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Miriam R. Conces

Miriam R. Conces

· Associate Professor-ClinicalVerified

Ohio State University · Translational and Molecular Pathology

Active 2007–2026

h-index14
Citations591
Papers8354 last 5y
Funding
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About

Miriam R. Conces, MD, is a pediatric pathologist at Nationwide Children’s Hospital in the Department of Pathology and Laboratory Medicine and an Associate Professor at The Ohio University College of Medicine. She serves as the Director of Surgical Pathology and Director of Immunopathology within the Division of Anatomic Pathology, with a focus on quality improvement. Her clinical expertise includes general pediatric pathology with specific interests in pediatric neoplasms, particularly neuroblastoma, as well as Hirschsprung disease and medical renal disease. Dr. Conces completed her medical education at Indiana University School of Medicine in Indianapolis, IN, followed by Anatomic Pathology and Clinical Pathology Residency at the University of Virginia Health System in Charlottesville, VA. She completed a fellowship in Pediatric Pathology at Nationwide Children’s Hospital.

Research topics

  • Medicine
  • Biology
  • Internal medicine
  • Pathology
  • Endocrinology
  • Genetics
  • Microbiology
  • Gastroenterology

Selected publications

  • Therapy-related mutational signatures in subsequent neoplasms among survivors of childhood cancer

    Cancer Discovery · 2026-04-19

    articleOpen access

    Childhood cancer survivors have heightened risk of developing subsequent neoplasms (SNs) related to therapy. We analyzed whole-genome, exome and RNA sequencing of 200 breast, meningioma, and thyroid SNs, which developed a median of 26.4 years after childhood cancer, among 160 survivors. Meningioma and thyroid SNs were enriched for driver gene rearrangements compared to de novo tumors, including NF2-disrupting alterations and kinase fusions potentially induced by radiation. Radiation correlated with increased insertion-deletion signature ID5. Nitrogen mustard treatment correlated with elevated "flat" signature SBS5 in breast and meningioma SNs; in vitro, these agents caused an unresolved flat signature associated with multiple flat COSMIC signatures. In meningioma, platinum therapy correlated with NF2 splice-site variants. Analysis of 19 multi-sample survivors revealed intrapatient heterogeneity in meningioma, including clonally independent tumors. These results demonstrate the long-term impact of childhood cancer treatment on the genomes of SNs developing in adulthood, which may guide SN treatment and prevention.

  • 1548 Benign, Atypical, or Malignant Granular Cell Tumor: Does Grading Correlate with Prognosis in Pediatric Patients? A 20-Year Institutional Experience

    Laboratory Investigation · 2026-03-01

    articleOpen access
  • Clinical and molecular characteristics of constitutional mismatch repair deficiency syndrome: a case series of five children and appraisal of diagnostic guidelines

    Diagnostic Pathology · 2026-01-22

    articleOpen access

    DNA mismatch repair (MMR) is critical for maintaining genome integrity through correction of single-base mismatches and insertion-deletion loops arising from DNA replication. Heterozygous germline alteration of MMR genes (MSH2, MSH6, MLH1, PMS2) cause autosomal dominant Lynch syndrome (LS), most commonly manifesting as colonic or endometrial cancers, although brain, ovarian, and other organ systems may be involved. Neoplasia in LS usually arises after the age of 30 years. Constitutional mismatch repair deficiency (CMMRD) is inherited in an autosomal recessive manner due to biallelic germline alteration in one of the four MMR genes. Individuals with CMMRD typically develop cancer in the first decade of life, although some may present during the second decade. We present a series of five children who developed cancer prior to the age of 20 years (range: 2-12 years) with malignancies including colonic adenocarcinoma (N = 1), T-lymphoblastic lymphoma (N = 3), and high-grade glioma (N = 4). Two patients with MSH6 alterations developed a constellation of three primary tumors: high-grade glioma, T-lymphoblastic lymphoma, and colonic neoplasia including colonic adenocarcinoma in one patient and a tubular adenoma in the other.

  • Pathology of peripheral neuroblastic tumors

    Diagnostic Pathology · 2026-01-29

    articleOpen access1st authorCorresponding

    Neuroblastoma is the most prevalent extracranial solid tumor in pediatric age populations worldwide and the most common neoplastic disease diagnosed in the first year of life. The term neuroblastoma often encompasses all peripheral neuroblastic tumors (pNTs including neuroblastoma, ganglioneuroblastoma, and ganglioneuroma) of neural crest origin. Since pNTs demonstrate a wide range of clinical behaviors, including spontaneous regression, tumor differentiation/maturation, and aggressive progression refractory to even intensive treatment modalities, these tumors are believed to be distinguished into different biological/molecular groups. For the practical purpose, risk classification systems have been developed based on combinations of so-called prognostic factors.In this review of pNTs, we describe a history of pathology, summarize epidemiology and clinical features, and outline International Neuroblastoma Pathology Classification (INPC). Then we discuss advantages and limitations of core needle biopsy and conventional biopsy of neuroblastoma. Besides the INPC, we also describe other prognostic factors, such as age at diagnosis, clinical stage, and molecular/genetic factors, since they are included in widely used Risk Classification Systems. Additionally, we discuss further molecular abnormalities closely associated with highly aggressive neruoblastomas. Towards the end, we touch on rapidly advancing technologies for establishing an artificial intelligence-assisted INPC system.

  • 486P Preliminary results from a first-in-human phase I study of a dual-conditionally binding EpCAM x CD3 bispecific T-cell engager, BA3182, in pts with treatment refractory metastatic adenocarcinoma

    Annals of Oncology · 2025-07-01

    articleOpen access
  • Safe Delivery of Ablative, Non-Adaptive Pancreas and Elective Nodal RT in Borderline Resectable and Locally Advanced Pancreatic Cancer

    International Journal of Radiation Oncology*Biology*Physics · 2025-09-01

    article
  • 877eP Non-alcoholic fatty liver disease and risk of early-onset colorectal cancer in patients with type 2 diabetes

    Annals of Oncology · 2025-09-01

    article
  • Appendiceal duplication leading to recurrent ileocolonic intussusception: A case report

    Journal of Pediatric Surgery Case Reports · 2025-11-06

    articleOpen access

    Appendiceal duplication is a rare congenital anomaly of the appendix, often identified incidentally, and is estimated to be present in 0.004–0.009% of the population. Rarely, an appendiceal duplication may act as a lead point for recurrent ileocolonic intussusception. This case describes a 15-year-old male with celiac disease who initially presented with ileocolonic intussusception for which he underwent exploratory laparotomy for intussusception reduction at a local institution. Intra-operatively, there was concern for an underlying colonic polyp. He subsequently underwent colonoscopy and CT enterography, which both revealed no evidence of a defined pathologic lead point. He then presented two months later to our institution with recurrent ileocolonic intussusception, which was reduced via air contrast enema. He was monitored overnight and discharged the following day. Three days after this, he again developed abdominal pain and was identified to have recurrent ileocolonic intussusception, which was successfully reduced via air contrast enema. Repeat CT enterography identified no pathologic lead point. He was monitored overnight and discharged with plans for outpatient ileocecectomy. One day later, however, his pain recurred, and he was again diagnosed with ileocolonic intussusception via abdominal ultrasound. This was successfully reduced via air contrast enema, and he was taken to the operating room for planned laparoscopic ileocecectomy to prevent further recurrence. Intra-operatively, there was no evidence of a clear pathologic lead point, but there were significant adhesive colonic peritoneal bands noted, as well as an enlarged but not inflamed appendix. On final pathology, he was found to have appendiceal duplication with otherwise benign ileocecal pathology. He recovered uneventfully in the hospital and was discharged on post-operative day two. He has had no further episodes of recurrence for four months post-operatively. Appendiceal duplication is a rare congenital anomaly that should be considered as a potential etiology for otherwise unexplained recurrent ileocolonic intussusception.

  • Molecular landscape of extra-pulmonary small cell neuroendocrine carcinomas based on site of origin

    Endocrine Abstracts · 2025-03-06

    article
  • Uncovering genomic differences between small and large cell extra-pulmonary neuroendocrine carcinomas

    Endocrine Abstracts · 2025-03-06

    article

Frequent coauthors

  • Michael Arnold

    University of Colorado Denver

    119 shared
  • Selene C. Koo

    St. Jude Children's Research Hospital

    85 shared
  • Sarah Beach

    Ohio University

    74 shared
  • Mai He

    Washington University in St. Louis

    73 shared
  • Louis P. Dehner

    Washington University Medical Center

    73 shared
  • Aadil Ahmed

    Loyola University Chicago

    72 shared
  • Joanna Kitlińska

    Georgetown University Medical Center

    72 shared
  • Brooj Abro

    Emory University

    72 shared

Awards & honors

  • Faculty Leadership Award, Nationwide Children’s Hospital, 20…
  • Excellence in Teaching Award, Nationwide Children’s Hospital…
  • Lotte Straus Prize, Society for Pediatric Pathology, 2017
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