Andrew X Zhu

University of Toronto, Toronto, Ontario, Canada

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Publications (165)1053.84 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: To compare the clinical outcomes of sorafenib plus either erlotinib or placebo in patients with advanced hepatocellular carcinoma (HCC) in a multicenter, multinational, randomized, phase III trial. Patients with advanced HCC and underlying Child-Pugh class A cirrhosis, who were naive to systemic treatment (N = 720), were randomly assigned to sorafenib plus either erlotinib (n = 362) or placebo (n = 358). The primary end point was overall survival (OS). Median OS was similar in the sorafenib plus erlotinib and sorafenib plus placebo groups (9.5 v 8.5 months, respectively; hazard ratio [HR], 0.929; P = .408), as was median time to progression (3.2 v 4.0 months, respectively; HR, 1.135; P = .18). In the sorafenib/erlotinib arm versus the sorafenib/placebo arm, the overall response rate trended higher (6.6% v 3.9%, respectively; P = .102), whereas the disease control rate was significantly lower (43.9% v 52.5%, respectively; P = .021). The median durations of treatment with sorafenib were 86 days in the sorafenib/erlotinib arm and 123 days in the sorafenib/placebo arm. In the sorafenib/erlotinib and sorafenib/placebo arms, the rates of treatment-emergent serious AEs (58.0% v 54.6%, respectively) and drug-related serious AEs (21.0% v 22.8%, respectively) were similar. AEs matched the known safety profiles of both agents, but rates of rash/desquamation, anorexia, and diarrhea were higher in the sorafenib/erlotinib arm, whereas rates of alopecia and hand-foot skin reaction were higher in the sorafenib/placebo arm. Withdrawal rates for AEs during cycles 1 to 3 were higher in the sorafenib/erlotinib arm. Adding erlotinib to sorafenib did not improve survival in patients with advanced HCC. © 2014 by American Society of Clinical Oncology.
    Journal of Clinical Oncology 12/2014; · 17.88 Impact Factor
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    ABSTRACT: Background Intrahepatic cholangiocarcinoma (ICC) often is a diagnosis determined by exclusion. Distinguishing ICC from other metastatic adenocarcinomas based on histopathologic or immunohistochemical analysis often is difficult and requires an extensive workup. This study aimed to determine whether albumin, whose expression is restricted to the liver, has potential as a biomarker for ICC using a novel and highly sensitive RNA in situ hybridization (ISH) platform. Methods Modified branched DNA probes were developed for albumin RNA ISH. The study evaluated 467 patient samples of primary and metastatic lesions. Results Of the 467 samples evaluated, 83 were ICCs, 42 were hepatocellular carcinomas (HCCs), and 332 were nonhepatic carcinomas including tumors arising from the perihilar region and bile duct, pancreas, stomach, esophagus, colon, breast, ovary, endometrium, kidney, and urinary bladder. Albumin RNA ISH was highly sensitive for cancers of liver origin, staining positive in 82 (99 %) of 83 ICCs and in 42 HCCs (100 %). Perihilar and distal bile duct carcinomas as well as carcinomas arising at other sites tested negative for albumin. Notably, 6 (22 %) of 27 intrahepatic tumors previously diagnosed as carcinomas of undetermined origin tested positive for albumin. Conclusions Albumin RNA ISH is a sensitive and highly specific diagnostic tool for distinguishing ICC from metastatic adenocarcinoma to the liver or carcinoma of unknown origin. Albumin RNA ISH could replace the extensive diagnostic workup, leading to timely confirmation of the ICC diagnosis. Additionally, the assay could serve as a guide to distinguish ICC from perihilar adenocarcinoma.
    Annals of Surgical Oncology 12/2014; · 3.94 Impact Factor
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    ABSTRACT: Sorafenib—a broad tyrosine kinase inhibitor—is the only approved systemic therapy for advanced hepatocellular carcinoma (HCC), but provides limited survival benefits. Recently, immunotherapy has emerged as a promising treatment strategy, but its role remains unclear in HCCs, which are associated with decreased cytotoxic CD8+ T-lymphocyte infiltration in both murine and human tumors. Moreover, we have shown in mouse models that after sorafenib treatment, intratumoral hypoxia is increased and may fuel evasive resistance. Using orthotopic HCC models, we now show that increased hypoxia after sorafenib treatment promotes immunosuppression, characterized by increased intratumoral expression of the immune checkpoint inhibitor programmed death-ligand 1 (PD-L1) and accumulation of T-regulatory cells and M2-type macrophages. We also show that the recruitment of the immunosuppressive cells is mediated in part by hypoxia-induced upregulation of stromal cell-derived 1 alpha (SDF1α). Inhibition of the SDF1α receptor (C-X-C receptor type 4 or CXCR4) using AMD3100 prevented the polarization toward an immunosuppressive microenvironment after sorafenib treatment, inhibited tumor growth, reduced lung metastasis, and improved survival. However, combination of AMD3100 and sorafenib did not significantly change cytotoxic CD8+ T-lymphocyte infiltration into HCC tumors and did not modify their activation status. In separate experiments, antibody blockade of the PD-L1 receptor PD-1 showed anti-tumor effects in treatment-naïve tumors in orthotopic (grafted and genetically engineered) models of HCC. However, anti-PD-1 antibody treatment had additional anti-tumor activity only when combined with sorafenib and AMD3100, and not when combined with sorafenib alone. Conclusion: Anti-PD-1 treatment can boost anti-tumor immune responses in HCC models. When used in combination with sorafenib, this immunotherapy approach shows efficacy only with concomitant targeting of the hypoxic and immunosuppressive microenvironment with agents such as CXCR4 inhibitors. This article is protected by copyright. All rights reserved.
    Hepatology 12/2014; · 11.19 Impact Factor
  • Richard L Hesketh, Andrew X Zhu, Rahmi Oklu
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    ABSTRACT: Personalized care in oncology is expected to significantly improve morbidity and mortality, facilitated by our increasing understanding of the molecular mechanisms driving tumors and the ability to target those drivers. Hepatocellular carcinoma has a very high mortality to incidence ratio despite localized disease being curable, emphasizing the importance of early diagnosis. Radiomics, the use of imaging technology to extrapolate molecular tumor data, and the detection of circulating tumor cells (CTCs) are two new technologies that could be incorporated into the clinical setting with relative ease. Here we discuss the molecular mechanisms leading to the development of hepatocellular carcinoma focusing on the latest developments in liver magnetic resonance imaging, CTC, and radiomic technology and their potential to improve diagnosis, staging, and therapy.
    Diagnostic and interventional radiology (Ankara, Turkey) 11/2014; · 1.43 Impact Factor
  • Amy R Deipolyi, Andrew X Zhu, Rahmi Oklu
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    ABSTRACT: Predicting which patients will benefit from radioembolization remains a challenge, as reliable prognostic indicators are not defined. Abnormal tumor vascular anatomy could not only impact the ability of cancer therapies to penetrate tumors, but may also contribute to a lesion's metastatic potential. Specifically, intratumoral vascular shunts could allow circulating tumor cells to initiate metastases by allowing them to gain access to distant sites in the body, bypassing capillary beds. Here, we describe how tumoral angiogenesis occurs and how intratumoral vascular shunts may form.
    American journal of clinical oncology. 10/2014;
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    ABSTRACT: Purpose To demonstrate the clinical translation of optical molecular imaging ( OMI optical molecular imaging ) for the localization of focal hepatic lesions during percutaneous hepatic interventions. Materials and Methods Institutional review board approval was obtained for this prospective, single-center, HIPAA-compliant trial. Patients who were suspected of having hepatocellular carcinoma or liver metastases from colorectal cancer and were scheduled for percutaneous liver biopsy or thermal ablation were eligible for this study. Patients (n = 5) received 0.5 mg per kilogram of body weight of indocyanine green ( ICG indocyanine green ) intravenously 24 hours prior to their scheduled procedure in this study. Intraprocedurally, a handheld device composed of an endoscope that fits coaxially through a standard 17-gauge introducer needle was advanced into the liver, and real-time measurements of ICG indocyanine green fluorescence were obtained. A point-of-care fluorescence imaging system was used to image ICG indocyanine green fluorescence in biopsy samples. Target-to-background ratios ( TBR target-to-background ratio s) were calculated by dividing the mean fluorescence intensity in the lesion by the mean fluorescence intensity in the adjacent liver parenchyma. The reference standard for determination of proper needle positioning in patients undergoing biopsy was final pathologic analysis of biopsy specimens or follow-up imaging. Results Intraprocedural OMI optical molecular imaging was successfully performed in six lesions (two lesions in patient 3) in five patients. The median size of the targeted lesions was 16 mm (range, 10-21 mm). Four of five biopsies (80%) yielded an accurate pathologic diagnosis, and one biopsy specimen showed benign liver parenchyma; both ablated lesions showed no residual disease 1 month after the procedure. The median overall added procedure time to perform OMI optical molecular imaging was 2 minutes. ICG indocyanine green was found to localize with TBR target-to-background ratio s greater than 2.0 (median, 7.9; range, 2.4-13.4) in all target lesions. No trial-related adverse events were reported. Conclusion The clinical translation of OMI optical molecular imaging to percutaneous hepatic interventions was demonstrated. © RSNA, 2014 Online supplemental material is available for this article.
    Radiology 10/2014; · 6.21 Impact Factor
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    ABSTRACT: Background Ganetespib (STA-9090) is an Hsp90 inhibitor that downregulates VEGFR, c-MET, HER2, IGF-IR, EGFR, and other Hsp90 client proteins involved in hepatocarcinogenesis, thereby making it an attractive therapy for HCC. This Phase I study was performed to establish the safety, tolerability, recommended Phase 2 dose (RP2D), and preliminary clinical activity of ganetespib in previously treated patients with advanced HCC. Methods Patients with advanced HCC, Child-Pugh A cirrhosis, progression on or intolerance to sorafenib, and ECOG PS ≤ 1 were enrolled in a standard 3x3 dose escalation study at doses of 100 mg/m(2), 150 mg/m(2), and 200 mg/m(2) IV given on days 1, 8, and 15 of each 28-day cycle. Objective response by RECIST version 1.1 criteria was evaluated by CT/MRI every 8 weeks. Results Fourteen patients were enrolled in this trial and received at least one dose of the study drug. Of the 14 patients: median age, 57 years old; male 71 %; Asian 36 %; HCC etiology (HBV 36 %, HCV 43 %, Hemachromatosis 7 %, unknown 21 %); Child Pugh Class (A 93 %, B 7 %); median number of prior treatments 2; median baseline AFP 70.1 ng/mL. The RP2D was determined to be 200 mg/m(2). The most commonly seen AEs were diarrhea (93 %), fatigue (71 %), AST elevation (64 %), and hyperglycemia (64 %). The most common Gr 3/4 AEs were hyperglycemia (21 %) and lipasemia (21 %). One (7 %) patient had a fatal AE, septic shock, within 30 days of receiving the study drug. One dose-limiting toxicity, grade 3 lipasemia, was observed at the 100 mg/m(2) dose. Pharmacokinetics studies showed a t1/2, CL, Tmax, and Vss of 6.45 h, 48.28 L/h (25.56 L/h/m(2)), 0.76 h, and 191 L (100.4 L/m(2)), respectively. No objective responses were seen; one patient (7 %) had stable disease at 16 weeks. Median time to progression was 1.8 months, and median overall survival was 7.2 months. Conclusion Ganetespib had a manageable safety profile in patients with advanced HCC who had progressed on at least one line of systemic therapy. The pharmacokinetic profile showed that ganetespib exposure in patients with mild hepatic dysfunction is similar to that seen in patients with normal liver function. Ganetespib showed limited clinical benefit in patients with advanced HCC in this phase I trial.
    Investigational New Drugs 09/2014; · 3.50 Impact Factor
  • Richard L Hesketh, Andrew X Zhu, Rahmi Oklu
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    ABSTRACT: The 'omics revolution is facilitating a personalized approach to improving outcome by refining diagnosis, staging, treatment, and monitoring of hepatocellular carcinoma. Furthermore, the promise of being able to target a range of specific tumor drivers at a molecular level offers exciting new therapy prospects for a disease that is notoriously difficult to treat. We provide a unique perspective combining our understanding of the molecular mechanisms of hepatocellular carcinoma development with the potential of circulating tumor cells and radiogenomics to change the drivers of decision-making used in current practice.
    American journal of clinical oncology. 09/2014;
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    ABSTRACT: Hepatobiliary cancers include a spectrum of invasive carcinomas arising in the liver (hepatocellular carcinoma), gall bladder, and bile ducts (cholangiocarcinomas). Gallbladder cancer and cholangiocarcinomas are collectively known as biliary tract cancers. Gallbladder cancer is the most common and aggressive type of all the biliary tract cancers. Cholangiocarcinomas are diagnosed throughout the biliary tree and are typically classified as either intrahepatic or extrahepatic cholangiocarcinoma. Extrahepatic cholangiocarcinomas are more common than intrahepatic cholangiocarcinomas. This manuscript focuses on the clinical management of patients with gallbladder cancer and cholangiocarcinomas (intrahepatic and extrahepatic).
    Journal of the National Comprehensive Cancer Network: JNCCN 08/2014; 12(8):1152-82. · 4.24 Impact Factor
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    ABSTRACT: To assess how intratumoral shunting relates to liver metastasis and to clinical outcome.
    Journal of vascular and interventional radiology: JVIR 07/2014; · 1.81 Impact Factor
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    ABSTRACT: Despite the historically limited role of radiotherapy in the management of primary hepatic malignancies, modern advances in treatment design and delivery have renewed enthusiasm for radiation as a potentially curative treatment modality. Surgical resection and/or liver transplantation are traditionally regarded as the most effective forms of therapy, although the majority of patients with hepatocellular carcinoma and intrahepatic cholangiocarcinoma present with locally advanced or unresectable disease on the basis of local vascular invasion or inadequate baseline hepatobiliary function. In this context, many efforts have focused on nonoperative treatment approaches including novel systemic therapies, transarterial chemoembolization, ethanol ablation, radiofrequency ablation, and stereotactic body radiation therapy (SBRT). This review aims to summarize modern advances in radiotherapy, particularly SBRT, in the treatment of primary hepatic malignancies.
    The Oncologist 07/2014; · 4.54 Impact Factor
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    ABSTRACT: IMPORTANCE Aside from the multikinase inhibitor sorafenib, there are no effective systemic therapies for the treatment of advanced hepatocellular carcinoma. OBJECTIVE To assess the efficacy of everolimus in patients with advanced hepatocellular carcinoma for whom sorafenib treatment failed. DESIGN, SETTING, AND PARTICIPANTS EVOLVE-1 was a randomized, double-blind, phase 3 study conducted among 546 adults with Barcelona Clinic Liver Cancer stage B or C hepatocellular carcinoma and Child-Pugh A liver function whose disease progressed during or after sorafenib or who were intolerant of sorafenib. Patients were enrolled from 17 countries between May 2010 and March 2012. Randomization was stratified by region (Asia vs rest of world) and macrovascular invasion (present vs absent). INTERVENTIONS Everolimus, 7.5 mg/d, or matching placebo, both given in combination with best supportive care and continued until disease progression or intolerable toxicity. Per the 2:1 randomization scheme, 362 patients were randomized to the everolimus group and 184 patients to the placebo group.
    JAMA The Journal of the American Medical Association 07/2014; 312(1):57-67. · 29.98 Impact Factor
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    ABSTRACT: Mutations in isocitrate dehydrogenase 1 (IDH1) and IDH2 are among the most common genetic alterations in intrahepatic cholangiocarcinoma (IHCC), a deadly liver cancer. Mutant IDH proteins in IHCC and other malignancies acquire an abnormal enzymatic activity allowing them to convert α-ketoglutarate (αKG) to 2-hydroxyglutarate (2HG), which inhibits the activity of multiple αKG-dependent dioxygenases, and results in alterations in cell differentiation, survival, and extracellular matrix maturation. However, the molecular pathways by which IDH mutations lead to tumour formation remain unclear. Here we show that mutant IDH blocks liver progenitor cells from undergoing hepatocyte differentiation through the production of 2HG and suppression of HNF-4α, a master regulator of hepatocyte identity and quiescence. Correspondingly, genetically engineered mouse models expressing mutant IDH in the adult liver show an aberrant response to hepatic injury, characterized by HNF-4α silencing, impaired hepatocyte differentiation, and markedly elevated levels of cell proliferation. Moreover, IDH and Kras mutations, genetic alterations that co-exist in a subset of human IHCCs, cooperate to drive the expansion of liver progenitor cells, development of premalignant biliary lesions, and progression to metastatic IHCC. These studies provide a functional link between IDH mutations, hepatic cell fate, and IHCC pathogenesis, and present a novel genetically engineered mouse model of IDH-driven malignancy.
    Nature 07/2014; · 42.35 Impact Factor
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    ABSTRACT: Background:Current data suggest that platinum-based combination therapy is the standard first-line treatment for biliary tract cancer. EGFR inhibition has proven beneficial across a number of gastrointestinal malignancies; and has shown specific advantages among KRAS wild-type genetic subtypes of colon cancer. We report the combination of panitumumab with gemcitabine (GEM) and oxaliplatin (OX) as first-line therapy for KRAS wild-type biliary tract cancer.Methods:Patients with histologically confirmed, previously untreated, unresectable or metastatic KRAS wild-type biliary tract or gallbladder adenocarcinoma with ECOG performance status 0-2 were treated with panitumumab 6 mg kg(-1), GEM 1000 mg m(-2) (10 mg m(-2) min(-1)) and OX 85 mg m(-2) on days 1 and 15 of each 28-day cycle. The primary objective was to determine the objective response rate by RECIST criteria v.1.1. Secondary objectives were to evaluate toxicity, progression-free survival (PFS), and overall survival.Results:Thirty-one patients received at least one cycle of treatment across three institutions, 28 had measurable disease. Response rate was 45% and disease control rate was 90%. Median PFS was 10.6 months (95% CI 5-24 months) and median overall survival 20.3 months (95% CI 9-25 months). The most common grade 3/4 adverse events were anaemia 26%, leukopenia 23%, fatigue 23%, neuropathy 16% and rash 10%.Conclusions:The combination of gemcitabine, oxaliplatin and panitumumab in KRAS wild type metastatic biliary tract cancer showed encouraging efficacy, additional efforts of genetic stratification and targeted therapy is warranted in biliary tract cancer.British Journal of Cancer advance online publication 24 June 2014; doi:10.1038/bjc.2014.343
    British Journal of Cancer 06/2014; · 4.82 Impact Factor
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    ABSTRACT: Immune checkpoint blockade has recently emerged as a promising therapeutic approach for various malignancies including hepatocellular carcinoma (HCC). Preclinical and clinical studies have shown the potential benefit of modulating immunogenicity of HCC. In addition, recent advances in tumor immunology have broadened our understanding of the complex mechanism of immune evasion. In this review, we summarize the current knowledge on HCC immunology, and discuss the potential of immune checkpoint blockade as a novel HCC therapy from the basic, translational, and clinical perspectives. (Hepatology 2014;).
    Hepatology 06/2014; · 11.19 Impact Factor
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    ABSTRACT: The molecular alterations that drive tumorigenesis in intrahepatic cholangiocarcinoma (ICC) remain poorly defined. We sought to determine the incidence and prognostic significance of mutations associated with ICC among patients undergoing surgical resection.
    Annals of Surgical Oncology 06/2014; · 3.94 Impact Factor
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    ABSTRACT: To evaluate the safety, efficacy and biomarkers of short-course proton beam radiation and capecitabine, followed by pancreaticoduodenectomy in a phase 1/2 study in pancreatic ductal adenocarcinoma (PDAC) patients.
    International journal of radiation oncology, biology, physics 05/2014; · 4.59 Impact Factor
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    ABSTRACT: Delivery of radiation therapy (RT) to unresectable liver tumors is sometimes limited by proximity of radiosensitive bowel. We sought to determine if biologic mesh spacers (BMS) could be used in this situation. BMS composed of acellular human dermis were placed via a laparoscopic or open approach to displace bowel away from unresectable liver tumors in patients previously unable to receive radiation therapy (RT) due to risk of bowel toxicity. In 1 year, 14 patients were treated. Median age was 64 years. Diagnoses included intrahepatic cholangiocarcinoma (n = 6), hepatocellular carcinoma (n = 3), and metastases (n = 5). A solitary lesion was present in 8 patients, while 4 patients had 2 lesions and 2 patients had 3 lesions. Median largest tumor size was 6.3 cm (range, 1.6-17.5 cm). Limited extrahepatic disease was present in 5 patients. The surgical approach was laparoscopic in 10 patients and open in 4 patients. Median length of stay was 2.5 days (1-8), and 3 patients developed low-grade complications. Folded, extra thick (2.3-3.3 mm) BMS, with a median area of 384 cm(2) (256-640 cm(2)), were used to displace stomach (n = 9), duodenum (7), colon (6), and small bowel (2). The mean displacement of these organs on postprocedure imaging was 23 mm, 23 mm, 24 mm, and 20 mm, respectively. Two patients did not receive RT due to extrahepatic disease progression. The remaining patients had 3-dimensional conformal proton RT (n = 5), stereotactic body RT (4), or intensity modulated RT (3). Median dose delivered was 54 Gy (40-58.5) in 5-15 fractions with only 1 patient with grade 3-4 toxicity. At short-term follow-up of at least 10 months, local disease control was obtained in 11 of 12 patients. Initial dual institution experience with this novel strategy demonstrates feasibility, allowing previously untreatable liver tumor patients to receive high-dose RT.
    Practical radiation oncology. 05/2014; 4(3):167-73.
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    ABSTRACT: Tumor vascular heterogeneity is a recognized biomarker for cancer progression. Our purpose was to assess the tumor perfusion heterogeneity during antiangiogenic therapy in hepatocellular carcinoma (HCC) by means of fractal analysis on computed tomography perfusion (CTP) images. Twenty-two patients (15 men and 7 women; mean age: 61.5 years) with advanced HCC underwent CTP at baseline and 2 weeks after administration of bevacizumab. Perfusion maps of blood flow (BF) were generated by the adiabatic approximation to the tissue homogeneity model with a motion registration, and fractal analyses were applied to gray-scale perfusion maps using a plugin tool on ImageJ software (NIH, Bethesda, MD). A differential box-counting method was applied, and the fractal dimension (FD) was calculated as a heterogeneity parameter. Patients were grouped into favorable progression-free survival (PFS) group (PFS>6 months, 11 patients) and unfavorable PFS group (PFS≤6, 11 patients). After 2 weeks of antiangiogenic therapy, the BF decreased significantly (P < .0001), whereas the FD showed no significant change (P = .69). The percent change of the FD in tumor BF was significantly different between patients with favorable PFS and those without (-2.52% vs. 3.72%, P = .01), whereas the change of tumor BF showed no significant difference between them (-28.93% vs. -25.47%, P = .64). In Kaplan-Meier analysis, patients with greater reduction in the percent change of FD and lower baseline FD in tumor BF showed significantly longer overall survival (P = .009, P = .005). Fractal analysis of tumor BF can be a biomarker for antiangiogenic therapy.
    Academic radiology 05/2014; 21(5):654-60. · 2.09 Impact Factor
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    ABSTRACT: Radiation therapy is emerging as a potentially effective treatment of locally advanced, unresectable hepatocellular carcinoma (HCC). Outcomes from early prospective studies seem promising, with improved survival compared with historical controls. Cure of early stage and unresectable HCC may be possible with high-quality radiation therapy. Many questions remain, including determination of the ideal radiation dose and fractionation schema, optimal patient selection criteria based on tumor size, tumor location, extent of vascular invasion, and baseline liver function, and the role of radiation therapy compared with other localized standard treatments including radiofrequency ablation or transarterial chemoembolization.
    Surgical Oncology Clinics of North America 04/2014; 23(2):353-368. · 1.67 Impact Factor

Publication Stats

6k Citations
1,053.84 Total Impact Points


  • 2014
    • University of Toronto
      Toronto, Ontario, Canada
  • 2003–2014
    • Harvard Medical School
      • Department of Medicine
      Boston, Massachusetts, United States
    • Massachusetts General Hospital
      • • Division of Hematology and Medical Oncology
      • • Department of Medicine
      • • Department of Radiation Oncology
      • • Department of Radiology
      • • Biostatistics Center
      • • Division of Surgical Oncology
      • • Cancer Center
      Boston, Massachusetts, United States
  • 2013
    • National Tsing Hua University
      Hsin-chu-hsien, Taiwan, Taiwan
    • University of Texas Southwestern Medical Center
      Dallas, Texas, United States
    • Johns Hopkins Medicine
      • Division of General Surgery and Surgical Oncology
      Baltimore, MD, United States
  • 2008–2013
    • Johns Hopkins University
      • Department of Surgery
      Baltimore, MD, United States
  • 2005–2013
    • Dana-Farber Cancer Institute
      • Department of Medical Oncology
      Boston, MA, United States
    • University of Texas MD Anderson Cancer Center
      • Department of Surgical Oncology
      Houston, Texas, United States
  • 2012
    • Second Military Medical University, Shanghai
      Shanghai, Shanghai Shi, China
  • 2010–2012
    • University of Rochester
      • James P. Wilmot Cancer Center
      Rochester, NY, United States
    • The University of Calgary
      • Department of Medicine
      Calgary, Alberta, Canada
    • Stanford University
      • Department of Surgery
      Stanford, CA, United States
  • 2011
    • Polytechnic Institute of New York University
      Brooklyn, New York, United States
  • 2009
    • Beth Israel Deaconess Medical Center
      • Department of Radiology
      Boston, Massachusetts, United States
    • University of California, Los Angeles
      • Department of Medicine
      Los Angeles, CA, United States
    • Columbia University
      • Department of Medicine
      New York City, NY, United States
    • NYU Langone Medical Center
      • Division of Hematology and Medical Oncology
      New York City, NY, United States
  • 2007
    • Vanderbilt University
      • Division of Hematology and Oncology
      Nashville, MI, United States
  • 2006
    • Brigham and Women's Hospital
      Boston, Massachusetts, United States