells, which would otherwise develop into a tumor, while leaving normal cells intact. Olaparib and veliparib are promising PARP inhibitors that are currently in clinical trials for breast cancer treatment; however, their role in cancer prevention has not been examined. Hence, this study evaluated the effect of these PARP inhibitors in chemoprevention in the BrcaCo/Co;MMTV-Cre;p53+/- mouse model. Mice were fed continuously with olaparib (200 mg/kg diet) or veliparib (100 mg/kg diet) and tumor development was assessed. Both olaparib and veliparib significantly delayed tumor development by 6.5 and 2.4 weeks respectively (p Citation Format: Ciric To, Charlotte R. Williams, Darlene B. Royce, Ryan M. Collins, Michael B. Sporn, Karen T. Liby. Olaparib and veliparib as effective PARP inhibitors for cancer prevention in a BRCA1-deficient mouse model. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2965. doi:10.1158/1538-7445.AM2014-2965
1 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
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
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
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