About

Eric Schiffman, DDS, MS, is a Professor and the Director of Clinical Research in the School of Dentistry at the University of Minnesota. He has received over $19 million in research funding from the National Institutes of Health (NIH) and has authored over 60 peer-reviewed publications, 12 book chapters, and holds 3 patents with another pending. His past research as an NIH study principal investigator includes developing and publishing validated Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) for the most common TMD, applicable in both clinical and research settings. He has also conducted research on TMD management, assessing the long-term effectiveness of medical management versus comprehensive rehabilitation with and without TMJ surgery, and the longitudinal impact of intra-articular TMJ disorders on jaw pain, function, and disability. Additionally, he contributed to the NIH-funded National Dental Practice-Based Research Network by evaluating how dentists manage TMD patients in their practices. His recent work includes developing and clinically testing a new version of the Restful Jaw device, designed to support the jaw during dental procedures, including third molar removal, funded through NIH/NIDCR’s STTR and SBIR grants.

Research topics

• Genetics
• Cell biology
• Biology
• Computational biology
• Computer Science
• Medicine
• Anatomy

Selected publications

• The Society for Craniofacial Genetics and Developmental Biology 48th Annual Meeting

  American Journal of Medical Genetics Part A · 2026-04-09

  article1st authorCorresponding

  The Society for Craniofacial Genetics and Developmental Biology (SCGDB) held its 48th Annual Meeting at the University of Minnesota in Minneapolis on September 29-October 1, 2025. On the first day of the meeting, Drs. Timothy Cox and Jennifer Fish were honored with Excellence in Craniofacial Research Awards for their exceptional contributions to the field of craniofacial biology. The following 2 days of the meeting featured five sessions that highlighted new discoveries in human genetics, systems biology of craniofacial development and disease, evolutionary connections, signaling mechanisms, and a special session on clinical and patient perspectives. The meeting also featured workshops on scientific writing and the role of artificial intelligence in advancing research and care. A poster session facilitated dynamic and insightful interactions among the 113 attendees, who represented diverse career stages and research backgrounds in developmental biology and genetics, further strengthening the SCGDB community.

  PublisherDOI

• Abstract 3500: Synergistic targeting of EP300/CBP and EYA co-activators collapses the rhabdomyosarcoma core regulatory circuit

  Cancer Research · 2026-04-03

  article

  Abstract Rhabdomyosarcoma (RMS) is a high-risk and lethal pediatric sarcoma that resembles developing skeletal muscle. RMS tumors have low mutation burdens, but these scant mutations often alter genes involved in transcriptional control. Transcriptional dysregulation is critical to RMS pathogenesis, supported by studies in both RMS tumors carrying mutationally derived chimeric transcription factors (“fusion positive (FP)”), or those without (“fusion negative” (FN)). However, mechanisms to selectively target dysregulated transcription in RMS remain outstanding. Here, we develop a novel approach targeting RMS transcription comprising simultaneous targeting of two distinctly acting transcriptional co-activators. We discover a common cell identity-controlling pan-RMS core regulatory circuit (CRC) composed of oncogenic and lineage-specific myogenic master transcription factors (mTFs). These mTFs are regulated by super-enhancers, and they co-bind genome-wide to control the malignant transcriptome of both FP- and FN-RMS. Using a super-enhancer-based reporter screen, we identify the EP300/CBP inhibitor A485 as a potent inhibitor of the pan-RMS CRC, though efficacy of this compound was limited by toxicity. To enhance on-target specificity, we identify the protein EYA2 as a co-factor that binds directly to SIX1, a member of the pan-RMS CRC and exploit a recently developed second-generation EYA1/2 tyrosine phosphatase inhibitor, LG1-34, to inactivate its function. While A485 and LG1-34 independently reduce mTF transcription and drive RMS cell death, in combination, these agents function synergistically to reduce RMS growth in vitro and in vivo. These results demonstrate that combined targeting of enhancer maintenance and CRC cofactors is a powerful strategy to suppress the RMS transcriptome and enforce RMS cell death. Citation Format: Annika Gustafson, Stephanie Nance, Berkley Gryder, Noha A. Shendy, Lars Wick, Grace McKay-Corkum, K. Elaine Ritter, Stephen Connor Purdy, Arthur R. Wolin, Sheera R. Rosenbaum, Sabateeshan Mathavarajah, Nickerson A. Demelfi, Yueyang Wang, Yang Zhang, Mark W. W. Zimmerman, Anoop M. Kavirayani, John Hardin, Alexander LaVeck, Xiang Wang, Neekesh V. Dharia, Andrew Hong, Guillaume Kugener, Jesse S. Boehm, Jennifer Roth, Javed Khan, Francisca Vasquez, Kristin B. Artinger, Rui Zhao, David M. Langenau, Jun Qi, Kimberly Stegmaier, Heide L. Ford, Adam D. Durbin, Brian J. Abraham. Synergistic targeting of EP300/CBP and EYA co-activators collapses the rhabdomyosarcoma core regulatory circuit [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 1 (Regular Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(7 Suppl):Abstract nr 3500.

  PublisherDOI

• PRDM paralogs are required for Meckel's cartilage formation during mandibular bone development

  Developmental Biology · 2025-12-04 · 1 citations

  articleOpen access
  PublisherOA PDFDOI

• PRDM paralogs are required for Meckel’s cartilage formation during mandibular bone development

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-07-22

  preprintOpen access

  Abstract Mandibular bone development utilizes both endochondral ossification, forming from the cartilaginous anlage Meckel’s cartilage derived from neural crest cells (NCC) and intramembranous ossification with direct differentiation of NCCs toward osteoblasts. Wnt/β-catenin signaling drives osteogenic vs chondrogenic differentiation and must be tightly controlled during the differentiation of osteochondroprogenitors. Chromatin remodelers add hierarchal regulation to the activation and repression of crucially timed gene regulatory networks and signaling cascades. In this study, we investigated the function of two chromatin remodelers—histone methyltransferases, PRDM3 and PRDM16 during murine craniofacial development. Conditionally ablating both Prdm3 and Prdm16 in the neural crest lineage using the Wnt1-Cre driver resulted in dramatic craniofacial phenotypes, including a severely hypoplastic mandible with complete absence of Meckel’s cartilage at E18.5. Focusing on the Meckel’s cartilage and mandibular bone phenotype, histological analysis demonstrated a significant increase in RUNX2+ osteoblast precursors, and loss of SOX9+ chondrogenic cells, suggesting an increase in osteoblast progenitors at the expense of chondrocytes that would otherwise form the Meckel’s cartilage. This was not due to alterations in proliferation or apoptosis, as we observed no significant changes in the number of phosphoH3+ or cleaved caspase3+ cells in the mandibular process at E11.5, suggesting lack of NCC-derived chondrocytes is due to a change in NCC osteochondroprogenitor fate decisions. mRNA transcripts and protein abundance of Wnt/β-catenin signaling components were elevated in the mandibular process during initial NCC osteochondroprogenitor condensation events, suggesting PRDM3 and PRDM16 normally restrict expression of Wnt/β-catenin signaling components during NCC-derived osteochondroprogenitor differentiation to promote chondrogenesis and Meckel’s cartilage formation. Taken together, PRDM3 and PRDM16 are required for NCC differentiation toward chondrocytes during Meckel’s cartilage formation by controlling proper spatiotemporal Wnt/β-catenin transcriptional activity and this process is necessary for morphogenesis of the developing mandible.

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• Myogenesis gone awry: the role of developmental pathways in rhabdomyosarcoma

  Frontiers in Cell and Developmental Biology · 2025-01-20 · 4 citations

  reviewOpen access

  Rhabdomyosarcoma is a soft-tissue sarcoma that occurs most frequently in pediatric patients and has poor survival rates in patients with recurrent or metastatic disease. There are two major sub-types of RMS: fusion-positive (FP-RMS) and fusion-negative (FN-RMS); with FP-RMS typically containing chromosomal translocations between the PAX3/7-FOXO1 loci. Regardless of subtype, RMS resembles embryonic skeletal muscle as it expresses the myogenic regulatory factors (MRFs), MYOD1 and MYOG. During normal myogenesis, these developmental transcription factors (TFs) orchestrate the formation of terminally differentiated, striated, and multinucleated skeletal muscle. However, in RMS these TFs become dysregulated such that they enable the sustained properties of malignancy. In FP-RMS, the PAX3/7-FOXO1 chromosomal translocation results in restructured chromatin, altering the binding of many MRFs and driving an oncogenic state. In FN-RMS, re-expression of MRFs, as well as other myogenic TFs, blocks terminal differentiation and holds cells in a proliferative, stem-cell-like state. In this review, we delve into the myogenic transcriptional networks that are dysregulated in and contribute to RMS progression. Advances in understanding the mechanisms through which myogenesis becomes stalled in RMS will lead to new tumor-specific therapies that target these aberrantly expressed developmental transcriptional pathways.

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• Human split hand/foot variants are not as functional as wildtype human <i>PRDM1</i> in the rescue of craniofacial defects

  Birth Defects Research · 2024-03-01 · 2 citations

  articleOpen accessSenior authorCorresponding

  Abstract Background Split hand/foot malformation (SHFM) is a congenital limb disorder presenting with limb anomalies, such as missing, hypoplastic, or fused digits, and often craniofacial defects, including a cleft lip/palate, microdontia, micrognathia, or maxillary hypoplasia. We previously identified three novel variants in the transcription factor, PRDM1 , that are associated with SHFM phenotypes. One individual also presented with a high arch palate. Studies in vertebrates indicate that PRDM1 is important for development of the skull; however, prior to our study, human variants in PRDM1 had not been associated with craniofacial anomalies. Methods Using transient mRNA overexpression assays in prdm1a −/− mutant zebrafish, we tested whether the PRDM1 SHFM variants were functional and could lead to a rescue of the craniofacial defects observed in prdm1a −/− mutants. We also mined previously published CUT&amp;RUN and RNA‐seq datasets that sorted EGFP‐positive cells from a Tg ( Mmu : Prx1‐EGFP ) transgenic line that labels the pectoral fin, pharyngeal arches, and dorsal part of the head to examine Prdm1a binding and the effect of Prdm1a loss on craniofacial genes. Results The prdm1a −/− mutants exhibit craniofacial defects including a hypoplastic neurocranium, a loss of posterior ceratobranchial arches, a shorter palatoquadrate, and an inverted ceratohyal. Injection of wildtype (WT) hPRDM1 in prdm1a −/− mutants partially rescues the palatoquadrate phenotype. However, injection of each of the three SHFM variants fails to rescue this skeletal defect. Loss of prdm1a leads to a decreased expression of important craniofacial genes by RNA‐seq, including emilin3a , confirmed by hybridization chain reaction expression. Other genes including dlx5a/dlx6a , hand2 , sox9b , col2a1a , and hoxb genes are also reduced. Validation by real‐time quantitative PCR in the anterior half of zebrafish embryos failed to confirm the expression changes suggesting that the differences are enriched in prx1 expressing cells. Conclusion These data suggest that the three SHFM variants are likely not functional and may be associated with the craniofacial defects observed in the humans. Finally, they demonstrate how Prdm1a can directly bind and regulate genes involved in craniofacial development.

  PublisherOA PDFDOI

• PRDM1 DNA-binding zinc finger domain is required for normal limb development and is disrupted in split hand/foot malformation

  Disease Models & Mechanisms · 2023-04-01 · 9 citations

  articleOpen accessSenior author

  Split hand/foot malformation (SHFM) is a rare limb abnormality with clefting of the fingers and/or toes. For many individuals, the genetic etiology is unknown. Through whole-exome and targeted sequencing, we detected three novel variants in a gene encoding a transcription factor, PRDM1, that arose de novo in families with SHFM or segregated with the phenotype. PRDM1 is required for limb development; however, its role is not well understood and it is unclear how the PRDM1 variants affect protein function. Using transient and stable overexpression rescue experiments in zebrafish, we show that the variants disrupt the proline/serine-rich and DNA-binding zinc finger domains, resulting in a dominant-negative effect. Through gene expression assays, RNA sequencing, and CUT&RUN in isolated pectoral fin cells, we demonstrate that Prdm1a directly binds to and regulates genes required for fin induction, outgrowth and anterior/posterior patterning, such as fgfr1a, dlx5a, dlx6a and smo. Taken together, these results improve our understanding of the role of PRDM1 in the limb gene regulatory network and identified novel PRDM1 variants that link to SHFM in humans.

  PublisherDOI

• SPLIT HAND/FOOT VARIANTS FAIL TO RESCUE PRDM1A MUTANT CRANIOFACIAL DEFECTS

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-05-22

  preprintOpen accessSenior authorCorresponding

  Abstract Background Split Hand/Foot Malformation (SHFM) is a congenital limb disorder presenting with limb anomalies, such as missing, hypoplastic, or fused digits, and often craniofacial defects, including a cleft lip/palate, microdontia, micrognathia, or maxillary hypoplasia. We previously identified three novel variants in the transcription factor, PRDM1 , that are associated with SHFM phenotypes. One individual also presented with a high arch palate. Studies in vertebrates indicate that PRDM1 is important for development of the skull; however, prior to our study, human variants in PRDM1 had not been associated with craniofacial anomalies. Methods Using transient mRNA overexpression assays in prdm1a -/- mutant zebrafish, we tested whether the PRDM1 SHFM variants were functional and could lead to a rescue of the craniofacial defects observed in prdm1a -/- mutants. We also mined a CUT&amp;RUN and RNA-seq dataset to examine Prdm1a binding and the effect of Prdm1a loss on craniofacial genes. Results prdm1a -/- mutants exhibit craniofacial defects including a hypoplastic neurocranium, a loss of posterior ceratobranchial arches, a shorter palatoquadrate, and an inverted ceratohyal. Injection of wildtype hPRDM1 in prdm1a -/- mutants partially rescues these structures. However, injection of each of the three SHFM variants fails to rescue the skeletal defects. Loss of prdm1a leads to a decreased expression of important craniofacial genes, such as dlx5a/dlx6a, hand2, sox9b, col2a1a , and hoxb genes. Conclusion These data suggest that the three SHFM variants are not functional and may have led to the craniofacial defects observed in the humans. Finally, they demonstrate how Prdm1a can directly bind and regulate craniofacial gene expression.

  PublisherOA PDFDOI

• Issue Information

  Birth Defects Research · 2023-01-15

  paratextOpen access
  PublisherOA PDFDOI

• Issue Information

  Birth Defects Research · 2023-04-02

  paratextOpen access
  PublisherOA PDFDOI

Recent grants

• NIH Grant R01DE017699

  NIH · $1.8M · 2014

• NIH Grant F32HD008209

  NIH · $94k

• NIH Grant U01DE020076

  NIH · $1.9M · 2015

• Function of chromatin modifiers in cranial neural crest development

  NIH · $3.2M · 2015–2022

• NIH Grant R01HD050698

  NIH · $1.2M · 2012

Frequent coauthors

• Brittany T. Truong

  University of Colorado Anschutz Medical Campus

  28 shared

• Linda Roberts

  24 shared

• Anne H. Monsoro-Burq

  Université Paris-Saclay

  22 shared

• James C. Costello

  University of Colorado Cancer Center

  22 shared

• Lomeli C. Shull

  University of Colorado Anschutz Medical Campus

  22 shared

• Laura Hernandez‐Lagunas

  University of Colorado Anschutz Medical Campus

  20 shared

• Heide L. Ford

  University of Colorado Anschutz Medical Campus

  19 shared

• Ezra Lencer

  Lafayette College

  18 shared