Dr. Delitto is a board certified complex general surgical oncologist with a focus on conditions of the liver, pancreas, and stomach. He is an assistant professor in Stanford Medicine’s Department of Surgery.
His education includes a decade of postgraduate training in complex general surgical oncology, as well as a PhD in immunology with an emphasis on cancer biology. He completed a clinical fellowship at Johns Hopkins University and continued his research at the postdoctoral level in the laboratory of Dr. Elizabeth Jaffee. His research focus is on advancing the field of cancer immunology and harnessing his findings to improve immunotherapies.
He was the principal investigator of two studies examining the immune response to pancreatic cancer, including one funded by the National Cancer Institute.
Dr. Delitto has presented the findings of his research at conferences such as the American Association for Cancer Research, Society for the Immunotherapy of Cancer, American Association of Immunologists, American College of Surgeons, Academic Surgical Congress and Pancreas Club. In addition to cancer immunology, he has also presented work focused on cancer cachexia, surgical outcomes, translational experimental models and a variety of other oncologic topics.
He has published original work in Nature Communications, the Journal of the National Cancer Institute, Cancer Research, Clinical Cancer Research, and other high impact journals. He is also a reviewer for Annals of Surgery, Scientific Reports, Surgery, Tumor Biology, Journal of Surgical Research, PLOS ONE, and the Journal of Translational Medicine.
Dr. Delitto has earned numerous honors related to clinical excellence, teaching and research. He is board certified by the American Board of Surgery and a member of the Society of Surgical Oncology, American Association for Cancer Research and American Association of Immunologists.
- General Surgery
- Pancreatic Cancer
- Gastric Cancer
- Bile Duct Cancers
- Gallbladder Cancer
- Cancer Immunology
Residency: University of Florida Dept of General Surgery (2019) FL
Board Certification, American Board of Surgery, Complex General Surgical Oncology (2022)
Fellowship: Johns Hopkins University Surgery Program (2021) MD
Board Certification: American Board of Surgery, General Surgery (2019)
PhD Training: University of Florida Office of the Registrar (2016) FL
Medical Education: University of Pittsburgh School of Medicine Registrar (2011) PA
- First Recurrence of Synovial Sarcoma Presenting With Solitary Pancreatic Mass CUREUS JOURNAL OF MEDICAL SCIENCE 2022; 14 (6)
Radiographic, Biochemical, or Pathologic Response to Neoadjuvant Chemotherapy in Resected Pancreatic Cancer: Which Is Best?
SPRINGER. 2022: 351
View details for Web of Science ID 000789811800041
- Surgical solution for a paraneoplastic neurodegenerative disorder TRAUMA SURGERY & ACUTE CARE OPEN 2022; 7 (1)
Implantation of a neoantigen-targeted hydrogel vaccine prevents recurrence of pancreatic adenocarcinoma after incomplete resection.
2021; 10 (1): 2001159
Tumor involvement of major vascular structures limits surgical options in pancreatic adenocarcinoma (PDAC), which in turn limits opportunities for cure. Despite advances in locoregional approaches, there is currently no role for incomplete resection. This study evaluated a gelatinized neoantigen-targeted vaccine applied to a grossly positive resection margin in preventing local recurrence. Incomplete surgical resection was performed in mice bearing syngeneic flank Panc02 tumors, leaving a 1 mm rim adherent to the muscle bed. A previously validated vaccine consisting of neoantigen peptides, a stimulator of interferon genes (STING) agonist and AddaVaxTM (termed PancVax) was embedded in a hyaluronic acid hydrogel and applied to the tumor bed. Tumor remnants, regional lymph nodes, and spleens were analyzed using histology, flow cytometry, gene expression profiling, and ELISPOT assays. The immune microenvironment at the tumor margin after surgery alone was characterized by a transient influx of myeloid-derived suppressor cells (MDSCs), prolonged neutrophil influx, and near complete loss of cytotoxic T cells. Application of PancVax gel was associated with enhanced T cell activation in the draining lymph node and expansion of neoantigen-specific T cells in the spleen. Mice implanted with PancVax gel demonstrated no evidence of residual tumor at two weeks postoperatively and healed incisions at two months postoperatively without local recurrence. In summary, application of PancVax gel at a grossly positive tumor margin led to systemic expansion of neoantigen-specific T cells and effectively prevented local recurrence. These findings support further work into locoregional adjuncts to immune modulation in PDAC.
View details for DOI 10.1080/2162402X.2021.2001159
View details for PubMedID 34777919
View details for PubMedCentralID PMC8583296
GSK3 suppression upregulates β-catenin and c-Myc to abrogate KRas-dependent tumors.
2018; 9 (1): 5154
Mutant KRas is a significant driver of human oncogenesis and confers resistance to therapy, underscoring the need to develop approaches that disable mutant KRas-driven tumors. Because targeting KRas directly has proven difficult, identifying vulnerabilities specific for mutant KRas tumors is an important alternative approach. Here we show that glycogen synthase kinase 3 (GSK3) is required for the in vitro and in vivo growth and survival of human mutant KRas-dependent tumors but is dispensable for mutant KRas-independent tumors. Further, inhibiting phosphorylation of GSK3 substrates c-Myc on T58 and β-catenin on S33/S37/T41 and their subsequent upregulation contribute to the antitumor activity of GSK3 inhibition. Importantly, GSK3 blockade inhibits the in vivo growth of G12D, G12V, and G12C mutant KRas primary and metastatic patient-derived xenografts from pancreatic cancer patients who progressed on chemo- and radiation therapies. This discovery opens new avenues to target mutant KRas-dependent cancers.
View details for DOI 10.1038/s41467-018-07644-6
View details for PubMedID 30514931
View details for PubMedCentralID PMC6279809
Prognostic Value of Clinical vs Pathologic Stage in Rectal Cancer Patients Receiving Neoadjuvant Therapy.
Journal of the National Cancer Institute
2018; 110 (5): 460-466
Neoadjuvant chemoradiation is currently standard of care in stage II-III rectal cancer, resulting in tumor downstaging for patients with treatment-responsive disease. However, the prognosis of the downstaged patient remains controversial. This work critically analyzes the relative contribution of pre- and post-therapy staging to the anticipated survival of downstaged patients.The National Cancer Database (NCDB) was queried for patients with rectal cancer treated with transabdominal resection between 2004 and 2014. Stage II-III patients downstaged with neoadjuvant radiation were compared with stage I patients treated with definitive resection alone. Patients with positive surgical margins were excluded. Overall survival was evaluated using both Kaplan-Meier analyses and Cox proportional hazards models. All statistical tests were two-sided.A total of 44 320 patients were eligible for analysis. Survival was equivalent for patients presenting with cT1N0 disease undergoing resection (mean survival = 113.0 months, 95% confidence interval [CI] = 110.8 to 115.3 months) compared with those downstaged to pT1N0 from both cT3N0 (mean survival = 114.9 months, 95% CI = 110.4 to 119.3 months, P = .12) and cT3N1 disease (mean survival = 115.4 months, 95% CI = 110.1 to 120.7 months, P = .22). Survival statistically significantly improved in patients downstaged to pT2N0 from cT3N0 disease (mean survival = 109.0 months, 95% CI = 106.7 to 111.2 months, P < .001) and cT3N1 (mean survival = 112.8 months, 95% CI = 110.0 to 115.7 months, P < .001), compared with cT2N0 patients undergoing resection alone (mean survival = 100.0 months, 95% CI = 97.5 to 102.5 months). Multiple survival analysis confirmed that final pathologic stage dictated long-term outcomes in patients undergoing neoadjuvant radiation (hazard ratio [HR] of pT2 = 1.24, 95% CI = 1.10 to 1.41; HR of pT3 = 1.81, 95% CI = 1.61 to 2.05; HR of pT4 = 2.72, 95% CI = 2.28 to 3.25, all P ≤ .001 vs pT1; HR of pN1 = 1.50, 95% CI = 1.41 to 1.59; HR of pN2 = 2.17, 95% CI = 2.00 to 2.35, both P < .001 vs pN0); while clinical stage at presentation had little to no predictive value (HR of cT2 = 0.81, 95% CI = 0.69 to 0.95, P = .008; HR of cT3 = 0.83, 95% CI = 0.72 to 0.96, P = .009; HR of cT4 = 1.02, 95% CI = 0.85 to 1.21, P = .87 vs cT1; HR of cN1 = 0.96, 95% CI = 0.91 to 1.02, P = .19; HR of cN2 = 0.96, 95% CI = 0.86 to 1.08, P = .48 vs cN0).Survival in patients with rectal cancer undergoing neoadjuvant radiation is driven by post-therapy pathologic stage, regardless of pretherapy clinical stage. These data will further inform prognostic discussions with patients.
View details for DOI 10.1093/jnci/djx228
View details for PubMedID 29165692
View details for PubMedCentralID PMC6279292
Human Pancreatic Cancer Cells Induce a MyD88-Dependent Stromal Response to Promote a Tumor-Tolerant Immune Microenvironment.
2017; 77 (3): 672-683
Cancer cells exert mastery over the local tumor-associated stroma (TAS) to configure protective immunity within the tumor microenvironment. The immunomodulatory character of pancreatic lysates of patients with cancer differs from those with pancreatitis. In this study, we evaluated the cross-talk between pancreatic cancer and its TAS in primary human cell culture models. Upon exposure of TAS to pancreatic cancer cell-conditioned media, we documented robust secretion of IL6 and IL8. This TAS response was MyD88-dependent and sufficient to directly suppress both CD4+ and CD8+ T-cell proliferation, inducing Th17 polarization at the expense of Th1. We found that patients possessed a similar shift in circulating effector memory Th17:Th1 ratios compared with healthy controls. The TAS response also directly suppressed CD8+ T-cell-mediated cytotoxicity. Overall, our results demonstrate how TAS contributes to the production of an immunosuppressive tumor microenvironment in pancreatic cancer. Cancer Res; 77(3); 672-83. ©2016 AACR.
View details for DOI 10.1158/0008-5472.CAN-16-1765
View details for PubMedID 27864347
View details for PubMedCentralID PMC5290036
Targeting tumor tolerance: A new hope for pancreatic cancer therapy?
Pharmacology & therapeutics
2016; 166: 9-29
With a 5-year survival rate of just 8%, pancreatic cancer (PC) is projected to be the second leading cause of cancer deaths by 2030. Most PC patients are not eligible for surgery with curative intent upon diagnosis, emphasizing a need for more effective therapies. However, PC is notoriously resistant to chemoradiation regimens. As an alternative, immune modulating strategies have recently achieved success in melanoma, prompting their application to other solid tumors. For such therapeutic approaches to succeed, a state of immunologic tolerance must be reversed in the tumor microenvironment and that has been especially challenging in PC. Nonetheless, knowledge of the PC immune microenvironment has advanced considerably over the past decade, yielding new insights and perspectives to guide multimodal therapies. In this review, we catalog the historical groundwork and discuss the evolution of the cancer immunology field to its present state with a specific focus on PC. Strategies currently employing immune modulation in PC are reviewed, specifically highlighting 66 clinical trials across the United States and Europe.
View details for DOI 10.1016/j.pharmthera.2016.06.008
View details for PubMedID 27343757