About

Peter Allen is the David C. Sabiston, Jr. Distinguished Professor of Surgery at Duke University. He serves as a Professor of Surgery and the Chair of Surgery within the Duke Department of Surgery. Additionally, he holds the position of Vice President for Cancer Services and is a member of the Duke Cancer Institute. His professional focus includes surgical oncology, hepatopancreatobiliary surgery, and complex general surgical oncology. Dr. Allen is involved in pancreatic cancer research and oversees the Pancreatic Cancer Research Laboratory. His work emphasizes advancing surgical techniques and cancer treatment, contributing significantly to the field through leadership roles and research initiatives at Duke University.

Research topics

• Internal medicine
• Medicine
• Oncology
• General surgery
• Surgery
• Economics
• Statistics

Selected publications

• Prognostic value of ctDNA monitoring in patients with resectable pancreatic ductal adenocarcinoma during surveillance.

  Journal of Clinical Oncology · 2026-01-10

  articleSenior author

  778 Background: Pancreatic ductal adenocarcinoma (PDAC) has a high recurrence rate, with up to 80% of patients experiencing disease recurrence within two years of surgical resection. Standard postoperative monitoring with imaging and serum tumor markers has significant limitations. Here, we evaluated the prognostic value of longitudinal circulating tumor (ct)DNA assessment in an updated cohort of patients with resected PDAC, representing a larger sample size and longer clinical follow-up during post-treatment surveillance. Methods: We retrospectively analyzed 292 banked plasma samples from 43 patients with localized PDAC who underwent surgical resection +/- neoadjuvant and/or adjuvant chemotherapy. Longitudinally collected blood samples during surveillance (from post-definitive treatment to the end of follow-up/recurrence) were used for ctDNA analysis using the personalized, tumor-informed 16-plex PCR-NGS assay (Signatera RUO, Natera, Inc.). The association of ctDNA status with recurrence-free survival (RFS) was evaluated using the Kaplan-Meier method, and comparisons were accomplished using log-rank tests. A multivariable Cox proportional hazards model was used to identify the most significant prognostic factor associated with RFS. Results: Among the 43 patients included in this analysis, 37% (16) had stage I, 30% (13) had stage II, and 33% (14) had stage III disease. The median patient age was 69 years (range: 51-86), and the median follow-up was 25 months (range: 1-52). The median plasma volume was 4.5 mL (range: 0.6-6.8), with ~half of the patient samples with <2 mL of plasma. 32.6% (14/43) received neoadjuvant chemotherapy (NAC) and 62.8% (27/43) received adjuvant chemotherapy (ACT). During follow-up, 72% (31/43) of patients relapsed, 68% (21/31) of whom tested ctDNA-positive at one or more time points post-surgery. In the surveillance window, 32% (10/31) of patients were positive for ctDNA, all of whom relapsed. ctDNA-positivity in the surveillance window was associated with significantly inferior RFS (HR: 16.1, 95% CI: 3.79-68.17, P=0.0002). Upon adjusting for other clinicopathological factors (stage and surgical margin), the multivariate analysis confirmed ctDNA-positivity during surveillance to be the most significant prognostic factor associated with RFS (HR: 8.4, 95%CI: 2.84–24.8, P<0.001). Conclusions: Despite the low sample quality in this cohort, ctDNA showed prognostic value, demonstrating the clinical utility of longitudinal ctDNA monitoring during surveillance.

  PublisherDOI

• Group Authors List 1 from The Global State of Blood Cancers: An Ongoing Challenge

  2026-01-12

  articleOpen access

  <p>List of committee members</p>

  PublisherDOI

• Prognostic Implications of Codon-Specific <i>KRAS</i> Mutations in Localized and Advanced Stages of Pancreatic Cancer

  JCO Precision Oncology · 2026-02-01

  articleOpen access

  PURPOSE Although KRAS mutations represent the primary oncogenic driver in pancreatic ductal adenocarcinoma (PDAC), the association between codon-specific alterations and patient outcomes remains poorly elucidated, largely because of a lack of data sets coupling genomic profiling with rich clinical annotations across disease stages. MATERIALS AND METHODS We used American Association for Cancer Research's GENIE Biopharma Consortium Pancreas v1.2 data set to test the association of codon-specific KRAS mutations with clinicogenomic features and patient outcomes in patients with PDAC diagnosed with localized (stages I to III) and advanced disease (stage IV). Overall survival (OS) was compared using Kaplan-Meier and multivariable Cox proportional hazards methods. RESULTS Among 1,032 eligible patients, 949 (92%) exhibited mutant KRAS . These mutations were predominantly observed at G12D (n = 390, 41%), G12V (n = 305, 32%), and G12R (n = 149, 16%). In the group of patients who presented with localized disease, those with G12V mutation had notably longer survival compared with G12D mutation ( P = .03). By contrast, patients with G12V mutation who presented with metastatic disease experienced shorter OS compared with those with G12R ( P = .04) and G12D mutations ( P = .04). Furthermore, no significant differences were observed in the frequencies of coaltered driver genes, including TP53 , CDKN2A , and SMAD4 , across the different KRAS mutations. CONCLUSION These findings demonstrated that codon-specific KRAS mutations affect PDAC outcomes differently based on disease stage at diagnosis. As studies testing KRAS inhibitors continue to emerge and mature, the prognostic variability of individual KRAS mutations must be carefully considered to avoid confounding and ensure accurate evaluation of therapeutic efficacy in early-phase studies.

  PublisherDOI

• Data from The Global State of Blood Cancers: An Ongoing Challenge

  2026-01-12

  articleOpen access

  &lt;div&gt;Summary:&lt;p&gt;The state of the blood cancer field and its toll on patient mortality and morbidity, adapted from the 15th edition of the annual &lt;i&gt;AACR Cancer Progress Report&lt;/i&gt; (&lt;a href="https://cancerprogressreport.aacr.org/progress/" target="_blank"&gt;https://cancerprogressreport.aacr.org/progress/&lt;/a&gt;), is presented to the US Congress and the public.&lt;/p&gt;&lt;/div&gt;

  PublisherDOI

• Prognostic Implications of Codon-Specific <i>KRAS</i> Mutations in Localized and Advanced Stages of Pancreatic Cancer

  medRxiv · 2025-02-05

  preprintOpen access

  Abstract Introduction While KRAS mutations represent the primary oncogenic driver in pancreatic ductal adenocarcinoma (PDAC), the association between codon-specific alterations and patient outcomes remains poorly elucidated, largely due to a lack of datasets coupling genomic profiling with rich clinical annotations across disease stages. Patients and Methods We utilized AACR’s GENIE Biopharma Consortium Pancreas v1.2 dataset to test the associating of codon-specific KRAS mutations with clinicogenomic features and patient outcomes in PDAC patients diagnosed with localized (stages I-III) and advanced disease (stage IV). Overall survival was compared using Kaplan–Meier and multivariable Cox proportional hazards methods. Results Among 1,032 eligible patients, 949 (92%) exhibited mutant KRAS . These mutations were predominantly observed at G12D (n=390, 41%), G12V (n=305, 32%), and G12R (n=149, 16%). In the group of patients who presented with localized disease, those with G12V mutation had notably longer survival compared to G12D mutation ( P = 0.002). In contrast, patients with G12V mutation who presented with metastatic disease experienced shorter overall survival compared to those with G12R ( P = 0.005), and G12D mutations ( P = 0.009). Furthermore, no significant differences were observed in the frequencies of co-altered driver genes, including TP53 , CDKN2A , and SMAD4 , across the different KRAS mutations. Conclusions These findings demonstrated that codon-specific KRAS mutations impact PDAC outcomes differently based on disease stage at diagnosis. As studies testing KRAS inhibitors continue to emerge and mature, these data offer important contextual insights regarding survival outcomes associated with codon-specific KRAS mutations based on existing therapeutic approaches.

  PublisherOA PDFDOI

• Prognostic factors for patients with T2/T3 gallbladder cancer: Does extent of resection matter?

  Surgical Oncology Insight · 2025-01-28

  articleOpen access
  PublisherOA PDFDOI

• ASO Visual Abstract: Perioperative and Oncologic Outcomes of Hepatic Arterial Infusion Pump Chemotherapy for Patients with Unresectable Colorectal Liver Metastases at an Expanding Hai Program

  Annals of Surgical Oncology · 2025-01-02

  article
  PublisherDOI

• Multiplexed glycan immunofluorescence identification of pancreatic cancer cell subpopulations in both tumor and blood samples

  Science Advances · 2025-03-07 · 3 citations

  articleOpen access

  Pancreatic ductal adenocarcinoma (PDAC) tumor heterogeneity impedes the development of biomarker assays for early disease detection. We hypothesized that PDAC cell subpopulations could be identified by aberrant glycan signatures in both tumor tissue and blood samples. We used multiplexed glycan immunofluorescence to distinguish between PDAC and noncancer cell subpopulations within tumor tissue, and we developed hybrid glycan sandwich assays to determine whether the aberrant glycan signatures could be detected in blood samples. We found that PDAC cells were identified by signatures of glycans detected by four glycan-binding proteins (VVL, CA19-9, sTRA, and GM2) and that there are three types of glycan-defined PDAC tumors: sTRA type, CA19-9 type, and intermixed. In patient-matched tumor and blood samples, the PDAC tumor type could be determined by the aberrant glycans in the blood. As a result, the combined assays of aberrant glycan signatures were more sensitive and specific than any individual assay. Our results demonstrate a methodology to detect and stratify PDAC.

  PublisherDOI

• Supplementary Tables S1-S9 from Spatial Transcriptomics of Intraductal Papillary Mucinous Neoplasms Reveals Divergent Indolent and Malignant States

  2025-05-01

  supplementary-materialsOpen accessSenior author

  &lt;p&gt;Table S1: Gene Sets; Table S2: Patient Clinical Information; Table S3: Clustering Results; Table S4: Differential expression analysis between clusters (full dataset); Table S5: GSEA results (full dataset); Table S6: Stromal highly variable genes; Table S7: DE analysis of NL-LGD subset; Table S8: GSEA results (NL-LGD subset); Table S9: Validation dataset clustering results&lt;/p&gt;

  PublisherDOI

• ASO Visual Abstract: Survival Outcomes and Genetic Characteristics of Resected Pancreatic Acinar Cell Carcinoma

  Annals of Surgical Oncology · 2025-06-18

  articleOpen access

  This multi-institutional series of resected pancreatic acinar cell carcinomas demonstrated a median overall survival longer than 70 months (https:// doi.org/ 10. 1245/ s10434-024-16331-4).Mutations within the Homologous Recombination Repair (HRR) pathway were identified in 45% of sequenced tumor specimen, with core HRR mutations in 26%, suggesting opportunities for informed targeted therapeutic options for pancreatic acinar cell carcinoma (pACC).

  PublisherOA PDFDOI

Frequent coauthors

• Sabino Zani

  Duke Medical Center

  70 shared

• Michael E. Lidsky

  Duke Medical Center

  58 shared

• Dan G. Blazer

  Duke Medical Center

  50 shared

• Daniel P. Nussbaum

  Duke University

  41 shared

• Kevin N. Shah

  Duke University

  34 shared

• Demetrios Moris

  Duke University Hospital

  32 shared

• William R. Jarnagin

  Memorial Sloan Kettering Cancer Center

  30 shared

• Austin M. Eckhoff

  Duke University

  25 shared