James Abbruzzese

Overview:

My research interests include the clinical study and treatment of pancreatic cancer.

Positions:

D. C. I. Distinguished Professor of Medical Oncology

Medicine, Medical Oncology
School of Medicine

Professor of Medicine

Medicine, Medical Oncology
School of Medicine

Chief, Division of Medical Oncology

Medicine, Medical Oncology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.D. 1978

The University of Chicago

Intern, Internal Medicine

Johns Hopkins University School of Medicine

Resident, Internal Medicine

Johns Hopkins University School of Medicine

Grants:

Topic Refinement, Task order 9 Topic Briefs

Administered By
Duke Clinical Research Institute
Awarded By
Patient Centered Outcomes Research Institute
Role
Co Investigator
Start Date
End Date

Publications:

Association of diabetes and perineural invasion in pancreatic cancer.

Diabetes and perineural invasion are frequently observed in pancreatic cancer. In this study, we tested possible relations between diabetes and perineural invasion in patients with resected pancreatic cancer. We conducted a retrospective study in 544 cases of resected pancreatic adenocarcinoma seen at the University of Texas MD Anderson Cancer Center during 1996-2011. Information on tumor characteristics, diabetes history, and survival time was collected by personal interview and medical record review. Patients with diabetes before or at the time of the pancreatic cancer diagnosis were considered diabetes only. Pearson χ(2) test was used to compare categorical variables in diabetic and nondiabetic groups. Kaplan-Meier plot, log-rank test, and Cox proportional regression models were applied in survival analysis. The prevalence of diabetes and perineural invasion was 26.5% and 86.9%, respectively, in this study population. Patients with diabetes had a significantly higher prevalence of perineural invasion (92.4%) than those without diabetes (85%) (P = 0.025, χ(2) test). Diabetes was not associated with other pathological characteristics of the tumor, such as tumor size, lymphovascular invasion, tumor grade, lymph node metastasis, and resection margin status. Diabetic patients had a significantly lower frequency of abdominal pain (P = 0.01), but a slightly higher frequency of weight loss (P = 0.078) as early symptoms of their cancer. Both diabetes and perineural invasion were related to worse survival and increased risk of death after adjusting for tumor grade and margin and node status (P = 0.036 and 0.019, respectively). The observed associations of diabetes and perineural invasion as well as reduced frequency of pain as early symptom of pancreatic cancer support the hypothesis that diabetes may contribute to pancreatic progression via the mechanism of nerve damage.
Authors
Sahin, IH; Shama, MA; Tanaka, M; Abbruzzese, JL; Curley, SA; Hassan, M; Li, D
MLA Citation
Sahin, Ibrahim Halil, et al. “Association of diabetes and perineural invasion in pancreatic cancer.Cancer Med, vol. 1, no. 3, Dec. 2012, pp. 357–62. Pubmed, doi:10.1002/cam4.43.
URI
https://scholars.duke.edu/individual/pub1427477
PMID
23342285
Source
pubmed
Published In
Cancer Medicine
Volume
1
Published Date
Start Page
357
End Page
362
DOI
10.1002/cam4.43

A phase 2 biomarker trial of combination cediranib and olaparib in relapsed platinum (plat) sensitive and plat resistant ovarian cancer (ovca).

Authors
Liu, JF; Barry, WT; Wenham, RM; Wahner Hendrickson, AE; Armstrong, DK; Chan, N; Cohn, DE; Lee, J-M; Penson, RT; Cristea, MC; Abbruzzese, JL; MATSUO, K; Olawaiye, A; Farooq, S; Swisher, EM; Van Allen, EM; Shapiro, G; Kohn, EC; Ivy, SP; Matulonis, UA
MLA Citation
Liu, Joyce F., et al. “A phase 2 biomarker trial of combination cediranib and olaparib in relapsed platinum (plat) sensitive and plat resistant ovarian cancer (ovca).Journal of Clinical Oncology, vol. 36, no. 15_suppl, American Society of Clinical Oncology (ASCO), 2018, pp. 5519–5519. Crossref, doi:10.1200/jco.2018.36.15_suppl.5519.
URI
https://scholars.duke.edu/individual/pub1441240
Source
crossref
Published In
Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology
Volume
36
Published Date
Start Page
5519
End Page
5519
DOI
10.1200/jco.2018.36.15_suppl.5519

Genetic variants of the peroxisome proliferator-activated receptor (PPAR) signaling pathway genes and risk of pancreatic cancer.

Because the peroxisome proliferator-activated receptor (PPAR) signaling pathway is involved in development and progression of pancreatic cancer, we investigated associations between genetic variants of the PPAR pathway genes and pancreatic cancer risk by using three published genome-wide association study datasets including 8477 cases and 6946 controls of European ancestry. Expression quantitative trait loci (eQTL) analysis was also performed for correlations between genotypes of the identified genetic variants and messenger RNA (mRNA) expression levels of their genes by using available databases of the 1000 Genomes, TCGA, and GTEx projects. In the single-locus logistic regression analysis, we identified 1141 out of 17 532 significant single-nucleotide polymorphisms (SNPs) in 112 PPAR pathway genes. Further multivariate logistic regression analysis identified three independent, potentially functional loci (rs12947620 in MED1, rs11079651 in PRKCA, and rs34367566 in PRKCB) for pancreatic cancer risk (odds ratio [OR] = 1.11, 95% confidence interval [CI], [1.06-1.17], P = 5.46 × 10-5 ; OR = 1.10, 95% CI, [1.04-1.15], P = 1.99 × 10-4 ; and OR = 1.09, 95% CI, [1.04-1.14], P = 3.16 × 10-4 , respectively) among 65 SNPs that passed multiple comparison correction by false discovery rate (< 0.2). When risk genotypes of these three SNPs were combined, carriers with 2 to 3 unfavorable genotypes (NUGs) had a higher risk of pancreatic cancer than those with 0 to 1 NUGs. The eQTL analysis showed that rs34367566 A>AG was associated with decreased expression levels of PRKCB mRNA in 373 lymphoblastoid cell lines. Our findings indicate that genetic variants of the PPAR pathway genes, particularly MED1, PRKCA, and PRKCB, may contribute to susceptibility to pancreatic cancer.
Authors
Liu, X; Qian, D; Liu, H; Abbruzzese, JL; Luo, S; Walsh, KM; Wei, Q
MLA Citation
Liu, Xiaowen, et al. “Genetic variants of the peroxisome proliferator-activated receptor (PPAR) signaling pathway genes and risk of pancreatic cancer.Mol Carcinog, vol. 59, no. 8, Aug. 2020, pp. 930–39. Pubmed, doi:10.1002/mc.23208.
URI
https://scholars.duke.edu/individual/pub1439325
PMID
32367578
Source
pubmed
Published In
Molecular Carcinogenesis
Volume
59
Published Date
Start Page
930
End Page
939
DOI
10.1002/mc.23208

Improved overall survival is still observed in patients receiving delayed adjuvant chemotherapy after pancreaticoduodenectomy for pancreatic adenocarcinoma.

BACKGROUND: Adjuvant chemotherapy (AC) is associated with improved survival following resection of pancreatic adenocarcinoma but is frequently delayed or deferred due to perioperative complications or patient deconditioning. The aim of this study was to assess impact of delayed AC on overall survival after pancreaticoduodenectomy for pancreatic head adenocarcinoma. METHODS: Patients with stage I-III pancreatic head adenocarcinoma in the 2006-2015 National Cancer Database were grouped by timing of AC (<6-weeks, 6-12-weeks, and 12-24-weeks). Overall survival was compared using Cox proportional hazard models adjusting for patient, tumor, and hospital factors. Subgroup analyses were conducted to assess the impact of comorbidities, readmission or extended hospital stay, and receipt of single- versus multi-agent chemotherapy. RESULTS: Of 13438 patients, 4552 (33.9%) received no AC, 2112 (15.7%) received AC <6-weeks following resection, 5580 (41.5%) within 6-12 weeks, and 1194 (8.9%) within 12-24 weeks. AC was associated with improved overall survival (adjusted hazard ratio [HR] <6-weeks: 0.765, 6-12-weeks: 0.744, and 12-24-weeks: 0.736 (p < 0.001)). This survival advantage persisted for patients with comorbidities, those with postoperative complications, and in those receiving single- or multi-agent regimens. CONCLUSIONS: For patients with stage I-III pancreatic adenocarcinoma, receipt of AC is associated with improved overall survival, even if delayed up to 24-weeks.
Authors
Turner, MC; Masoud, SJ; Cerullo, M; Adam, MA; Shah, KN; Blazer, DG; Abbruzzese, JL; Zani, S
MLA Citation
URI
https://scholars.duke.edu/individual/pub1437923
PMID
32299656
Source
pubmed
Published In
Hpb (Oxford)
Published Date
DOI
10.1016/j.hpb.2020.03.006

Abstract A074: Correlation of homologous recombination deficiency (HRD) status by BROCA-HR sequencing with response to combination cediranib and olaparib in relapsed ovarian cancer

Authors
Liu, JF; Cheng, S-C; Wenham, RM; Hendrickson, AEW; Armstrong, DK; Chan, N; Cohn, DE; Lee, J-M; Penson, RT; Cristea, M; Abbruzzese, J; Matsuo, K; Olawaiye, AB; Curtis, J; Shapiro, G; Matulonis, UA; Kohn, E; Ivy, P; Swisher, EM
MLA Citation
Liu, Joyce F., et al. “Abstract A074: Correlation of homologous recombination deficiency (HRD) status by BROCA-HR sequencing with response to combination cediranib and olaparib in relapsed ovarian cancer.” Clinical Trials, American Association for Cancer Research, 2019. Crossref, doi:10.1158/1535-7163.targ-19-a074.
URI
https://scholars.duke.edu/individual/pub1434259
Source
crossref
Published In
Clinical Trials
Published Date
DOI
10.1158/1535-7163.targ-19-a074

Research Areas:

Adolescent
Adult
Age Distribution
Albumins
Animals
Blood Transfusion
Cell Differentiation
Cell Growth Processes
Cell Lineage
Cell Movement
Cell Transformation, Neoplastic
Chemotherapy, Adjuvant
Chi-Square Distribution
Child
Cisplatin
Clinical Competence
Combined Modality Therapy
Cytokines
DNA Repair
Diabetes Complications
Diabetes Mellitus, Type 2
Diagnosis, Differential
Disease Models, Animal
Disease-Free Survival
Drug Delivery Systems
Drug Therapy, Combination
Dyspnea
Epithelial Cells
False Positive Reactions
Fibrosis
Genetic Variation
Genotype
HEK293 Cells
HT29 Cells
Health Status
Homozygote
Hypothyroidism
Immunohistochemistry
Inflammation
Intercellular Signaling Peptides and Proteins
Islets of Langerhans
Isotope Labeling
Liver
Liver Neoplasms
Liver Neoplasms, Experimental
Lymph Nodes
Membrane Proteins
Mesoderm
Models, Biological
Mutation
Neoadjuvant Therapy
Neoplasm Invasiveness
Neoplasm Metastasis
Neoplasm Proteins
Neoplasm Recurrence, Local
Neoplasm Staging
Neoplasms
Nervous System
Odds Ratio
Organoplatinum Compounds
Oxidative Stress
Pain
Pancreas
Pancreatectomy
Pancreatic Ducts
Pancreatic Neoplasms
Pancreaticoduodenectomy
Patient Care Team
Phenotype
Physicians
Polymorphism, Genetic
Probability
Prognosis
Proteolysis
Pyrimidines
Quinazolines
Radiation Tolerance
Radiotherapy, Adjuvant
Reactive Oxygen Species
Reference Values
Reproducibility of Results
Risk
Sensitivity and Specificity
Sepsis
Sex Distribution
Signal Transduction
Thiazoles
Time Factors
Treatment Outcome
Tumor Cells, Cultured
Tumor Markers, Biological
Water
Xenograft Model Antitumor Assays