Jaffer A Ajani

Szent László Hospital, Budapest, Budapeŝto, Budapest, Hungary

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Publications (600)3507.77 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Gastric cancer (GC) continues to be a significant problem worldwide and is the third leading cause of cancer death. Armamentarium to treat GC whether it is potentially curable or metastatic (incurable) has changed little over the last decades with only two new agents being approved (trastuzumab and ramucirumab). Many relatively healthy patients after second-line therapy have limited and generally ineffective options. The recent The Cancer Genome Atlas analysis has uncovered four genotypes of GC; however, it is not sufficient to change our treatment strategies and more work needs to be done. The popular front-line regimen containing a platinum compound and a fluoropyrimidine is widely used for drug development and has worked well globally. Thus, this combination appears suitable for adding a biologic agent. The search for new classes of cytotoxics has almost stopped, but it is clear that cytotoxic therapy continues to contribute and it is here to stay. Biologic agents that modulate the immune system of the host appear promising along with many other biologics that can potentially inhibit signaling pathways that are often employed by GC cells. We will briefly describe the efforts that have targeted EGFR, mTOR, angiogenesis and MET pathways.
    Expert Opinion on Pharmacotherapy 04/2015; 16(7):1-6. DOI:10.1517/14656566.2015.1025750 · 3.09 Impact Factor
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    ABSTRACT: Background The purpose of this study was to determine the survival of patients with metastatic gastric cancer treated with surgery.Methods We reviewed the medical records of 7,404 patients with gastric or gastroesophageal cancer seen from January 1995 to August 2012 at MD Anderson Cancer Center and identified patients with stage IV disease treated with surgery. Kaplan–Meier curves were created to compare overall survival (OS) between groups.ResultsOf the 82 patients who met inclusion criteria, sites of metastatic disease included peritoneum (N = 34, 42%), positive cytology only (N = 17, 21%), distant lymph nodes (N = 12, 15%), and distant organs (N = 19, 23%). The median time from initial cancer diagnosis to surgery for metastatic disease was 10 months (range, 0–70). Surgery included exploratory surgery only (N = 16, 20%), primary tumor resection with or without resection of distant disease (N = 50, 61%), and distant disease resection only (N = 16, 20%). Median follow-up for living patients was 3 years (range, 0.1–14). Median survival for all patients was 1.5 years (range, 0.1–14). Five year OS for patients with peritoneal metastases, positive cytology only, distant lymph nodes, and distant organ involvement was 13, 42, 20, and 34%, respectively.Conclusions Surgery in the setting of metastatic disease is an uncommon clinical scenario and has a considerable risk of exploration without resection, although long-term survival is possible. J. Surg. Oncol. © 2015 Wiley Periodicals, Inc.
    Journal of Surgical Oncology 04/2015; DOI:10.1002/jso.23907 · 2.84 Impact Factor
  • Seminars in Oncology 04/2015; 42 Suppl 1:S1-S2. DOI:10.1053/j.seminoncol.2015.02.020 · 3.94 Impact Factor
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    ABSTRACT: We have limited knowledge of the geographic distribution of resistant esophageal adenocarcinoma (EAC) in resected specimens, but its clinical importance can be enormous. We selected patients with baseline stage III EAC who had had chemoradiation followed by surgery and had residual EAC (resistant cases only). Outcomes were correlated with various endpoints (percentage of resistant EAC and anatomic distribution). A total of 100 clinical stage III patients were studied; 90% had an R0 resection, and 99% had either moderate or poorly differentiated EAC. Twelve percent had >50% residual cancer, 31% had 11-50% residual cancer, 53% had 1-10% residual cancer, and 3% had positive nodes only. Each compartment was frequently involved: mucosa/submucosa (66%), muscularis propria (76%), and serosa (62%); all compartments were involved in 35% of the cases. Lack of EAC (meaning response) was observed in the mucosa/submucosa (34%), muscularis propria (24%), serosa (38%), and nodes (42%). Although the endoscopic biopsies prior to surgery showed no EAC in 79% of the patients, in the surgical specimens, resistant EAC was frequently occurring in the mucosa/submucosa (66%). Contrary to our hypothesis that resistant EAC would be frequent in the nodes, our data show that its distribution is heterogeneous and unpredictable. Most importantly, the postchemoradiation biopsies are misleading, and a decision to delay/avoid surgery based on negative biopsies can be detrimental for the patients. © 2015 S. Karger AG, Basel.
    Oncology 03/2015; DOI:10.1159/000371889 · 2.61 Impact Factor
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    ABSTRACT: Purpose:Esophageal cancer (EC) is an aggressive malignancy and often resistant to therapy. Overexpression of EGFR has been associated with poor prognosis of EC patients. However, clinical trials using EGFR inhibitors have not provided benefit for EC patients. Failure of EGFR inhibition may be due to crosstalk with other oncogenic pathways. Experimental Design:In this study, expression of YAP1 and EGFR were examined in EAC resistant tumor tissues vs sensitive tissues by immunohistochemistry. Western blot, immunofluorescence, real-time PCR, promoter analysis, site-directed mutagenesis and in vitro and in vivo functional assays were performed to elucidate the YAP1 mediate EGFR expression and transcription and the relationship with chemoresistance in esophageal cancer. Results:We demonstrate that Hippo pathway coactivator YAP1 can induce EGFR expression and transcription in multiple cell systems. Both YAP1 and EGFR are overexpressed in resistant EC tissues compared to sensitive EC tissues. Further, we found that YAP1 increases EGFR expression at the level of transcription requiring an intact TEAD binding site in the EGFR promoter. Most importantly, exogenous induction of YAP1 induces resistance to 5-FU and docetaxcel, while knockdown of YAP sensitizes EC cells to these cytotoxics. Verteporfin, a YAP1 inhibitor, effectively inhibits both YAP1 and EGFR expression and sensitizes cells to cytotoxics. Conclusions:Our data provide evidence that YAP1 up-regulation of EGFR plays an important role in conferring therapy resistance in EC cells. Targeting YAP1-EGFR axis may be more efficacious than targeting EGFR alone in EC. Copyright © 2015, American Association for Cancer Research.
    Clinical Cancer Research 03/2015; DOI:10.1158/1078-0432.CCR-14-2191 · 8.19 Impact Factor
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    ABSTRACT: Malignant nodes in patients with localized esophageal adenocarcinoma (L-EAC) portend a poor prognosis. We assessed the correlation of the distribution of nodes with the outcome of patients undergoing chemoradiation/surgery (trimodality therapy). We studied 209 L-EAC patients who had confirmed or suspicious nodes at baseline staging. All patients received trimodality therapy and were grouped according to the nodal geography: above the diaphragm (AD), below the diaphragm (BD), or above and below the diaphragm (ABD). Survival estimates were calculated using the Kaplan-Meier method, and the outcomes of the groups were assessed by the log-rank test. Patients were primarily Caucasian (91%) and male (93%), with a baseline stage III L-EAC (89%). The median follow-up was 2.8 years (range, 0.4-11.7). Of the 209 patients, 35% (n = 73) had AD nodes, 20% (n = 41) had BD nodes, and 45% (n = 95) had ABD nodes. ABD patients had a 5-year overall survival rate of 33%, whereas this rate was 55% in AD patients and 60% in BD patients (p = 0.02). Patients with a higher histology grade were also at a higher risk of relapse and had a poor survival (p < 0.01 for both). L-EAC patients in the ABD group had the worst outcome after trimodality treatment compared to those in the AD or BD group. Novel strategies are needed for ABD patients. © 2015 S. Karger AG, Basel.
    Oncology 02/2015; DOI:10.1159/000368611 · 2.61 Impact Factor
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    ABSTRACT: Patient-reported outcomes (PRO) of health-related quality of life (HRQoL) and time to worsening of clinical benefit parameters were evaluated as secondary end points in the phase 3 first-line advanced gastric cancer study (FLAGS) trial of cisplatin/S-1 versus cisplatin/5-fluorouracil (5-FU) in patients with previously untreated advanced gastric cancer. The primary PRO end point was the Trial Outcome Index of the Functional Assessment of Cancer Therapy-Gastric (FACT-Ga). FACT-Ga was completed at the beginning of the first 4 cycles, cycle 6, and then every 3 cycles thereafter. The Chemotherapy Convenience and Satisfaction Questionnaire (CCSQ) was administered before the first 4 cycles; clinical benefit parameters (performance status, weight loss, and anorexia) were assessed at baseline, prior to study drug administration on day 1 of each cycle after cycle 1, and at the end of study treatment. Compliance to questionnaire fulfillment was more than 80 % through cycle 9. Significantly, fewer patients treated with cisplatin/S-1 reported worsened physical well-being (PWB) scores (45.1 versus 51.7 %, p = 0.044) and experienced significantly longer time to worsening in PWB scores, with a median of 4.5 months (95 % confidence interval (CI), 3.1-5.1) compared to 3.0 months (2.8-4.6) with cisplatin/5-FU (CF) (p = 0.01). Patients receiving cisplatin/S-1 also reported significantly higher best and worst score of PWB as well as CCSQ scores and a longer median time to worsening in clinical benefit parameters. Differences in secondary end points of PWB, CCSQ scores, and clinical benefit parameters favoring the cisplatin/S-1 arm provide further evidence for considering this combination a standard therapeutic option for first-line treatment of advanced gastric cancer.
    Journal of Gastrointestinal Cancer 02/2015; DOI:10.1007/s12029-014-9680-1
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    ABSTRACT: Pathologic complete response (pCR) to neoadjuvant chemoradiation for esophageal cancer is associated with improved outcomes. We evaluated whether a nomogram designed to predict who would have a pCR after trimodality therapy could also predict outcome after definitive chemoradiation. Patients in this retrospective, single-institution analysis had received chemoradiation without surgery for esophageal cancer from 1998 through 2010; 333 such patients had complete information on all variables required for the pCR nomogram: sex; T status (by endoscopic sonography); tumor grade; tumor avidity on positron emission tomography (PET); and esophagogastroduodenoscopy (EGD)-directed biopsy results after chemoradiation. We used multivariate Cox regression to test potential associations between clinical outcomes [overall survival (OS), locoregional recurrence, and distant metastasis] and patient or treatment factors and the pCR nomogram score; the component variables of the nomogram were not reintroduced into the multivariate analysis. The median follow-up time for all patients (median age 66 years) was 18.2 months (30.7 months for those alive at the time of analysis). Patients with nomogram scores ≤125 (median for all patients) had significantly worse outcomes than patients with scores >125: median OS time 19.7 vs. 48.2 months; disease-free survival (DFS) time 6.1 vs. 31.1 months; locoregional failure-free survival time 17.7 months vs. not reached; and distant metastasis-free survival time 11.7 months vs. not reached (all P<0.001). Multivariate Cox regression analysis indicated that nomogram score independently predicted each survival outcome, along with other patient and disease factors. The pCR nomogram score predicted survival outcomes in patients receiving definitive chemoradiation for esophageal cancer. Although this nomogram requires further validation, it may prove useful for stratifying patients for clinical trials designed to intensify treatments for patients at the highest risk of relapse.
    Journal of gastrointestinal oncology 02/2015; 6(1):45-52. DOI:10.3978/j.issn.2078-6891.2014.054
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    ABSTRACT: Despite the advancement of treatment modalities, many cancer patients experience tumor recurrence and metastasis at regional or distant sites. Evolving understanding of tumor biology has led to the hypothesis that tumors may possess a stem cell-like subpopulation known as cancer stem cells (CSCs) that may be involved in driving tumor propagation and pathogenesis. Like normal stem cells (NSCs), CSCs can be identified by markers such as CD133, CD44, and ALDH. CSCs have the ability to self-renew and differentiate into different tumor components through stemness pathways, such as Wnt, TGF-β, STAT, and Hippo-YAP/TAZ, among others. In NSCs, stemness pathways are strictly regulated and control many important biologic processes, including embryogenesis and intestinal crypt cellular regulation. In contrast, stemness pathways in CSCs are significantly dysregulated. Combining current drugs with the targeting of these stemness pathways may significantly improve patient prognosis. The aim of this supplement is to update clinicians on the accumulated evidence characterizing the role of CSCs in tumor initiation, heterogeneity, therapy resistance, and recurrence and metastasis, and the potential for effectively treating patients. Copyright © 2015 Elsevier Inc. All rights reserved.
    Seminars in Oncology 01/2015; 42 Suppl 1. DOI:10.1053/j.seminoncol.2015.01.001 · 3.94 Impact Factor
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    ABSTRACT: BACKGROUND In the current study we present a validated miRNA signature to predict pathologic complete response (pCR) to neoadjuvant chemoradiation in esophageal adenocarcinoma.METHODS Three patient cohorts (discovery, n = 10; model, n = 43; and validation, n = 65) with locally advanced esophageal adenocarcinoma were analyzed. In the discovery cohort 754 miRNAs were examined in pretreatment tumor biopsy specimens using a TaqMan array. Of these, the 44 most significantly altered between tumors with pCR and non-pCR were examined in an additional 43 tumors using a Fluidigm 48.48 array. The 4 miRNAs (mir-505*, mir-99b, mir-451, and mir-145*) significantly predicting pCR in both cohorts were examined in an additional validation cohort (n = 65) using an Illumina array. These 4 miRNAs were used to generate an miRNA expression profile (MEP) score.RESULTSThe 4 miRNAs profiled are highly significantly associated with pCR in the model cohort (Ptrend = .008), the validation cohort (Ptrend = .025), and the combined cohort (Ptrend = 4.6 × 10−4). The receiver-operator characteristic areas under the curves (AUCs) for the MEP score were 0.78 for the model cohort, 0.71 for the validation cohort, and 0.72 for the combined cohort. When combined with clinical variables, the MEP score AUCs increased to 0.89, 0.77, and 0.81, respectively Estimates from logistic regression based on the MEP were determined and used to generate a probability of pCR plot, which identifies a group of patients with very high (≥80%) and very low (≤10%) probability of pCR.CONCLUSIONS The MEP score provides a validated means of predicting pCR to neoadjuvant chemoradiotherapy in esophageal adenocarcinoma that is robust across several analysis platforms. Cancer 2014. © 2014 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society.
    Cancer 12/2014; 120(23). DOI:10.1002/cncr.28911 · 4.90 Impact Factor
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    ABSTRACT: Objective Differences in gastric cancer (GC) clinical outcomes between patients in Asian and non-Asian countries has been historically attributed to variability in clinical management. However, recent international Phase III trials suggest that even with standardised treatments, GC outcomes differ by geography. Here, we investigated gene expression differences between Asian and non-Asian GCs, and if these molecular differences might influence clinical outcome. Design We compared gene expression profiles of 1016 GCs from six Asian and three non-Asian GC cohorts, using a two-stage meta-analysis design and a novel biostatistical method (RUV-4) to adjust for technical variation between cohorts. We further validated our findings by computerised immunohistochemical analysis on two independent tissue microarray (TMA) cohorts from Asian and non-Asian localities (n=665). Results Gene signatures differentially expressed between Asians and non-Asian GCs were related to immune function and inflammation. Non-Asian GCs were significantly enriched in signatures related to T-cell biology, including CTLA-4 signalling. Similarly, in the TMA cohorts, non-Asian GCs showed significantly higher expression of T-cell markers (CD3, CD45R0, CD8) and lower expression of the immunosuppressive T-regulatory cell marker FOXP3 compared to Asian GCs (p<0.05). Inflammatory cell markers CD66b and CD68 also exhibited significant cohort differences (p<0.05). Exploratory analyses revealed a significant relationship between tumour immunity factors, geographic locality-specific prognosis, and postchemotherapy outcomes. Conclusions Analyses of >1600 GCs suggest that Asian and non-Asian GCs exhibit distinct tumour immunity signatures related to T-cell function. These differences may influence geographical differences in clinical outcome, and the design of future trials particularly in immuno-oncology. INTRODUCTION
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    ABSTRACT: Gastric cancer represents a serious health problem on a global scale. It is the second leading cause of cancer-related death worldwide. Novel therapeutic targets are desperately needed because the meager improvement in the cure rate of about 10% realized by adjunctive treatments to surgery is unacceptable as > 50% patients with localized gastric cancer succumb to their disease. Either postoperative chemoradiotherapy (United States), pre-and post-operative chemotherapy (Europe), and adjuvant chemotherapy after a D2 resection (Asia) can all be regarded as standards of care in the localized gastric cancer management. In metastatic disease the addition of trastuzumab to chemotherapy is standard of care in Her2 positive disease. In the HER2 negative population, the treatments remain limited. In the first line setting, the standard of care is a combination of fluoropyrimidine and platinum containing chemotherapy, with or without epirubicin or docetaxel. The results of targeted therapy trials have by and large been disappointing, but none of these trials looked at an appropriately enriched population. Finally there is a meager overall survival benefit in treating patients with metastatic disease in the second line setting, with either irinotecan, docetaxel or ramucirumab however none of these drugs have been compared head to head in a well-powered randomized controlled trial.
    World Journal of Gastroenterology 10/2014; 20(38):13637-13647. DOI:10.3748/wjg.v20.i38.13637 · 2.43 Impact Factor
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    ABSTRACT: BACKGROUND: Hispanics are the largest nonwhite ethnic group in the US population, and they have higher incidence and mortality rates for gastric cancer (GC) than whites and Asians. Studies have identified several genetic susceptibility loci and intermediate phenotypic biomarkers for GC in whites and Asians. No studies have evaluated genetic susceptibility and intermediate phenotypic biomarkers in Hispanics. METHODS: In a case-control study of 132 Hispanic patients with GC (cases) and a control group of 125 Hispanics (controls), the authors evaluated the association of 5 single nucleotide polymorphisms (SNPs) that predispose whites and/or Asians to GC and of 2 intermediate phenotypic markers in peripheral blood leukocytes, ie, telomere length and mitochondrial DNA (mtDNA) copy number, with the GC risk. RESULTS: The variant C allele of the reference SNP rs2294008 in the PSCA gene was associated with a significantly reduced risk of GC (per allele-adjusted odds ratio [aOR], 0.51; 95% confidence interval [CI], 0.33-0.77; P=.002). Leukocyte mtDNA copy numbers were significantly lower in GC cases (mean+/-standard deviation, 0.9160.28) than in controls (1.2960.42; P<. 001). When individuals were dichotomized into high and low mtDNA copy number groups based on the median mtDNA copy number value in the controls, those who had a low mtDNA copy number had a significantly increased risk of GC (aOR, 11.00; 95% CI, 4.79-25.23; P<. 001) compared with those who had a high mtDNA copy number. Telomere length was not associated significantly with the risk of GC (aOR, 1.21; 95% CI, 0.65-2.27; P5.551). CONCLUSIONS: Hispanics share certain genetic susceptibility loci and intermediate phenotypic GC biomarkers with whites and Asians and may also have distinct genetic susceptibility factors (C) 2014 American Cancer Society.
    Cancer 10/2014; 120(19). DOI:10.1002/cncr.28792 · 4.90 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):2486-2486. DOI:10.1158/1538-7445.AM2014-2486 · 9.28 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):3896-3896. DOI:10.1158/1538-7445.AM2014-3896 · 9.28 Impact Factor
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    ABSTRACT: VEGFR-2 has a role in gastric cancer pathogenesis and progression. We assessed whether ramucirumab, a monoclonal antibody VEGFR-2 antagonist, in combination with paclitaxel would increase overall survival in patients previously treated for advanced gastric cancer compared with placebo plus paclitaxel.
    The Lancet Oncology 09/2014; 15(11). DOI:10.1016/S1470-2045(14)70420-6 · 24.73 Impact Factor
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    ABSTRACT: Purpose Patients with esophageal carcinoma (EC) who are treated with definitive chemoradiotherapy (bimodality therapy [BMT]) experience frequent relapses. In a large cohort, we assessed the timing, frequency, and types of relapses during an aggressive surveillance program and the value of the salvage strategies. Patients and Methods Patients with EC (N = 276) who received BMT were analyzed. Patients who had surgery within 6 months of chemoradiotherapy were excluded to reduce bias. We focused on local relapse (LR) and distant metastases (DM) and the salvage treatment of patients with LR only. Standard statistical methods were applied. Results The median follow-up time was 54.3 months (95% CI, 48.4 to 62.4). First relapses included LR only in 23.2% (n = 64), DM with or without LR in 43.5% (n = 120), and no relapses in 33.3% (n = 92) of patients. Final relapses included no relapses in 33.3%, LR only in 14.5%, DM only in 15.9%, and DM plus LR in 36.2% of patients. Ninety-one percent of LRs occurred within 2 years and 98% occurred within 3 years of BMT. Twenty-three (36%) of 64 patients with LR only underwent salvage surgery, and their median overall survival was 58.6 months (95% CI, 28.8 to not reached) compared with those patients with LR only who were unable to undergo surgery (9.5 months; 95% CI, 7.8 to 13.3). Conclusion Unlike in patients undergoing trimodality therapy, for whom surveillance/salvage treatment plays a lesser role, 1 in the BMT population, approximately 8% of all patients (or 36% of patients with LR only) with LRs occurring more than 6 months after chemoradiotherapy can undergo salvage treatment, and their survival is excellent. Our data support vigilant surveillance, at least in the first 24 months after chemotherapy, in these patients.
    Journal of Clinical Oncology 09/2014; DOI:10.1200/JCO.2014.56.7156 · 17.88 Impact Factor
  • Journal of the American College of Surgeons 09/2014; 219(3):S22. DOI:10.1016/j.jamcollsurg.2014.07.041 · 4.45 Impact Factor
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    ABSTRACT: Background The purpose of this study was to examine the significance of signet ring cell histology to predict response to preoperative chemoradiotherapy in patients with esophageal adenocarcinoma. Methods Two groups of patients with locoregional esophageal adenocarcinoma treated with neoadjuvant chemoradiation and surgery were studied: those with signet ring cell adenocarcinoma (n = 85) and a reference group (n = 638) with usual and other types of adenocarcinoma. Surgical specimens were reviewed for degree of pathologic response and pathologic stage. Cox regression models were used to assess the effects of clinicopathologic variables on survival. Results Tumors from patients in the signet ring cell group had a lower rate of complete pathologic response (9% versus 26%, p < 0.001) and more frequent positive margins (24% versus 10%, p < 0.001) compared with tumors from the reference group. Median overall survival (22 versus 48 months, p = 0.003) and disease-free survival (16 versus 35 months, p = 0.007) were shorter in the signet ring cell group than in the reference group. Signet ring cell histology and high pathologic stage were significant predictors of decreased overall survival and disease-free survival. Survival durations for patients whose resected specimens showed downstaging after neoadjuvant chemoradiation did not significantly differ from survival durations of patients whose specimens did not show downstaging in the signet ring cell group, unlike the reference group. Conclusions Signet ring cell histology on pretreatment biopsy predicts a decreased likelihood of complete pathologic response and survival for patients with esophageal adenocarcinoma treated with preoperative chemoradiation and surgery.
    The Annals of Thoracic Surgery 09/2014; 98(3). DOI:10.1016/j.athoracsur.2014.04.099 · 3.63 Impact Factor

Publication Stats

18k Citations
3,507.77 Total Impact Points


  • 2015
    • Szent László Hospital, Budapest
      Budapeŝto, Budapest, Hungary
  • 1985–2015
    • University of Texas MD Anderson Cancer Center
      • • Department of Medical Oncology
      • • Division of Cancer Medicine
      • • Division of Diagnostic Imaging
      • • Department of Thoracic Cardiovascular Surgery
      • • Department of NeuroSurgery
      • • Department of Gastrointestinal Medical Oncology and Digestive Diseases
      • • Department of Surgical Oncology
      • • Department of Radiotherapy
      • • Department of General Surgery
      Houston, Texas, United States
  • 1998–2014
    • University of Houston
      Houston, Texas, United States
  • 2013
    • Mayo Clinic - Scottsdale
      Scottsdale, Arizona, United States
    • Moffitt Cancer Center
      • Department of Cancer Epidemiology
      Tampa, Florida, United States
  • 1994–2013
    • Memorial Sloan-Kettering Cancer Center
      • Department of Medicine
      New York, New York, United States
  • 2011
    • University of Utah
      • Huntsman Cancer Institute
      Salt Lake City, UT, United States
    • Baylor College of Medicine
      • Department of Medicine
      Houston, TX, United States
  • 2009
    • Penn State Hershey Medical Center and Penn State College of Medicine
      • Department of Surgery
      Hershey, PA, United States
    • Krankenhaus Nordwest
      Frankfurt, Hesse, Germany
  • 2007
    • University of Santiago, Chile
      CiudadSantiago, Santiago Metropolitan, Chile
    • Georgetown University
      Washington, Washington, D.C., United States
    • Mayo Clinic - Rochester
      • Department of Gastroenterology and Hepatology
      Rochester, Minnesota, United States
  • 2006–2007
    • Duke University
      Durham, North Carolina, United States
    • N.N. Blokhin Cancer Research Center
      Moskva, Moscow, Russia
    • Ruhr-Universität Bochum
      Bochum, North Rhine-Westphalia, Germany
    • Peking Union Medical College Hospital
      Peping, Beijing, China
  • 2004
    • Washington University in St. Louis
      San Luis, Missouri, United States
    • Kitasato University
      • Department of Gastroenterology
      Tokyo, Tokyo-to, Japan
  • 2003
    • University of Geneva
      Genève, Geneva, Switzerland
  • 1990
    • University of Texas Health Science Center at Houston
      Houston, Texas, United States