To serve patients, health care providers, research scientists, scholars, and society by providing excellence and innovation in diagnostic services and educational resources in a respectful, professional and culturally diverse atmosphere.
To become a preeminent leader in academic anatomic and clinical pathology while translating basic science discovery to improved clinical care.
Robert C Wilson, Ph.D.
Associate Professor Research
Department of Pathology and Laboratory Medicine
The James E. Clyburn Research Center
Medical University of South Carolina
68 President Street
Charleston, SC 29425
Office: BEB BE414
Laboratory: BEB BE432
Office Phone: (843) 876-2217
B.A., 1985, University of California, Santa Cruz
M.S., 1987, Columbia University, New York
M.Phil., 1988,Columbia University, New York
Ph.D., 1992, Columbia University, New York
I oversee the Hollings Cancer Genomics Core Laboratory. My goal is to utilize my expertise in molecular biology and next generation sequencing by offering my services as a shared resource center manager but also to form collaborations by becoming intimately involved with my colleagues’ research projects here at MUSC.
George MM, Sinha S, Mamkin I, Philibert P, New MI, Wilson RC, Sultan C, Ten S, Bhangoo A. Isolated mild clitoral hypertrophy may reveal 46,XY disorders of sex development in infancy due to 17βHSD-3 defect confirmed by molecular analysis. Gynecol Endocrinol. 2011 Nov;27(11):890-4. Epub 2011 Jan 10.
Baş F, Kayserili H, Darendeliler F, Uyguner O, Günöz H, Yüksel Apak M, Atalar F, Bundak R, Wilson RC, New MI, Wollnik B, Saka N. CYP21A2 gene mutations in congenital adrenal hyperplasia: genotype-phenotype correlation in Turkish children. J Clin Res Pediatr Endocrinol. 2009;1(3):116-28. Epub 2009 Feb 2.
Wilson RC, Nimkarn S, Dumic M, Obeid J, Azar MR, Najmabadi H, Saffari F, New MI. Ethnic-specific distribution of mutations in 716 patients with congenital adrenal hyperplasia owing to 21-hydroxylase deficiency. Mol Genet Metab. 2007 Apr;90(4):414-21. Epub 2007 Feb 1. Erratum in: Mol Genet Metab. 2008 Feb;93(2):219. Azar, Maryam [corrected to Azar, Maryam Razzaghy].
Nimkarn S, Lin-Su K, Berglind N, Wilson RC, New MI. Aldosterone-to-renin ratio as a marker for disease severity in 21-hydroxylase deficiency congenital adrenal hyperplasia. J Clin Endocrinol Metab. 2007 Jan;92(1):137-42. Epub 2006 Oct 10.
Ergun-Longmire B, Auchus R, Papari-Zareei M, Tansil S, Wilson RC, New MI. Two novel mutations found in a patient with 17alpha-hydroxylase enzyme deficiency. J Clin Endocrinol Metab. 2006 Oct;91(10):4179-82. Epub 2006 Jul 18.
Bhangoo A, Wilson R, New MI and Ten S. donor Splice Mutation In The 11Beta-Hydroxylase (Cypllb1) Gene Resulting In Sex Reversal: A Case Report And Review Of The Literature. J Pediatr Endocrinol Metab. 2006 Oct;19(10):1267-82.
Motaghedi R, Betensky BP, Slowinska B, Cerame B, Cabrer M, New MI, Wilson RC. Update on the prenatal diagnosis and treatment of congenital adrenal hyperplasia due to 11beta-hydroxylase deficiency. J Pediatr Endocrinol Metab. 2005 Feb;18(2):133-42.
Chemaitilly W, Betensky BP, Marshall I, Wei JQ, Wilson RC, New MI. The natural history and genotype-phenotype nonconcordance of HLA identical siblings with the same mutations of the 21-hydroxylase gene. J Pediatr Endocrinol Metab. 2005 Feb;18(2):143-53.
New MI, Geller DS, Fallo F, Wilson RC. Monogenic low renin hypertension. Trends Endocrinol Metab. 2005 Apr;16(3):92-7. Review.
Lin-Su K, Zhou P, Arora N, Betensky BP, New MI, Wilson RC. In vitro expression studies of a novel mutation D299 in a patient affected with apparent mineralocorticoid excess. J Clin Endocrinol Metab. 2004 May;89(5):2024-7
Chemaitilly W, Wilson RC, New MI. Hypertension and adrenal disorders. Curr Hypertens Rep. 2003 Dec;5(6):498-504. Review.
New MI, Carlson A, Obeid J, Marshall I, Cabrera MS, Goseco A, Lin-Su K, Putnam AS, Wei JQ, Wilson RC. Prenatal diagnosis for congenital adrenal hyperplasia in 532 pregnancies. J Clin Endocrinol Metab. 2001 Dec;86(12):5651-7.
Wilson RC, Nimkarn S, New MI. Apparent mineralocorticoid excess. Trends Endocrinol Metab. 2001 Apr;12(3):104-11. Review.
Ugrasbul F, Wiens T, Rubinstein P, New MI, Wilson RC. Prevalence of mild apparent mineralocorticoid excess in Mennonites. J Clin Endocrinol Metab. 1999 Dec;84(12):4735-8.
New MI, Wilson RC. Steroid disorders in children: congenital adrenal hyperplasia and apparent mineralocorticoid excess. Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12790-7.
Cerame BI, Newfield RS, Pascoe L, Curnow KM, Nimkarn S, Roe TF, New MI, Wilson RC. Prenatal diagnosis and treatment of 11beta-hydroxylase deficiency congenital adrenal hyperplasia resulting in normal female genitalia. J Clin Endocrinol Metab. 1999 Sep;84(9):3129-34.
Nimkarn S, Cerame BI, Wei JQ, Dumic M, Zunec R, Brkljacic L, Skrabić V, New MI, Wilson RC. Congenital adrenal hyperplasia (21-hydroxylase deficiency) without demonstrable genetic mutations. J Clin Endocrinol Metab. 1999 Jan;84(1):378-81.
Wilson RC, Dave-Sharma S, Wei JQ, Obeyesekere VR, Li K, Ferrari P, Krozowski ZS, Shackleton CH, Bradlow L, Wiens T, New MI. A genetic defect resulting in mild low-renin hypertension. Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):10200-5. Review.
Obeyesekere VR, Ferrari P, Andrews RK, Wilson RC, New MI, Funder JW, Krozowski ZS. The R337C mutation generates a high Km 11 beta-hydroxysteroid dehydrogenase type II enzyme in a family with apparent mineralocorticoid excess. J Clin Endocrinol Metab. 1995 Nov;80(11):3381-3.
Wilson RC, Harbison M.D., Krozowski ZS, Funder JW, Shackleton CH, Hanauske-Abel HM, Wei JQ, Hertecant J, Moran A, Neiberger RE, et al. Several homozygous mutations in the gene for 11 beta-hydroxysteroid dehydrogenase type 2 in patients with apparent mineralocorticoid excess. J Clin Endocrinol Metab. 1995 Nov;80(11):3145-50.
Wilson RC, Mercado AB, Cheng KC, New MI. Steroid 21-hydroxylase deficiency: genotype may not predict phenotype. J Clin Endocrinol Metab. 1995 Aug;80(8):2322-9.
Wilson RC, Krozowski ZS, Li K, Obeyesekere VR, Razzaghy-Azar M, Harbison M.D., Wei JQ, Shackleton CH, Funder JW, New MI. A mutation in the HSD11B2 gene in a family with apparent mineralocorticoid excess. J Clin Endocrinol Metab. 1995 Jul;80(7):2263-6.