Professor, Medicine, Perelman School of Medicine

Endocrinology

Doris A. Stoffers is an expert in the field of Endocrinology. She went to Johns Hopkins University School of Medicine. Johns Hopkins University School of Medicine is a one of the best medicals schools. Johns Hopkins University School of Medicine is ranked 3/29 in Research/PrimaryCare. She over the years received 1 awards: "Elected Member". Doris Stoffers is also a published physician. She has 67 publication published. The most recent publication is: Misexpression of the pancreatic homeodomain protein IDX-1 by the Hoxa-4 promoter associated with agenesis of the cecum.

Publications

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• The Polycomb protein, Bmi1, regulates insulin sensitivity.
• Islet-1 is essential for pancreatic β-cell function.
• The diabetes susceptibility gene clec16a regulates mitophagy.
• Insulin regulates carboxypeptidase E by modulating translation initiation scaffolding protein eIF4G1 in pancreatic β cells.
• The Role of β Cell Glucagon-like Peptide-1 Signaling in Glucose Regulation and Response to Diabetes Drugs.
• Pdx1 Maintains β Cell Identity and Function by Repressing an α Cell Program.
• Transient cytokine treatment induces acinar cell reprogramming and regenerates functional beta cell mass in diabetic mice.
• The pancreatic β cell and type 1 diabetes: innocent bystander or active participant?
• Vertical Sleeve Gastrectomy is Effective in Two Genetic Mouse Models of Glucagon-like Peptide-1 Receptor Deficiency.
• MicroRNA-7 Regulates the mTOR Pathway and Proliferation in Adult Pancreatic β-Cells.
• Endoplasmic Reticulum Oxidoreductase-1-Like {beta} (ERO1l{beta}) Regulates Susceptibility to Endoplasmic Reticulum Stress and Is Induced by Insulin Flux in {beta}-Cells.
• Neonatal Diabetes and Congenital Malabsorptive Diarrhea Attributable to a Novel Mutation in the Human Neurogenin-3 Gene Coding Sequence.
• Calcineurin signaling regulates human islet {beta}-cell survival.
• Three-amino-acid-loop-extension homeodomain factor Meis3 regulates cell survival via PDK1.
• Reversal of preexisting hyperglycemia in diabetic mice by acute deletion of the Men1 gene.
• Pcif1 modulates Pdx1 protein stability and pancreatic β cell function and survival in mice.
• A novel hypomorphic PDX1 mutation responsible for permanent neonatal diabetes with subclinical exocrine deficiency.
• Neonatal exendin-4 treatment reduces oxidative stress and prevents hepatic insulin resistance in intrauterine growth-retarded rats.
• Pdx1 (MODY4) regulates pancreatic beta cell susceptibility to ER stress.
• The diabetes gene Pdx1 regulates the transcriptional network of pancreatic endocrine progenitor cells in mice.
• Exendin-4 normalizes islet vascularity in intrauterine growth restricted rats: potential role of VEGF.
• Minireview: Meeting the demand for insulin: molecular mechanisms of adaptive postnatal beta-cell mass expansion.
• Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice.
• Exendin-(9-39) corrects fasting hypoglycemia in SUR-1-/- mice by lowering cAMP in pancreatic beta-cells and inhibiting insulin secretion.
• Toward a cell-based cure for diabetes: advances in production and transplant of beta cells.
• On the origin of the beta cell.
• Development of type 2 diabetes following intrauterine growth retardation in rats is associated with progressive epigenetic silencing of Pdx1.
• Preexisting pancreatic acinar cells contribute to acinar cell, but not islet beta cell, regeneration.
• The PDX1 homeodomain transcription factor negatively regulates the pancreatic ductal cell-specific keratin 19 promoter.
• Regeneration of pancreatic islets after partial pancreatectomy in mice does not involve the reactivation of neurogenin-3.
• Identification of transcriptional targets during pancreatic growth after partial pancreatectomy and exendin-4 treatment.
• Successful growth and characterization of mouse pancreatic ductal cells: functional properties of the Ki-RAS(G12V) oncogene.
• Identification of PCIF1, a POZ domain protein that inhibits PDX-1 (MODY4) transcriptional activity.
• The role of Brn4/Pou3f4 and Pax6 in forming the pancreatic glucagon cell identity.
• The mutant K-ras oncogene causes pancreatic periductal lymphocytic infiltration and gastric mucous neck cell hyperplasia in transgenic mice.
• Neonatal exendin-4 prevents the development of diabetes in the intrauterine growth retarded rat.
• Role of endogenous glucagon-like peptide-1 in islet regeneration after partial pancreatectomy.
• Foxa2 controls Pdx1 gene expression in pancreatic beta-cells in vivo.
• Hedgehog signaling is required for effective regeneration of exocrine pancreas.
• Two conserved domains in PCIF1 mediate interaction with pancreatic transcription factor PDX-1.
• Pancreatic epithelial plasticity mediated by acinar cell transdifferentiation and generation of nestin-positive intermediates.
• Role of glucagon-like peptide-1 in the pathogenesis and treatment of diabetes mellitus.
• Origin of exocrine pancreatic cells from nestin-positive precursors in developing mouse pancreas.
• Improved glucose tolerance and acinar dysmorphogenesis by targeted expression of transcription factor PDX-1 to the exocrine pancreas.
• Tissue-specific deletion of Foxa2 in pancreatic beta cells results in hyperinsulinemic hypoglycemia.
• Insulinotropic glucagon-like peptide 1 agonists stimulate expression of homeodomain protein IDX-1 and increase islet size in mouse pancreas.
• Exendin-4 does not promote Beta-cell proliferation or survival during the early post-islet transplant period in mice.
• Developmental expression of the homeodomain protein IDX-1 in mice transgenic for an IDX-1 promoter/lacZ transcriptional reporter.
• Misexpression of the pancreatic homeodomain protein IDX-1 by the Hoxa-4 promoter associated with agenesis of the cecum.
• The development of beta-cell mass: recent progress and potential role of GLP-1.
• Exendin-4 increases histone acetylase activity and reverses epigenetic modifications that silence Pdx1 in the intrauterine growth retarded rat.
• Exendin-4 stimulates both beta-cell replication and neogenesis, resulting in increased beta-cell mass and improved glucose tolerance in diabetic rats.
• Insulin promoter factor-1 gene mutation linked to early-onset type 2 diabetes mellitus directs expression of a dominant negative isoprotein.
• Alternative mRNA splicing generates multiple forms of peptidyl-glycine alpha-amidating monooxygenase in rat atrium.
• The multifunctional peptidylglycine alpha-amidating monooxygenase gene: exon/intron organization of catalytic, processing, and routing domains.
• Impaired insulin secretion and increased insulin sensitivity in familial maturity-onset diabetes of the young 4 (insulin promoter factor 1 gene).
• Tissue specific expression of rat peptidylglycine alpha-amidating monooxygenase activity and mRNA.
• Defective mutations in the insulin promoter factor-1 (IPF-1) gene in late-onset type 2 diabetes mellitus.
• Alternative splicing and endoproteolytic processing generate tissue-specific forms of pituitary peptidylglycine alpha-amidating monooxygenase (PAM).
• Characterization of novel mRNAs encoding enzymes involved in peptide alpha-amidation.
• Proadrenocorticotropin/endorphin production and messenger ribonucleic acid levels in primary intermediate pituitary cultures: effects of serum, isoproterenol, and dibu...
• Insulin promoter factor 1 gene is not a major cause of maturity-onset diabetes of the young in French Caucasians.
• Pancreatic agenesis attributable to a single nucleotide deletion in the human IPF1 gene coding sequence.
• A newly discovered role of transcription factors involved in pancreas development and the pathogenesis of diabetes mellitus.
• Early-onset type-II diabetes mellitus (MODY4) linked to IPF1.
• The biosynthesis of neuropeptides: peptide alpha-amidation.

Schools

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• Johns Hopkins University School of Medicine

• Brigham and Women39s Hospital

• Mass Gen Hospital

• Massachusetts General Hospital

Doctors Specialties

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• Endocrinology

Accepted Insurances

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Awards

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• Elected Member

Education

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• Massachusetts General Hospital
• Brigham and Women's Hospital
• Johns Hopkins University School of Medicine

Hospital

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• Hospital of the University of Pennsylvania

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