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The Layman Lab
PI Information Page

Principal investigator:

Dr. Lawrence C. Layman
Professor and Chief, Reproductive Endocrinology, Infertility and Genetics Section
Department of Obstetrics and Gynecology
Developmental Neurobiology Program
Institute of Molecular Medicine and Genetics
Lab: CA 4046,  ph: 706-721-7591
IMMAG Office: CA 4016 
Reproductive Endocrinology Office: BB 7514, ph: 706-721-3832
Email: llayman@mcg.edu 

Institution and Location:

Dickinson College, Carlisle, PA BS 1977 Biology
University of Cincinnati, Cincinnati, OH MD 1981 MD
Jewish Hospital, Cincinnati, OH Resident 1982 Internal Medicine
University of Louisville, Louisville, KY Resident 1986 OB/GYN
Medical College of Georgia, Augusta, GA Fellow 1988 Reprod Endocr/Genetics

A. Positions and Honors

Academic Appointments

7/88-6/92 Assistant Professor, Dept. of Obstetrics and Gynecology, Section of Reproductive Endocrinology, Infertility, & Genetics, Medical College of Georgia, Augusta, GA
3/91-6/92 Joint appointment, Department of Oral Biology, Medical College of Georgia
7/92-10/95 Assistant Professor (7/92-9/94), Associate Professor (9/94-10/95), Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology, Tufts University
10/95-7/99 Associate Professor, Chief, Section of Reproductive Endocrinology & Infertility,
Department of Obstetrics and Gynecology, The University of Chicago
7/99–present Professor, Section Chief, Reproductive Endocrinology, Infertility,& Genetics section, Dept. OB/GYN, Developmental Biology Program, Institute of Molecular Medicine & Genetics, Medical College of GA
1/00–present School of Graduate Studies Faculty, Medical College of Georgia

Board Certification

1989 American Board of Obstetrics and Gynecology (recertified, 2004)
1990 American Board of Obstetrics and Gynecology, Reproductive Endocrinology (recertified, 2004)
1990 American Board of Medical Genetics, Clinical Genetics (lifetime recertification)
1993 American Board of Medical Genetics, Clinical Molecular Genetics (recertified, 2002)

Honors:

Chair of Study Section, Reproductive Medicine Network, NIH, December, 1999.
Distinguished Faculty Award for Clinical Science Research, MCG, May 14, 2002.
SCCPRR NIH Study Section Member, 2004, 2005.
Inducted as Member, American Gynecologic & Obstetrical Society, 2004.
Selected for Best Doctors in America, 2005-2006.

B. Selected peer-reviewed publications (in chronological order)

  1. Layman LC, Edwards JL, Osborne WE, Peak DB, Wall SW, Gallup DG, Reindollar RH, McDonough PG, KD Lanclos. Human chorionic gonadotropin-beta gene mutations in women with disorders of hCG production: recurrent abortion, unexplained infertility, and gestational trophoblastic neoplasia. Mol Hum Reprod 1997;3:315-320.
  2. Layman LC, Lee EJ, Peak DB, Namnoum AB, Vu KK, van Lingen BL, Gray MR, McDonough PG, Reindollar RH, Jameson JL. Delayed puberty and hypogonadism caused by a mutation in the follicle stimulating hormone beta-subunit gene. N Engl J Med 1997;337:607-611.
  3. Layman LC, Peak DB, Reindollar RH, Sohn SH, Gray MR. Mutation analysis of the gonadotropin releasing hormone receptor gene structure in idiopathic hypogonadotropic hypogonadism. Fertil Steril 1997;68:1079-1085.
  4. Layman LC, Cohen DP, Jin M, Xie J, Li Z, Reindollar RH, Bolbolan S, Bick DP, Sherins RJ, Duck LW, Musgrove LC, Sellers JC, Neill JD. Mutations in gonadotropin-releasing hormone receptor cause hypogonadotropic hypogonadism. Nat Genet 1998;18:14-15.
  5. Layman LC, Amde S, DP Cohen, Jin M, Xie J. The Finnish follicle stimulating hormone receptor (FSHR) gene mutation in women with 46,XX ovarian failure is rare in the United States. Fertil Steril 1998;69:300-302.
  6. Layman LC. Mutations in human gonadotropin genes and their physiologic significance in puberty and reproduction. Fertil Steril 1999; 71:201-218.
  7. Cohen DP, Stein EM, Li Z, Matulis CK, Ehrmann DA, Layman LC. Molecular analysis of the gonadotropin releasing hormone receptor in polycystic ovarian syndrome. Fertil Steril 1999;72:360-363.
  8. Layman LC. The molecular basis of human hypogonadotropic hypogonadism. Mol Genet Metab 1999;68:191-99.
  9. Taylor H, Block K, Olive D, Bick DP, Sherins RJ, Layman LC. Absence of EMX2 gene mutations in Kallmann syndrome. Fertil Steril 1999;72:910-914.
  10. Achermann JC, Gu W-X, Kotlar TJ, Meeks JJ, Sabacan LP, Seminara SB, Habiby RL, Hindmarsh PC, Bick DP, Sherins RJ, Crowley Jr. WF, Layman LC, Jameson JL. Mutational analysis of DAX1 in patients with hypogonadotropic hypogonadism or pubertal delay. J Clin Endocrinol Metab 1999;84:4497-4500.
  11. Layman LC. The genetics of human hypogonadotropic hypogonadism. Am J Med Genet 1999;89:240-248.
  12. Barnes RB, Namnoum A, Rosenfield RL, Layman LC. Effect of follicle stimulating hormone on ovarian androgen production in a woman with isolated follicle-stimulating hormone deficiency. N Engl J Med 2000;343:1197-1198.
  13. Layman LC, McDonough PG, Cohen DP, Maddox M, Tho SPT, Reindollar RH. Familial gonadotropin releasing hormone resistance and hypogonadotropic hypogonadism in a family with multiple affected individuals. Fertil Steril 2001;75:1148-1155.
  14. Barnes RB, Namnoum A, Rosenfield RL, Layman LC. The role of LH and FSH in ovarian androgen secretion and ovarian follicular development: Clinical studies in a patient with isolated FSH deficiency and multicystic ovaries. Hum Reprod 2002;17:88-91.
  15. Layman LC, Porto ALA, Xie J, da Motta LACR, da Motta LDC, Weiser W, Sluss PM. Partial deficiency of follicle stimulating hormone (FSH)-dependent phenotype due to an FSH gene mutation, J Clin Endocrinol Metab 2002;87:3702-3707.
  16. Layman LC, Xie J, Cohen DP, Smith GD. Clinical phenotype and infertility treatment in a male with hypogonadotropic hypogonadism due to Ala129Asp/Arg262Gln gonadotropin releasing hormone receptor mutations. Fertil Steril 2002; 78:1317-20.
  17. Clark AD, Layman LC. Analysis of the Cys82Arg mutation in FSH using a novel FSH expression vector. Fertil Steril 2003;79:379-385.
  18. Park JK, Ozata M, Chorich LP, Bick DP, Sherins RJ, Ozdemir IE, Cogan J, Phillips III JA, Layman LC. Study of the PROP1 gene in a large sample of patients with idiopathic hypogonadotropic hypogonadism. Clin Endocr 2004;60:147-149.
  19. Layman LC. Autoantibodies against the follicle stimulating hormone receptor—association or causation? Clin Endocrinol 2004;61:414-5.
  20. Xu N, Podolsky RH, Chudgar P, Chorich LP, Liu C, McDonough PG, Warrington JA, Layman LC. Screening candidate genes for mutations in patients with hypogonadotropic hypogonadism using genome custom resequencing microarrays. Am J Obstet Gynecol 2005;192:1274-1284.
  21. Bhagavath B, Ozata M, Ozdemir IC, Bolu E, Bick DP, Sherins RJ, Layman LC. The prevalence of GNRHR mutations in a large cohort of patients with hypogonadotropic hypogonadism. Fertil Steril (In press).
  22. Bhagavath B, Podolsky RH, Ozata M, Bolu E, Bick DP, Kulharya A, Sherins RJ, Layman LC. Clinical and molecular characterization of a large sample of patients with hypogonadotropic hypogonadism. Fertil Steril (In press).

C. Research Support

Ongoing Research Support

  1. “Genotype/phenotype correlations in infertility.”
    Principal Investigator: Lawrence C.Layman, M.D.
    Agency: NICHD
    NIH K24 HD040287, August 15,2002 – August 14, 2007.
    The goal of this proposal is to characterize genes involved in the pathogenesis of idiopathic hypogonadotropic hypogonadism (IHH). Specific aims include: (1) increase our sample size of IHH patients; (2) characterize the patients clinically including pedigree analysis; and (3) study candidate genes and chromosomal regions for linkage and association.
     
  2. "Genetics of delayed puberty.”
    Principal Investigator: Lawrence C.Layman, M.D.
    Agency: NICHD
    NIH R01 HD033004, July 15, 2003-May 31, 2008.
    Our overlying hypothesis is that the genes that regulate gonadotropin production and/or secretion are important in normal puberty and possess mutations in IHH patients. Specific Aims include: (1) To identify locations of possible candidate genes by determining the prevalence of chromosomal abnormalities in IHH patients; (2) To test candidate genes, determined by their possible effects upon GnRH and gonadotropin function or by their location in chromosomal breakpoints regions, for association and for mutations in patients with IHH vs. fertile controls; (3) To determine the effects upon transcription and protein function; (4) To perform clinical endocrinologic studies on patients with gene mutations in order to make genotype/phenotype correlations.
  1. “Genetics of delayed puberty.”
    NIH Underrepresented Minority Supplement, 8/10/2005 - 5/31/2006, 3 R01 HD033004-09S1.

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Medical College of Georgia
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December 12, 2005