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Pancreatic Neoplasms: HELP
Articles by Emily Chan
Based on 8 articles published since 2008
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Between 2008 and 2019, Emily Chan wrote the following 8 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Editorial Timing versus duration of adjuvant therapy for pancreatic cancer: all the lessons we need in life are taught to us as children. 2014

Chan, Emily / Berlin, Jordan. ·Vanderbilt University Medical Center, Nashville, TN. ·J Clin Oncol · Pubmed #24419124.

ABSTRACT: -- No abstract --

2 Clinical Trial Phase I/II study of mocetinostat in combination with gemcitabine for patients with advanced pancreatic cancer and other advanced solid tumors. 2018

Chan, Emily / Chiorean, E Gabriela / O'Dwyer, Peter J / Gabrail, Nashat Y / Alcindor, Thierry / Potvin, Diane / Chao, Richard / Hurwitz, Herbert. ·Vanderbilt-Ingram Cancer Center, Nashville, TN, USA. · Fred Hutchinson Cancer Research Center, University of Washington, Seattle, WA, USA. · Indiana University Cancer Center, Indianapolis, IN, USA. · Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA. · Gabrail Cancer Center, Canton, OH, USA. · McGill University Health Centre, Montreal, QC, Canada. · Mirati Therapeutics Inc., 9393 Towne Centre Drive, Suite 200, San Diego, CA, 92121, USA. · Mirati Therapeutics Inc., 9393 Towne Centre Drive, Suite 200, San Diego, CA, 92121, USA. chaor@MIRATI.COM. · Duke University Medical Center, Durham, NC, USA. ·Cancer Chemother Pharmacol · Pubmed #29238851.

ABSTRACT: PURPOSE: To evaluate the safety and efficacy of mocetinostat (a Class I/IV HDAC inhibitor) in combination with gemcitabine in patients with solid tumors, including pancreatic cancer. METHODS: In this open-label, non-randomized Phase I/II study (NCT00372437) sequential cohorts of patients with solid tumors received gemcitabine (1000 mg/m RESULTS: Forty-eight patients were enrolled into the Phase I (n = 25) and Phase II (n = 23) studies. In the Phase I study, the MTD/RP2D was mocetinostat 90 mg TIW + gemcitabine 1000 mg/m CONCLUSIONS: Mocetinostat TIW in combination with gemcitabine was associated with significant toxicities in patients with advanced pancreatic cancer. The level of clinical activity of this treatment combination was not considered high enough to merit further testing in this setting.

3 Clinical Trial Dual Src and EGFR inhibition in combination with gemcitabine in advanced pancreatic cancer: phase I results : A phase I clinical trial. 2018

Cardin, Dana B / Goff, Laura W / Chan, Emily / Whisenant, Jennifer G / Dan Ayers, G / Takebe, Naoko / Arlinghaus, Lori R / Yankeelov, Thomas E / Berlin, Jordan / Merchant, Nipun. ·Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN, USA. dana.cardin@vanderbilt.edu. · Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. dana.cardin@vanderbilt.edu. · Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN, USA. · Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. · Amgen Inc., Thousand Oaks, CA, USA. · Department of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, USA. · Center for Quantitative Sciences, Vanderbilt University Medical Center, Nashville, TN, USA. · Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD, USA. · Vanderbilt University Institute of Imaging Science, Vanderbilt University Medical Center, Nashville, TN, USA. · Institute for Computational and Engineering Sciences, Departments of Biomedical Engineering and Diagnostic Medicine, Livestrong Cancer Institutes, University of Texas, Austin, TX, USA. · Department of Surgery, Sylvester Comprehensive Cancer Center, University of Miami School of Medicine, Miami, FL, USA. ·Invest New Drugs · Pubmed #28990119.

ABSTRACT: Pancreatic adenocarcinoma remains a major therapeutic challenge, as the poor (<8%) 5-year survival rate has not improved over the last three decades. Our previous preclinical data showed cooperative attenuation of pancreatic tumor growth when dasatinib (Src inhibitor) was added to erlotinib (EGFR inhibitor) and gemcitabine. Thus, this study was designed to determine the maximum-tolerated dose of the triplet combination. Standard 3 + 3 dose escalation was used, starting with daily oral doses of 70 mg dasatinib and 100 mg erlotinib with gemcitabine on days 1, 8, and 15 (800 mg/m

4 Clinical Trial Phase I trial of vorinostat added to chemoradiation with capecitabine in pancreatic cancer. 2016

Chan, Emily / Arlinghaus, Lori R / Cardin, Dana B / Goff, Laura / Berlin, Jordan D / Parikh, Alexander / Abramson, Richard G / Yankeelov, Thomas E / Hiebert, Scott / Merchant, Nipun / Bhaskara, Srividya / Chakravarthy, Anuradha Bapsi. ·Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, United States. · Vanderbilt University Institute of Imaging Science, United States. · Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, United States; Vanderbilt University Institute of Imaging Science, United States; Departments of Radiology and Radiological Sciences, Biomedical Engineering, Physics, and Cancer Biology, Vanderbilt University, United States. · Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, UHealth - University of Miami Health System, United States. · Department of Radiation Oncology and Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, United States. · Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, United States. Electronic address: bapsi.chak@vanderbilt.edu. ·Radiother Oncol · Pubmed #27106554.

ABSTRACT: BACKGROUND AND PURPOSE: This single institution phase I trial determined the maximum tolerated dose (MTD) of concurrent vorinostat and capecitabine with radiation in non-metastatic pancreatic cancer. MATERIAL AND METHODS: Twenty-one patients received escalating doses of vorinostat (100-400mg daily) during radiation. Capecitabine was given 1000mg q12 on the days of radiation. Radiation consisted of 30Gy in 10 fractions. Vorinostat dose escalation followed the standard 3+3 design. No dose escalation beyond 400mg vorinostat was planned. Diffusion-weighted (DW)-MRI pre- and post-treatment was used to evaluate in vivo tumor cellularity. RESULTS: The MTD of vorinostat was 400mg. Dose limiting toxicities occurred in one patient each at dose levels 100mg, 300mg, and 400mg: 2 gastrointestinal toxicities and one thrombocytopenia. The most common adverse events were lymphopenia (76%) and nausea (14%). The apparent diffusion coefficient (ADC) increased in most tumors. Nineteen (90%) patients had stable disease, and two (10%) had progressive disease at time of surgery. Eleven patients underwent surgical exploration with four R0 resections and one R1 resection. Median overall survival was 1.1years (95% confidence interval 0.78-1.35). CONCLUSIONS: The combination of vorinostat 400mg daily M-F and capecitabine 1000mg q12 M-F with radiation (30Gy in 10 fractions) was well tolerated with encouraging median overall survival.

5 Clinical Trial Phase II trial of sorafenib and erlotinib in advanced pancreatic cancer. 2014

Cardin, Dana B / Goff, Laura / Li, Chung-I / Shyr, Yu / Winkler, Charles / DeVore, Russell / Schlabach, Larry / Holloway, Melanie / McClanahan, Pam / Meyer, Krista / Grigorieva, Julia / Berlin, Jordan / Chan, Emily. ·Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. ·Cancer Med · Pubmed #24574334.

ABSTRACT: This trial was designed to assess efficacy and safety of erlotinib with sorafenib in the treatment of patients with advanced pancreatic adenocarcinoma. An exploratory correlative study analyzing pretreatment serum samples using a multivariate protein mass spectrometry-based test (VeriStrat®), previously shown to correlate with outcomes in lung cancer patients treated with erlotinib, was performed. Patients received sorafenib 400 mg daily along with erlotinib 150 mg daily with a primary endpoint of 8-week progression free survival (PFS) rate. Pretreatment serum sample analysis by VeriStrat was done blinded to clinical and outcome data; the endpoints were PFS and overall survival (OS). Difference between groups (by VeriStrat classification) was assessed using log-rank P values; hazard ratios (HR) were obtained from Cox proportional hazards model. Thirty-six patients received study drug and were included in the survival analysis. Eight-week PFS rate of 46% (95% confidence interval (CI): 0.32-0.67) did not meet the primary endpoint of a rate ≥70%. Thirty-two patients were included in the correlative analysis, and VeriStrat "Good" patients had superior PFS (HR = 0.18, 95% CI: 0.06-0.57; P = 0.001) and OS (HR = 0.31 95% CI: 0.13-0.77, P = 0.008) compared to VeriStrat "Poor" patients. Grade 3 toxicities of this regimen included fever, anemia, diarrhea, dehydration, rash, and altered liver function. This study did not meet the primary endpoint, and this combination will not be further pursued. In this small retrospective analysis, the proteomic classification was significantly associated with clinical outcomes and is being further evaluated in ongoing studies.

6 Clinical Trial A phase I trial of CEP-701 + gemcitabine in patients with advanced adenocarcinoma of the pancreas. 2008

Chan, Emily / Mulkerin, Daniel / Rothenberg, Mace / Holen, Kyle D / Lockhart, A Craig / Thomas, James / Berlin, Jordan. ·Department of Medicine, Division of Hematology and Oncology, Vanderbilt University Medical Center, Nashville, TN, USA. Emily.chan@vanderbilt.edu ·Invest New Drugs · Pubmed #18217204.

ABSTRACT: INTRODUCTION: Current standard therapy for advanced pancreas cancer includes the use of gemcitabine or a gemcitabine-based chemotherapy regimen. Based on pre-clinical data, the combination of CEP-701, an inhibitor of tyrosine kinases including Flt-3, TRK-A/B and JCK-2, with gemcitabine appeared promising. METHODS: Two clinical sites were chosen for this phase I trial, one scheduled to start gemcitabine prior to CEP-701 and one scheduled to start CEP-701 prior to gemcitabine. Gemcitabine was given at a dose of 1,000 mg/m2 over 30 min each week for 3 weeks in a row followed by 1 week off. CEP 701 was taken orally twice daily at doses ranging from 20 mg bid to 40 mg bid. Pharmacokinetics of both drugs were determined to assess for any drug-drug interactions. RESULTS: Eighteen patients were enrolled and 17 received at least one dose of study drug. Nine patients experienced serious adverse events, but only one patient's toxicity was attributed as possibly secondary to study drug. No radiologic responses were seen. No significant pharmacokinetic interactions were observed between gemcitabine and CEP 701. The combination was well-tolerated, and the MTD was not reached in this study. CONCLUSIONS: No unexpected toxicities were seen for this combination. Although too few patients were enrolled to fully evaluate efficacy, there was not significant evidence for pursuing this combination further in pancreas cancer. The maximum tolerated dose of the combination was not determined secondary to the early termination of the study.

7 Article Cotargeting of MEK and PDGFR/STAT3 Pathways to Treat Pancreatic Ductal Adenocarcinoma. 2017

Sahu, Nisebita / Chan, Emily / Chu, Felix / Pham, Thinh / Koeppen, Hartmut / Forrest, William / Merchant, Mark / Settleman, Jeff. ·Department of Discovery Oncology, Genentech, South San Francisco, California. · Department of Translational Oncology, Genentech, South San Francisco, California. · Department of Pathology, Genentech, South San Francisco, California. · Department of Bioinformatics and Computational Biology, Genentech, South San Francisco, California. · Department of Discovery Oncology, Genentech, South San Francisco, California. settleman@calicolabs.com. ·Mol Cancer Ther · Pubmed #28619758.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is among the most lethal human diseases and remains largely refractory to available drug treatments. Insufficient targeting of the known oncogenic drivers and activation of compensatory feedback loops and inability to prevent metastatic spread contribute to poor prognosis for this disease. The

8 Article Modeling targeted inhibition of MEK and PI3 kinase in human pancreatic cancer. 2015

Junttila, Melissa R / Devasthali, Vidusha / Cheng, Jason H / Castillo, Joseph / Metcalfe, Ciara / Clermont, Anne C / Otter, Douglas Den / Chan, Emily / Bou-Reslan, Hani / Cao, Tim / Forrest, William / Nannini, Michelle A / French, Dorothy / Carano, Richard / Merchant, Mark / Hoeflich, Klaus P / Singh, Mallika. ·Genentech Inc., South San Francisco, California. junttila.melissa@gene.com msingh@patronustx.com. · Genentech Inc., South San Francisco, California. ·Mol Cancer Ther · Pubmed #25376606.

ABSTRACT: Activating mutations in the KRAS oncogene occur in approximately 90% of pancreatic cancers, resulting in aberrant activation of the MAPK and the PI3K pathways, driving malignant progression. Significant efforts to develop targeted inhibitors of nodes within these pathways are underway and several are currently in clinical trials for patients with KRAS-mutant tumors, including patients with pancreatic cancer. To model MEK and PI3K inhibition in late-stage pancreatic cancer, we conducted preclinical trials with a mutant Kras-driven genetically engineered mouse model that faithfully recapitulates human pancreatic ductal adenocarcinoma development. Treatment of advanced disease with either a MEK (GDC-0973) or PI3K inhibitor (GDC-0941) alone showed modest tumor growth inhibition and did not significantly enhance overall survival. However, combination of the two agents resulted in a significant survival advantage as compared with control tumor-bearing mice. To model the clinical scenario, we also evaluated the combination of these targeted agents with gemcitabine, the current standard-of-care chemotherapy for pancreatic cancer. The addition of MEK or PI3K inhibition to gemcitabine, or the triple combination regimen, incrementally enhanced overall survival as compared with gemcitabine alone. These results are reminiscent of the survival advantage conferred in this model and in patients by the combination of gemcitabine and erlotinib, an approved therapeutic regimen for advanced nonresectable pancreatic cancer. Taken together, these data indicate that inhibition of MEK and PI3K alone or in combination with chemotherapy do not confer a dramatic improvement as compared with currently available therapies for patients with pancreatic cancer.