David L Bartlett

University of Pittsburgh, Pittsburgh, Pennsylvania, United States

Are you David L Bartlett?

Claim your profile

Publications (287)1316.44 Total impact

  • No preview · Conference Paper · Feb 2016
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and objectives: To evaluate whether urologic procedures during cytoreductive surgery with hyperthermic intraperitoneal chemotherapy (CRS-HIPEC) are associated with adverse postoperative outcomes. Methods: We identified patients who underwent CRS-HIPEC at our institution from 2001 to 2012 and compared outcomes between operations that did and did not include a urologic procedure. Results: A total of 938 CRS-HIPEC procedures were performed, 71 of which included a urologic intervention. Urologic interventions were associated with longer operative times (547 vs. 459 min, P < 0.001) and greater length of stay (15 vs. 12 days, P = 0.003). Major complications (Clavien III and IV) were more common in the urologic group (31% vs. 20%, P = 0.028). On multivariable analysis, urologic procedures were associated with a low anterior resection (OR: 2.25, 95%CI 1.07-4.74, P = 0.033) and a greater number of enteric anastomoses (OR: 1.83, 95%CI 1.31-2.56, P < 0.001). At a median follow up of 17 months (IQR 5.6-35 months), addition of a urologic procedure did not significantly impact overall survival for appendiceal or colorectal cancers. Conclusion: Urologic surgery at the time of CRS-HIPEC is associated with longer operative times, length of stay and increased risk of major complications, but not with decreased overall survival. J. Surg. Oncol. © 2016 Wiley Periodicals, Inc.
    No preview · Article · Jan 2016 · Journal of Surgical Oncology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Introduction: Patients with peritoneal carcinomatosis (PC) of appendiceal origin demonstrate variable oncologic outcomes, despite aggressive cytoreductive surgery and hyperthermic intraperitoneal chemotherapy (CRS-HIPEC). We sought to devise a prognostic risk stratification system for oncologic outcomes following CRS-HIPEC. Methods: A total of 197 patients undergoing CRS-HIPEC for the treatment of appendiceal PC were reviewed from a prospective database. Kaplan-Meier survival curves and multivariate Cox regression models were used to identify prognostic factors affecting oncologic outcomes. Clinicopathologic variables affecting overall survival (OS) were utilized to develop a prognostic staging system and nomograms. Results: Univariate and multivariate Cox regression analysis indicated that high-grade tumor histology, lymph node metastasis, and incomplete cytoreduction were high-risk features, adversely affecting OS. Patients were stratified on the presence of high-risk features as follows: low-risk patients had no risk factors (n = 102); intermediate-risk patients had one risk factor (n = 49); and high-risk patients had more than one risk factor (n = 46). Median OS for low-risk patients was not reached, and was 43 and 22 months for intermediate-risk and high-risk patients, respectively. Five-year OS was 72, 43, and 13 % for low-, intermediate- and high-risk patients, respectively (p < 0.0003 for low vs. intermediate risk, and p = 0.06 for intermediate vs. high risk). Conclusions: We propose a three-tier staging system for appendiceal PC following CRS-HIPEC, based on histologic grade, lymph node involvement, and completeness of cytoreduction. The presence of any one or more of these high-risk features significantly decreased survival in our single-institution database and provided the basis for a prognostic staging system and corresponding nomograms.
    No preview · Article · Jan 2016 · Annals of Surgical Oncology

  • No preview · Article · Jan 2016 · Annals of Surgical Oncology
  • Source

    Preview · Article · Nov 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: We have armed a tumor-selective oncolytic vaccinia virus (vvDD) with the chemokine (CK) CXCL11, in order to enhance its ability to attract CXCR3+ antitumor CTLs and possibly NK cells to the tumor microenvironment (TME) and improve its therapeutic efficacy. As expected, vvDD-CXCL11 attracted high numbers of tumor-specific T cells to the TME in a murine AB12 mesothelioma model. Intratumoral virus-directed CXCL11 expression enhanced local numbers of CD8+ CTLs and levels of granzyme B, while reducing expression of several suppressive molecules, TGF-β, COX2, and CCL22 in the TME. Unexpectedly, we observed that vvDD-CXCL11, but not parental vvDD, induced a systemic increase in tumor-specific IFN-γ-producing CD8+ T cells in the spleen and other lymph organs, indicating the induction of systemic anti-tumor immunity. This effect was associated with enhanced therapeutic efficacy and a survival benefit in tumor-bearing mice treated with vvDD-CXCL11, mediated by CD8+ T cells and IFN-γ, but not CD4+ T cells. These results demonstrate that intratumoral expression of CXCL11, in addition to promoting local trafficking of T cells and to a lesser extent NK cells, has a novel function as a factor eliciting systemic immunity to cancer-associated antigens. Our data provide a rationale for expressing CXCL11 to enhance the therapeutic efficacy of oncolytic viruses and cancer vaccines.
    No preview · Article · Oct 2015 · OncoImmunology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cytoreductive surgery and hyperthermic intraperitoneal chemoperfusion for patients with malignant peritoneal mesothelioma has resulted in improved disease control and increased survival. Despite these results, there are significant perioperative risks associated with this aggressive procedure that necessitate consideration of prognostic markers during patient selection. The molecular pathogenesis of peritoneal mesothelioma remains relatively unknown, but extrapolation of findings from their pleural counterpart would suggest frequent alterations in CDKN2A, NF2, and BAP1. Homozygous deletions in CDKN2A portend a worse overall survival in peritoneal mesothelioma. However, the prevalence and prognostic significance of NF2 and BAP1 abnormalities has not been studied. Dual-color fluorescence in situ hybridization using CDKN2A and NF2 locus-specific probes and BAP1 immunohistochemistry identified homozygous CDKN2A deletions (n=25, 29%), hemizygous NF2 loss (n=30, 35%), and/or loss of BAP1 protein expression (n=49, 57%) in 68 of 86 (79%) peritoneal mesotheliomas. Homozygous CDKN2A deletions or hemizygous NF2 loss correlated with shorter progression-free survival (P<0.02) and poor overall survival (P<0.03). Moreover, the significance of these findings was cumulative. Patients harboring both homozygous CDKN2A deletions and hemizygous NF2 loss had a 2-year progression-free survival rate of 9% with a median of 6 months (P<0.01) and overall survival rate of 18% with a median of 8 months (P<0.01). By multivariate analysis, combined homozygous CDKN2A deletions and hemizygous NF2 loss was a negative prognostic factor for both progression-free survival and overall survival, independent of patient age, peritoneal cancer index, completeness of cytoreduction, and extent of invasion. In contrast, loss of BAP1 was not associated with clinical outcome. In summary, homozygous deletions in CDKN2A and hemizygous loss of NF2 as detected by fluorescence in situ hybridization would confer a poor clinical outcome and may guide future treatment decisions for patients with peritoneal mesothelioma.Modern Pathology advance online publication, 23 October 2015; doi:10.1038/modpathol.2015.121.
    No preview · Article · Oct 2015 · Modern Pathology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: High-grade (HG) mucinous appendiceal neoplasms (MAN) have a worse prognosis than low-grade histology. Our objective was to assess the safety and efficacy of cytoreductive surgery with hyperthermic intraperitoneal chemoperfusion (CRS/HIPEC) in patients with high-grade, high-volume (HG-HV) peritoneal metastases in whom the utility of this aggressive approach is controversial. Methods: Prospectively collected perioperative data were compared between patients with peritoneal metastases from HG-HV MAN, defined as simplified peritoneal cancer index (SPCI) ≥12, and those with high-grade, low-volume (HG-LV; SPCI <12) disease. Kaplan-Meier curves and multivariate Cox regression models identified prognostic factors affecting oncologic outcomes. Results: Overall, 54 patients with HG-HV and 43 with HG-LV peritoneal metastases underwent CRS/HIPEC. The HG-HV group had longer operative time, increased blood loss/transfusion, and increased intensive care unit length of stay (p < 0.05). Incomplete macroscopic cytoreduction (CC-1/2/3) was higher in the HG-HV group compared with the HG-LV group (68.5 vs. 32.6 %; p = 0.005). Patients with HG-HV disease demonstrated worse survival than those with HG-LV disease (overall survival [OS] 17 vs. 42 m, p = 0.009; time to progression (TTP) 10 vs. 14 m, p = 0.024). However, when complete macroscopic resection (CC-0) was achieved, the OS and progression-free survival of patients with HG-HV disease were comparable with HG-LV disease (OS 56 vs. 52 m, p = 0.728; TTP 20 vs. 19 m, p = 0.393). In a multivariate Cox proportional hazard regression model, CC-0 resection was the only significant predictor of improved survival for patients with HG-HV disease. Conclusions: Although patients with HG-HV peritoneal metastases from MAN have worse prognosis compared with patients with HG-LV disease, their survival is comparable when complete macroscopic cytoreduction is achieved.
    No preview · Article · Oct 2015 · Annals of Surgical Oncology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Excessive accumulation of mucin 2 (MUC2; a gel-forming secreted mucin) protein in the peritoneal cavity is the major cause of morbidity and mortality in pseudomyxoma peritonei (PMP). Hypoxia/hypoxia-inducible factor-1α (HIF-1α) has been shown to regulate the expression of similar mucins (eg, MUC5AC). We hypothesized that hypoxia/HIF-1α drives MUC2 expression in PMP and is therefore a novel target to reduce mucinous tumor growth. The regulation of MUC2 by 2% hypoxia/HIF-1α was evaluated in MUC2-secreting LS174T cells. The effect of BAY 87-2243, an inhibitor of HIF-1α, on MUC2 expression and mucinous tumor growth was evaluated in LS174T cells, PMP explant tissue, and in a unique intraperitoneal murine xenograft model of PMP. In vitro exposure of LS174T cells to hypoxia increased MUC2 messenger RNA (mRNA) and protein expression and increased HIF-1α binding to the MUC2 promoter. Hypoxia-mediated MUC2 protein overexpression was downregulated by transfected HIF-1α small interfering RNA (siRNA) compared with scrambled siRNA in LS174T cells. BAY 87-2243 inhibited hypoxia-induced MUC2 mRNA and protein expression in LS174T cells and PMP explant tissue. In a murine xenograft model of PMP, chronic oral therapy with BAY 87-2243 inhibited mucinous tumor growth and MUC2/HIF-1α expression in the tumor tissue. Our data suggest that hypoxia/HIF-1α induces MUC2 promoter activity to increase MUC2 expression. HIF-1α inhibition decreases MUC2 production and mucinous tumor growth, providing a preclinical rationale for the use of HIF-1α inhibitors to treat patients with PMP.
    No preview · Article · Oct 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: Colorectal peritoneal carcinomatosis (CPC) exhibits severe tumor hypoxia, leading to drug resistance and disease aggressiveness. This study demonstrates that the combination of the chemotherapeutic agent mitomycin C with the proteasome inhibitor bortezomib induced synergistic cytotoxicity and apoptosis, which was even more effective under hypoxia in colorectal cancer cells. The combination of mitomycin C and bortezomib at sublethal doses induced activation of c-Jun NH2-Terminal kinase and p38 mitogen-Activated protein kinase and resulted in Bcl-xL phosphorylation at Serine 62, leading to dissociation of Bcl-xL from proapoptotic Bak. Interestingly, the intracellular level of p53 became elevated and p53 translocated to the mitochondria during the combinatorial treatment, in particular under hypoxia. The coordinated action of Bcl-xL phosphorylation and p53 translocation to the mitochondria resulted in conformational activation of Bak oligomerization, facilitating cytochrome c release and apoptosis induction. In addition, the combinatorial treatment with mitomycin C and bortezomib significantly inhibited intraperitoneal tumor growth in LS174T cells and increased apoptosis, especially under hypoxic conditions in vivo. This study provides a preclinical rationale for the use of combination therapies for CPC patients. Implications: The combination of a chemotherapy agent and proteasome inhibitor at sublethal doses induced synergistic apoptosis, in particular under hypoxia, in vitro and in vivo through coordinated action of Bcl-xL and p53 on Bak activation.
    No preview · Article · Sep 2015 · Molecular Cancer Research
  • [Show abstract] [Hide abstract]
    ABSTRACT: Complement is a central part of both the innate and adaptive immune response and its activation has traditionally been considered part of the immunosurveillance response against cancer. Its pro-inflammatory role and its contribution to the development of many illnesses associated with inflammatory states implicate complement in carcinogenesis. We evaluated the role of three protein inhibitors of complement-cobra venom factor, humanized cobra venom factor, and recombinant staphylococcus aureus superantigen-like protein 7-in the setting of a transplantable murine colon cancer model. Outcomes were evaluated by monitoring tumor growth, and flow cytometry, ELISPOT, and quantitative real-time PCR were used to determine the impact of complement inhibition on the host immune response. Complement inhibitors were effective at depleting complement component C3 in tumor bearing mice and this was temporally correlated with a decreased rate of tumor growth during the establishment of tumors. Treatment with cobra venom factor resulted in increased CD8(+) T cells as a percentage of tumor-infiltrating cells as well as a reduced immunosuppressive environment evidenced by decreased myeloid derived suppressor cells in splenocytes of treated mice. Complement inhibition resulted in increased expression of the chemoattractive cytokines CCL5, CXCL10, and CXCL11. Complement depletion represents a promising mode of immunotherapy in cancer by its ability to impair tumor growth by increasing the host's effective immune response to tumor and diminishing the immunosuppressive effect created by the tumor microenvironment and ultimately could be utilized as a component of combination immunotherapy.
    No preview · Article · Aug 2015 · Annals of Surgical Oncology
  • [Show abstract] [Hide abstract]
    ABSTRACT: The prognostic significance of histological subtyping of epithelioid pleural mesotheliomas has been recently reported, but similar data are lacking in peritoneal mesotheliomas. We investigated possible relationships between histological growth patterns of epithelioid peritoneal mesotheliomas, clinicopathologic features and patient outcome. 84 cases of chemotherapy-naive epithelioid peritoneal mesothelioma were classified into tubulopapillary, micropapillary, papillary, tubular, solid and trabecular growth patterns. Pathologic features such as depth of invasion, lymphocytic host response, mitotic count, nuclear grade, lymphovascular invasion, lymph node metastasis, and stromal desmoplasia were analyzed. The most common histological patterns were solid (n = 37, 44%), tubulopapillary (n = 24, 29%) and micropapillary (n = 11, 13%). The overall median survival was 36 months. Patients with solid mesothelioma had shorter overall survival (median, 29 months) compared to patients with tubulopapillary and micropapillary growth patterns (median, 51 months and 53 months, respectively; p=.053). A high mitotic index (>5 in 50 hpf) was found to be associated with poor survival (p<.03). Moderate to severe lymphocytic host response was associated with longer median survival (p=.13) CONCLUSIONS: Our study highlights the prognostic importance of the solid growth pattern among diffuse epithelioid peritoneal mesotheliomas and reaffirms mitotic index as a predictor of overall survival. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    No preview · Article · Aug 2015 · Histopathology
  • Source
    Glen C Balch · David L Bartlett

    Preview · Article · Aug 2015 · Annals of Surgical Oncology
  • [Show abstract] [Hide abstract]
    ABSTRACT: It is well known that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis can be initially triggered by surface death receptors (the extrinsic pathway) and subsequently amplified through mitochondrial dysfunction (the intrinsic pathway). However, little is known about signaling pathways activated by the TRAIL-induced endoplasmic reticulum (ER) stress response. In this study, we report that TRAIL-induced apoptosis is associated with the endoplasmic reticulum (ER) stress response. Human colorectal carcinoma HCT116 cells were treated with TRAIL and the ER stress-induced signal transduction pathway was investigated. During TRAIL treatment, expression of ER stress marker genes, in particular the BiP (binding immunoglobulin protein) gene, was increased and activation of the PERK (PKR-like ER kinase)-eIF2α (eukaryotic initiation factor 2α)-ATF4 (activating transcription factor 4)-CHOP (CCAAT-enhancer-binding protein homologous protein) apoptotic signal transduction pathway occurred. Experimental data from use of a siRNA (small interfering RNA) technique, caspase inhibitor, and caspase-3-deficient cell line revealed that TRAIL-induced caspase activation is a prerequisite for the TRAIL-induced ER stress response. TRAIL-induced ER stress was triggered by caspase-8-mediated cleavage of BAP31 (B cell receptor-associated protein 31). The involvement of the proapoptotic PERK-CHOP pathway in TRAIL-induced apoptosis was verified by using a PERK knockout (PERK(-/-) ) mouse embryo fibroblast (MEF) cell line and a CHOP(-/-) MEF cell line. These results suggest that TRAIL-induced the activation of ER stress response plays a role in TRAIL-induced apoptotic death. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc.
    No preview · Article · Jul 2015 · Journal of Cellular Biochemistry
  • [Show abstract] [Hide abstract]
    ABSTRACT: Proponents of the robotic platform site its potential advantages in complex reconstructions such as the pancreaticojejunal anastomosis; however, the incidence and risk factors for postoperative pancreatic fistula (POPF) after robotic pancreaticoduodenectomy (RPD) have not been characterized. To identify independent risk factors for POPF after RPD. A prospectively maintained database of patients that underwent RPD (2008-2013) with a standardized pancreaticojejunostomy was analyzed. Univariate and multivariate analyses (UVA/MVA) were used to identify independent predictors for POPF. The POPF prognostic scores developed by Braga and Callery for open pancreaticoduodenectomy were then applied with logistic regression analysis on this RPD cohort. One hundred and fifty consecutive RPDs were analyzed. POPF occurred in 26 (17.3 %); 13 (8.6 %) of which were ISGPF category B and C. On UVA, patients with POPF had larger body mass index (BMI), smaller pancreatic duct diameter, smaller tumor size, longer OR time, larger estimated blood loss (EBL) and RBC transfusion (all p < 0.05). Higher EBL, duct size <4 mm, larger BMI and small tumor size remained the best independent risk factors for POPF on MVA. Increased Callery (OR 1.46, 95 % CI, p = 0.001) and Braga (OR 1.2, 95 % CI, p = 0.005) scores predicted an increased risk of POPF in this RPD cohort. Larger BMI, higher EBL, smaller tumor size and smaller duct diameter are the main predictors of POPF in RPD.
    No preview · Article · Jul 2015 · Surgical Endoscopy
  • [Show abstract] [Hide abstract]
    ABSTRACT: In adrenal tumors, size ≥4 cm has been an indication for adrenalectomy due to concern for malignancy. We compared mass size to imaging features (ImF) for accuracy in diagnosing adrenal malignancy. Data were retrieved for 112 consecutive patients who had adrenalectomy from January 2011 to August 2014. ImF was classified as nonbenign if HU > 10 on unenhanced CT scan or if loss of signal on out-of-phase imaging was absent on chemical-shift MRI. Indications for resection included hormonal hypersecretion, nonbenign ImF, and/or size ≥4 cm. Of 113 resected adrenals, 37 % were functional. Histologic malignancy occurred in 18 % (20/113) and included 3 adrenocortical carcinomas (ACC), 1 epithelioid liposarcoma, 1 lymphoma, 1 malignant nerve sheath tumor, and 14 adrenal metastases. Patients with malignancies were older (mean age, 60 ± 13 vs. 51 ± 14 years, p = 0.01). Malignant tumors were larger on preoperative imaging (mean 5.3 ± 3.2 vs. 3.9 ± 2.4 cm, p = 0.03). All 20 malignant masses had nonbenign ImF. In predicting malignancy, the sensitivity, specificity, NPV, and PPV of nonbenign ImF was 100, 57, 100, and 33 %, respectively. Size ≥4 cm was less predictive with sensitivity, specificity, NPV, and PPV of 55, 61, 86, and 23 %, respectively. If size ≥4 cm had been used as the sole criterion for surgery, 45 % of malignancies (9/20) would have been missed including 8 metastases and an ACC. In resected adrenal tumors, the presence of nonbenign ImF is more sensitive for malignancy than mass size (100 vs. 55 %) with equivalent specificity. Regardless of mass size, adrenalectomy should be strongly considered when non-benign ImF are present.
    No preview · Article · Jun 2015 · Annals of Surgical Oncology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cytoreductive surgery (CRS) and heated intraperitoneal chemotherapy (HIPEC) are used to treat peritoneal carcinomatosis from a variety of primary tumor sites. Little is known about the in vivo effects of CRS and HIPEC. We examined tumor and non-neoplastic peritoneal tissue samples from 38 patients undergoing CRS and HIPEC for appendiceal or colorectal carcinomatosis, using conventional histologic analysis and immunohistochemical analysis for markers of early DNA damage (phosphorylated H2AX, γH2AX) and early necrosis (extracellular HMGB1). Findings were correlated with clinicopathologic features and oncologic outcome. Histologic findings corresponding with CRS and HIPEC included extensive submesothelial inflammatory infiltrate, endothelial activation, mesothelial karyolysis and surface fibrin deposition. Endothelial activation in submesothelial vessels exhibited high specificity for samples obtained following HIPEC relative to samples obtained following CRS but prior to HIPEC. Mesothelial nuclear γH2AX staining and submesothelial extracellular HMGB1 staining increased progressively following CRS and HIPEC, consistent with DNA damage and necrosis. No significant increase in tumor staining for markers was seen with CRS or HIPEC. Submesothelial HMGB1 staining was associated with increased progression-free survival on univariate analysis. The immediate histologic effects of CRS and HIPEC are defined and provide evidence that DNA damage and early steps of necrosis are underway in mesothelial tissues at the conclusion of the procedure. Further research will be necessary to investigate the impact of these findings on long-term oncologic outcome, and may provide insight into the downstream effects of CRS and HIPEC that could facilitate refinement of regional therapeutic regimens for carcinomatosis.
    No preview · Article · May 2015 · Annals of Surgical Oncology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Autophagy is a cell survival mechanism that plays a critical role in pancreatic carcinogenesis. Murine studies have previously demonstrated that treatment with the late-autophagy inhibitor chloroquine in combination with chemotherapy limited tumor growth. In this phase 1/2 trial, we examined treatment with hydroxychloroquine (HCQ) and gemcitabine for patients with pancreatic adenocarcinoma. The primary endpoints were safety and tolerability, evaluated by Storer's dose escalation design. Secondary endpoints were CA 19-9 biomarker response, R0 resection rates, survival, and correlative studies of autophagy. Thirty-five patients were enrolled. There were no dose-limiting toxicities and no grade 4/5 events related to treatment. Nineteen patients (61 %) had a decrease in CA 19-9 after treatment. Twenty-nine patients (94 %) underwent surgical resection as scheduled, with a 77 % R0 resection rate. Median overall survival was 34.8 months (95 % confidence interval, 11.57 to not reached). Patients who had more than a 51 % increase in the autophagy marker LC3-II in circulating peripheral blood mononuclear cells had improvement in disease-free survival (15.03 vs. 6.9 months, p < 0.05) and overall survival (34.83 vs. 10.83 months, p < 0.05). No outcome differences were demonstrated in the 81 % of patients with abnormal p53 expression assessed by immunohistochemistry in the resected specimens. Preoperative autophagy inhibition with HCQ plus gemcitabine is safe and well tolerated. Surrogate biomarker responses (CA 19-9) and surgical oncologic outcomes were encouraging. p53 status was not associated with adverse outcomes.
    No preview · Article · Apr 2015 · Annals of Surgical Oncology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Robotic distal pancreatectomy (RDP) is performed increasingly, but knowledge of the number of cases required to attain procedural proficiency is lacking. The aim of this study was to identify the learning curve associated with RDP at a high-volume pancreatic centre. Metrics of perioperative safety and efficiency for all consecutive RDPs were evaluated. Outcomes were followed to 90 days. Cumulative sum (CUSUM) analysis was used to identify inflexion points corresponding to the learning curve. Between 2008 and 2013, 100 patients underwent RDP. There was no 90-day mortality. In two patients (2.0%), surgery was converted to laparotomy. Thirty procedures were performed for pancreatic adenocarcinoma. Precipitous operative time reductions from an initial operative time of 331 min were observed after the first 20 and 40 cases to 266 min and 210 min, respectively (P < 0.0001). The likelihood of readmission was significantly lower after the first 40 cases (P = 0.04), and non-significant reductions were observed in incidences of major (Clavien-Dindo Grade II or higher) morbidity and Grade B and C leaks, and length of stay. In this experience, RDP outcomes were optimized after 40 cases. Familiarity with the platform and dedicated training are likely to contribute to significantly shorter learning curves in future adopters. © 2015 International Hepato-Pancreato-Biliary Association.
    No preview · Article · Apr 2015 · HPB
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Hepatic arterial anomalies (HAAs) are not infrequently encountered during pancreatic resections. In view of the current emergence of the robotic platform as a safe alternative to open surgery in experienced centres, this study sought to determine the implications of HAAs on the safety and oncologic outcomes of robotic pancreaticoduodenectomy (RPD).MethodsA prospectively maintained database of patients with HAAs who underwent RPD (RPD + HAA) at a single institution between 2008 and 2013 was retrospectively reviewed. Demographic information and perioperative outcomes of RPD were compared for patients with and without HAAs.ResultsA total of 142 patients underwent RPD; 112 (78.9%) did not have and 30 (21.1%) did have HAAs. The majority (90.0%) of RPDs in patients with HAAs were performed for malignant indications and all aberrant vessels were preserved without conversion to laparotomy. There were no statistically significant differences between RPD patients with and without HAAs with respect to preoperative demographics, tumour characteristics, operative metrics (operative time, estimated blood loss, conversion) and postoperative outcomes, including complications, length of stay and readmissions. Negative margin (R0) rates were similar in both groups.Conclusions Robot-assisted pancreaticoduodenectomy is safe and feasible in patients with HAAs and has outcomes similar to those in patients with normal arterial anatomy.
    No preview · Article · Apr 2015 · HPB

Publication Stats

8k Citations
1,316.44 Total Impact Points


  • 2001-2016
    • University of Pittsburgh
      • • Department of Surgery
      • • Division of Surgical Oncology
      Pittsburgh, Pennsylvania, United States
    • Cancer Research and Biostatistics
      Seattle, Washington, United States
  • 1998-2011
    • National Cancer Institute (USA)
      • • Surgery Branch
      • • Center for Cancer Research
      Maryland, United States
    • The National Institute of Diabetes and Digestive and Kidney Diseases
      베서스다, Maryland, United States
  • 1998-2009
    • National Institutes of Health
      • • Branch of Surgery
      • • Section on Human Iron Metabolism
      Maryland, United States
  • 2005
    • University of Chicago
      Chicago, Illinois, United States
  • 2004
    • UPMC
      Pittsburgh, Pennsylvania, United States
  • 2002
    • National Institute of Allergy and Infectious Diseases
      베서스다, Maryland, United States
  • 1995-2002
    • Memorial Sloan-Kettering Cancer Center
      • • Department of Surgery
      • • Gastroenterology and Nutrition Service
      New York, New York, United States
  • 1999-2001
    • NCI-Frederick
      Фредерик, Maryland, United States
    • University of Vienna
      Wien, Vienna, Austria
    • Technische Universität München
      München, Bavaria, Germany
  • 1996
    • University of Pennsylvania
      • Department of Surgery
      Philadelphia, Pennsylvania, United States
  • 1994
    • Philadelphia College of Pharmacy and Science
      Filadelfia, Pennsylvania, United States