Ralph H. Hruban

Johns Hopkins University

Full Professor(heuristic)

Pancreatic and Hepatic Oncology Research · Oncology

h-index209

i10-index938

Publications1,972

Citations206,095

Grants

No NSF/NIH grants on record.

Career Trajectory

Research Cluster Map

Direct collaborators. Node size = influence, colour = community, dashed = past collaboration.

Potential Collaborators

Recent Publications

Last 2 years · showing 20 of 137

Insulinomatosis: A case report of a multifocal insulin-secreting entity
Radiology Case Reports · 2026-06-14
Virtual multiplex staining of the pancreatic islets across type 1 diabetes progression using a Schrödinger bridge
bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-17
Follow-up of prior CT scans as part of patient care and continuous learning: A call to action
Clinical Imaging · 2026-01-29
Metastatic Pancreatic Acinar Cell Carcinoma to the Liver Mimicking Neuroendocrine Tumor (NET) and Pancreatic Ductal Adenocarcinoma (PDAC): A series of 7 casesPreprint
SSRN Electronic Journal · 2026-01-01
Figure S4 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Supplementary Notes 1-5 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Figure S3 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Figure S1 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
PancreaSeq Genomic Classifier (PancreaSeq GC) Improves Pancreatic Cyst Classification and Detection of Advanced Neoplasia: A Multi-institutional Validation Study
Annals of Surgical Oncology · 2025-12-12 · 5 citations
Figure S10 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Figure S8 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Figure S6 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Figure S7 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Figure S9 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Figure S2 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Supplementary Tables S1 and S2 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Figure S5 from The Origin of Highly Elevated Cell-Free DNA in Healthy Individuals and Patients with Pancreatic, Colorectal, Lung, or Ovarian Cancer
2025-12-12
Supplementary Table 4 from Comprehensive DNA Methylation Analysis Indicates That Pancreatic Intraepithelial Neoplasia Lesions Are Acinar-Derived and Epigenetically Primed for Carcinogenesis
2025-11-24
Supplementary Table 5 from Comprehensive DNA Methylation Analysis Indicates That Pancreatic Intraepithelial Neoplasia Lesions Are Acinar-Derived and Epigenetically Primed for Carcinogenesis
2025-11-24
Supplementary Table 1 from Comprehensive DNA Methylation Analysis Indicates That Pancreatic Intraepithelial Neoplasia Lesions Are Acinar-Derived and Epigenetically Primed for Carcinogenesis
2025-11-24

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