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Pancreatic Neoplasms: HELP
Articles by Vincent M. Chung
Based on 9 articles published since 2009
(Why 9 articles?)

Between 2009 and 2019, Vincent Chung wrote the following 9 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Guideline Pancreatic Adenocarcinoma, Version 2.2017, NCCN Clinical Practice Guidelines in Oncology. 2017

Tempero, Margaret A / Malafa, Mokenge P / Al-Hawary, Mahmoud / Asbun, Horacio / Bain, Andrew / Behrman, Stephen W / Benson, Al B / Binder, Ellen / Cardin, Dana B / Cha, Charles / Chiorean, E Gabriela / Chung, Vincent / Czito, Brian / Dillhoff, Mary / Dotan, Efrat / Ferrone, Cristina R / Hardacre, Jeffrey / Hawkins, William G / Herman, Joseph / Ko, Andrew H / Komanduri, Srinadh / Koong, Albert / LoConte, Noelle / Lowy, Andrew M / Moravek, Cassadie / Nakakura, Eric K / O'Reilly, Eileen M / Obando, Jorge / Reddy, Sushanth / Scaife, Courtney / Thayer, Sarah / Weekes, Colin D / Wolff, Robert A / Wolpin, Brian M / Burns, Jennifer / Darlow, Susan. · ·J Natl Compr Canc Netw · Pubmed #28784865.

ABSTRACT: Ductal adenocarcinoma and its variants account for most pancreatic malignancies. High-quality multiphase imaging can help to preoperatively distinguish between patients eligible for resection with curative intent and those with unresectable disease. Systemic therapy is used in the neoadjuvant or adjuvant pancreatic cancer setting, as well as in the management of locally advanced unresectable and metastatic disease. Clinical trials are critical for making progress in treatment of pancreatic cancer. The NCCN Guidelines for Pancreatic Adenocarcinoma focus on diagnosis and treatment with systemic therapy, radiation therapy, and surgical resection.

2 Review Current and future therapies for advanced pancreatic cancer. 2017

Gupta, Rohan / Amanam, Idoroenyi / Chung, Vincent. ·City of Hope National Medical Center, Duarte, California. ·J Surg Oncol · Pubmed #28591939.

ABSTRACT: Pancreatic cancer remains a deadly disease with a 5-year survival rate of only 8%. Even after surgical resection, most patients have recurrence of their cancer. Over the last 10 years, improvements in chemotherapy regimens led to a doubling in median overall survival. Here we review the management of advanced pancreatic cancer and highlight vaccine therapy as a novel modality of treatment.

3 Clinical Trial Effect of Selumetinib and MK-2206 vs Oxaliplatin and Fluorouracil in Patients With Metastatic Pancreatic Cancer After Prior Therapy: SWOG S1115 Study Randomized Clinical Trial. 2017

Chung, Vincent / McDonough, Shannon / Philip, Philip A / Cardin, Dana / Wang-Gillam, Andrea / Hui, Laifong / Tejani, Mohamedtaki A / Seery, Tara E / Dy, Irene A / Al Baghdadi, Tareq / Hendifar, Andrew E / Doyle, L Austin / Lowy, Andrew M / Guthrie, Katherine A / Blanke, Charles D / Hochster, Howard S. ·City of Hope National Medical Center, Duarte, California. · SWOG Statistical Center, Fred Hutchinson Cancer Research Center, Seattle, Washington. · Karmanos Cancer Institute, Wayne State University, Detroit, Michigan. · Vanderbilt University Medical Center, Nashville, Tennessee. · Washington University in St Louis, St Louis, Missouri. · Kaiser Permanente NCORP, Sacramento, California. · University of Rochester, Rochester, New York. · University of California, Irvine, Orange. · Crossroads Cancer Center/Heartland NCORP, Effingham, Illinois. · St Joseph Mercy Hospital/Michigan CRC NCORP, Ann Arbor. · Cedars-Sinai Medical Center, Los Angeles, California. · Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, Maryland. · University of California, San Diego, La Jolla. · SWOG Group Chair's Office/Knight Cancer Institute, Oregon Health and Science University, Portland. · Yale Cancer Center, New Haven, Connecticut. ·JAMA Oncol · Pubmed #27978579.

ABSTRACT: Importance: KRAS mutations are common in pancreatic cancer, but directly targeting the KRAS protein has thus far been unsuccessful. The aim of this trial was to block the MEK and PI3K/AKT pathways downstream of the KRAS protein as an alternate treatment strategy to slow cancer growth and prolong survival. This was the first cooperative group trial to evaluate this strategy using molecularly targeted oral combination therapy for the treatment of chemotherapy-refractory pancreatic cancer. Objective: To compare selumetinib and MK-2206 vs modified FOLFOX (mFOLFOX) in patients with metastatic pancreatic cancer for whom gemcitabine-based therapy had failed. Design, Setting, and Participants: SWOG S1115 was a randomized phase 2 clinical trial. Between September 2012 and May 2014, 137 patients with metastatic pancreatic adenocarcinoma for whom gemcitabine-based chemotherapy had failed were randomized to selumetinib plus MK-2206 or mFOLFOX. Patients were randomized in a 1:1 fashion and stratified according to duration of prior systemic therapy and presence of liver metastases. Interventions: Patients received selumetinib 100 mg orally per day plus MK-2206 135 mg orally once per week or mFOLFOX (oxaliplatin, 85 mg/m2 intravenous, and fluorouracil, 2400 mg/m2 intravenous infusion over 46-48 hours) on days 1 and 15 of a 28-day cycle. Main Outcomes and Measures: The primary end point of the study was overall survival. Secondary objectives included evaluating toxic effects, objective tumor response, and progression-free survival. Results: There were 58 patients in the selumetinib plus MK-2206 (experimental) arm (60% male; median [range] age, 69 [54-88] years) and 62 patients in the mFOLFOX arm (35% male; median [range] age, 65 [34-82] years). In the experimental arm, median overall survival was shorter (3.9 vs 6.7 months; HR, 1.37; 95% CI, 0.90-2.08; P = .15), as was median progression-free survival (1.9 vs 2.0 months; HR, 1.61; 95% CI, 1.07-2.43; P = .02). One vs 5 patients had a partial response and 12 vs 14 patients had stable disease in the experimental arm vs mFOLFOX arm. Grade 3 or higher toxic effects were observed in 39 patients treated with selumetinib and MK-2206 vs 23 patients treated with mFOLFOX. More patients in the experimental arm discontinued therapy due to adverse events (13 vs 7 patients). Conclusions and Relevance: Dual targeting of the MEK and PI3K/AKT pathways downstream of KRAS by selumetinib plus MK-2206 did not improve overall survival in patients with metastatic pancreatic adenocarcinoma for whom gemcitabine-based chemotherapy had failed. This was the first randomized prospective evaluation of mFOLFOX in the US population that showed comparable results to CONKO-003 and PANCREOX. Trial Registration: clinicaltrials.gov Identifier: NCT01658943.

4 Clinical Trial Gene-mediated cytotoxic immunotherapy as adjuvant to surgery or chemoradiation for pancreatic adenocarcinoma. 2015

Aguilar, Laura K / Shirley, Lawrence A / Chung, Vincent M / Marsh, Christopher L / Walker, Jon / Coyle, Walter / Marx, Howard / Bekaii-Saab, Tanios / Lesinski, Gregory B / Swanson, Benjamin / Sanchez, Daniel / Manzanera, Andrea G / Aguilar-Cordova, Estuardo / Bloomston, Mark. ·Advantagene, Inc., Auburndale, MA, 02466, USA. ·Cancer Immunol Immunother · Pubmed #25795132.

ABSTRACT: BACKGROUND: While surgical resection of pancreatic adenocarcinoma provides the only chance of cure, long-term survival remains poor. Immunotherapy may improve outcomes, especially as adjuvant to local therapies. Gene-mediated cytotoxic immunotherapy (GMCI) generates a systemic anti-tumor response through local delivery of an adenoviral vector expressing the HSV-tk gene (aglatimagene besadenovec, AdV-tk) followed by anti-herpetic prodrug. GMCI has demonstrated synergy with standard of care (SOC) in other tumor types. This is the first application in pancreatic cancer. METHODS: Four dose levels (3 × 10(10) to 1 × 10(12) vector particles) were evaluated as adjuvant to surgery for resectable disease (Arm A) or to 5-FU chemoradiation for locally advanced disease (Arm B). Each patient received two cycles of AdV-tk + prodrug. RESULTS: Twenty-four patients completed therapy, 12 per arm, with no dose-limiting toxicities. All Arm A patients were explored, eight were resected, one was locally advanced and three had distant metastases. CD8(+) T cell infiltration increased an average of 22-fold (range sixfold to 75-fold) compared with baseline (p = 0.0021). PD-L1 expression increased in 5/7 samples analyzed. One node-positive resected patient is alive >66 months without recurrence. Arm B RECIST response rate was 25 % with a median OS of 12 months and 1-year survival of 50 %. Patient-reported quality of life showed no evidence of deterioration. CONCLUSIONS: AdV-tk can be safely combined with pancreatic cancer SOC without added toxicity. Response and survival compare favorably to expected outcomes and immune activity increased. These results support further evaluation of GMCI with more modern chemoradiation and surgery as well as PD-1/PD-L1 inhibitors in pancreatic cancer.

5 Article The spectrum of genetic variants in hereditary pancreatic cancer includes Fanconi anemia genes. 2018

Slavin, Thomas P / Neuhausen, Susan L / Nehoray, Bita / Niell-Swiller, Mariana / Solomon, Ilana / Rybak, Christina / Blazer, Kathleen / Adamson, Aaron / Yang, Kai / Sand, Sharon / Guerrero-Llamas, Nancy / Castillo, Danielle / Herzog, Josef / Wu, Xiwei / Tao, Shu / Raja, Shivali / Chung, Vincent / Singh, Gagandeep / Nadesan, Sue / Brown, Sandra / Cruz-Correa, Marcia / Petersen, Gloria M / Weitzel, Jeffrey / Anonymous671109. ·Department of Population Sciences, City of Hope National Medical Center, 1500 E. Duarte Rd, Bldg. 173, Duarte, CA, 91010, USA. tslavin@coh.org. · Division of Clinical Cancer Genetics, Department of Medical Oncology, City of Hope National Medical Center, 1500 E. Duarte Rd, Bldg. 173, Room # 131, Duarte, CA, 91010, USA. tslavin@coh.org. · Department of Population Sciences, City of Hope National Medical Center, 1500 E. Duarte Rd, Bldg. 173, Duarte, CA, 91010, USA. · HealthQuest, Dyson Center for Cancer Care, 45 Reade Place, Poughkeepsie, NY, 12603, USA. · Department of Molecular and Cellular Biology, City of Hope National Medical Center, 1500 E. Duarte Rd, Duarte, CA, 91010, USA. · Division of Clinical Cancer Genetics, Department of Medical Oncology, City of Hope National Medical Center, 1500 E. Duarte Rd, Bldg. 173, Room # 131, Duarte, CA, 91010, USA. · Department of Surgery, City of Hope National Medical Center, 1500 E. Duarte Rd, Duarte, CA, 91010, USA. · Harrington Cancer Center, 1500 Wallace Blvd, Amarillo, TX, 79106, USA. · St. Joseph Hospital, 1100 W Stewart Dr., Orange, CA, 92868, USA. · University of Puerto Rico, Paseo Dr. Jose Celso Barbosa, San Juan, 00921, Puerto Rico. · Mayo Clinic, 216 2nd St. SW, Rochester, MN, 55902, USA. ·Fam Cancer · Pubmed #28687971.

ABSTRACT: Approximately 5-10% of all pancreatic cancer patients carry a predisposing mutation in a known susceptibility gene. Since >90% of patients present with late stage disease, it is crucial to identify high risk individuals who may be amenable to early detection or other prevention. To explore the spectrum of hereditary pancreatic cancer susceptibility, we evaluated germline DNA from pancreatic cancer participants (n = 53) from a large hereditary cancer registry. For those without a known predisposition mutation gene (n = 49), germline next generation sequencing was completed using targeted capture for 706 candidate genes. We identified 16 of 53 participants (30%) with a pathogenic (P) or likely pathogenic (LP) variant that may be related to their hereditary pancreatic cancer predisposition; seven had mutations in genes associated with well-known cancer syndromes (13%) [ATM (2), BRCA2 (3), MSH2 (1), MSH6 (1)]. Many had mutations in Fanconi anemia complex genes [BRCA2 (3 participants), FANCF, FANCM]. Eight participants had rare protein truncating variants of uncertain significance with no other P or LP variants. Earlier age of pancreatic cancer diagnosis (57.5 vs 64.8 years) was indicative of possessing a P or LP variant, as was cancer family history (p values <0.0001). Our multigene panel approach for identifying known cancer predisposing genetic susceptibility in those at risk for hereditary pancreatic cancer may have direct applicability to clinical practice in cases with mutations in actionable genes. Future pancreatic cancer predisposition studies should include evaluation of the Fanconi anemia genes.

6 Article Pilot study of an interdisciplinary supportive care planning intervention in pancreatic cancer. 2016

Sun, Virginia / Ruel, Nora / Chung, Vincent / Singh, Gagandeep / Leong, Lucille / Fakih, Marwan / Fong, Yuman / Ferrell, Betty. ·Division of Nursing Research and Education, Department of Population Sciences, City of Hope, 1500 East Duarte Road, Duarte, CA, 91010, USA. vsun@coh.org. · Division of Biostatistics, Department of Information Sciences, City of Hope, Duarte, CA, USA. · Department of Medical Oncology and Therapeutics Research, City of Hope, Duarte, CA, USA. · Division of Surgical Oncology, Department of Surgery, City of Hope, Duarte, CA, USA. · Division of Nursing Research and Education, Department of Population Sciences, City of Hope, 1500 East Duarte Road, Duarte, CA, 91010, USA. ·Support Care Cancer · Pubmed #26984248.

ABSTRACT: PURPOSE: A diagnosis of pancreatic cancer is often associated with higher symptom burden, lower functional status, and worse quality of life (QOL). To date, few interventions have focused on the unique QOL needs of patients with pancreatic cancer. The purpose of this pilot study is to determine the feasibility of an interdisciplinary supportive care planning intervention in patients with pancreatic cancer during disease-focused treatments. METHODS: Patients enrolled in this prospective, pre- and post-intervention pilot study received a supportive care intervention that included the following three components: comprehensive QOL assessment, case presentation at interdisciplinary care meetings, and two nurse-administered educational sessions on QOL concerns. Patients completed outcome measures that included the FACT-Hep, FACIT-Sp-12, and self-report of finances and out-of-pocket costs since diagnosis. Measures were completed at baseline prior to receiving the intervention, and follow-up occurred at 1 and 2 months post-intervention. RESULTS: A total of 10 patients were enrolled during a 4-month period who provided informed consent, received the intervention, and completed the study (58 % accrual). Examination of pre- and post-intervention QOL outcomes revealed changes across the three evaluation time points that were not statistically significant. Patients were highly satisfied with the intervention, with 80 % reporting that the intervention was "excellent." Discussions during the interdisciplinary care meetings and educational sessions were largely focused on physical and psychosocial needs. CONCLUSIONS: An interdisciplinary supportive care planning intervention was potentially feasible and acceptable for pancreatic cancer patients in an ambulatory care setting.

7 Article Epidermal Growth Factor Receptor Signaling to the Mitogen Activated Protein Kinase Pathway Bypasses Ras in Pancreatic Cancer Cells. 2016

Lee, Sangjun / Heinrich, Eileen L / Lu, Jianming / Lee, Wendy / Choi, Audrey H / Luu, Carrie / Chung, Vincent / Fakih, Marwan / Kim, Joseph. ·From the *Division of Surgical Oncology, Departments of Surgery and †Medical Oncology and Experimental Therapeutics, City of Hope National Medical Center, Duarte, CA; and ‡Department of Surgery, Stony Brook Medicine, Stony Brook, NY. ·Pancreas · Pubmed #26262587.

ABSTRACT: OBJECTIVE: Epidermal growth factor (EGF) receptor (EGFR/HER1) is overexpressed in human pancreatic cancers. However, anti-EGFR therapy does not exhibit significant therapeutic activity with oncogenic K-ras mutation. We sought to assess the signaling relationship between EGFR and mutant K-ras, which is commonly detected in pancreatic cancer. METHODS: Pancreatic cancer cells harboring mutated K-ras were treated with EGF to assess signaling from EGFR to mitogen-activated protein kinase (MAPK) pathway. The role of Ras family of proteins in transducing EGFR signals was assessed using short interfering RNA. Other components of MAPK and PI3K (phosphoinositide 3-kinase) pathways were examined for their roles in EGFR signaling. RESULTS: First, EGF signaling in pancreatic cancer cells occurs selectively through HER1. Second, knockdown of all Ras isoforms failed to block EGF-mediated phosphorylation of extracellular signal-regulated kinase (ERK). Inhibition of Raf was observed to partially abrogate ERK phosphorylation, whereas MEK inhibition resulted in complete attenuation of EGF-mediated ERK phosphorylation. Finally, inhibition of phosphoinositide 3-kinase/AKT and CDC42/PAK pathways did not block EGFR signaling. CONCLUSIONS: Our study results demonstrate that EGFR-mediated signaling in mutant K-ras pancreatic cancer cells does not follow canonical MAPK signaling. Our novel findings suggest the existence of alternate signaling pathways to downstream MAPK in the presence of mutant K-ras.

8 Article Salmonella-Based Therapy Targeting Indoleamine 2,3-Dioxygenase Coupled with Enzymatic Depletion of Tumor Hyaluronan Induces Complete Regression of Aggressive Pancreatic Tumors. 2015

Manuel, Edwin R / Chen, Jeremy / D'Apuzzo, Massimo / Lampa, Melanie G / Kaltcheva, Teodora I / Thompson, Curtis B / Ludwig, Thomas / Chung, Vincent / Diamond, Don J. ·Department of Experimental Therapeutics, Beckman Research Institute of City of Hope, Duarte, California. emanuel@coh.org ddiamond@coh.org. · Department of Experimental Therapeutics, Beckman Research Institute of City of Hope, Duarte, California. · Department of Pathology, City of Hope Comprehensive Cancer Center, Duarte, California. · Halozyme Therapeutics, Inc., San Diego, California. · Department of Molecular Virology, Immunology and Medical Genetics, Ohio State University, Columbus, Ohio. · Department of Medical Oncology and Therapeutics Research, City of Hope Comprehensive Cancer Center, Duarte, California. ·Cancer Immunol Res · Pubmed #26134178.

ABSTRACT: Bacterial-based therapies are emerging as effective cancer treatments and hold promise for refractory neoplasms, such as pancreatic ductal adenocarcinoma (PDAC), which has not shown significant improvement in therapy for more than 25 years. Using a novel combination of shIDO-ST, a Salmonella-based therapy targeting the immunosuppressive molecule indoleamine 2,3-dioxygenase (IDO), with an enzyme, PEGPH20, which depletes extracellular matrix hyaluronan, we observed extended survival with frequent total regression of autochthonous and orthotopic PDAC tumors. This observation was associated with migration and accumulation of activated polymorphonuclear neutrophils (PMN) from spleens into tumors, which was not seen using a scrambled control (shScr-ST). Purified splenic PMNs from PEGPH20/shIDO-ST-treated mice exhibited significant IDO knockdown and were able to kill tumor targets ex vivo through mechanisms involving FasL and serine proteases. In addition, CD8(+) T cells were observed to contribute to late control of pancreatic tumors. Collectively, our data demonstrate that entry of shIDO-ST and PMNs into otherwise impermeable desmoplastic tumors is facilitated by PEGPH20-mediated HA removal, further highlighting an important component of effective treatment for PDAC.

9 Article Pancreatic adenocarcinoma, version 2.2014: featured updates to the NCCN guidelines. 2014

Tempero, Margaret A / Malafa, Mokenge P / Behrman, Stephen W / Benson, Al B / Casper, Ephraim S / Chiorean, E Gabriela / Chung, Vincent / Cohen, Steven J / Czito, Brian / Engebretson, Anitra / Feng, Mary / Hawkins, William G / Herman, Joseph / Hoffman, John P / Ko, Andrew / Komanduri, Srinadh / Koong, Albert / Lowy, Andrew M / Ma, Wen Wee / Merchant, Nipun B / Mulvihill, Sean J / Muscarella, Peter / Nakakura, Eric K / Obando, Jorge / Pitman, Martha B / Reddy, Sushanth / Sasson, Aaron R / Thayer, Sarah P / Weekes, Colin D / Wolff, Robert A / Wolpin, Brian M / Burns, Jennifer L / Freedman-Cass, Deborah A. ·From UCSF Helen Diller Family Comprehensive Cancer Center; Moffitt Cancer Center; St. Jude Children's Research Hospital/The University of Tennessee Health Science Center; Robert H. Lurie Comprehensive Cancer Center of Northwestern University; Memorial Sloan Kettering Cancer Center; Fred Hutchinson Cancer Research Center/Seattle Cancer Care Alliance; City of Hope Comprehensive Cancer Center; Fox Chase Cancer Center; Duke Cancer Institute; Pancreatic Cancer Action Network (PanCAN); University of Michigan Comprehensive Cancer Center; Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine; The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins; Stanford Cancer Institute; UC San Diego Moores Cancer Center; Roswell Park Cancer Institute; Vanderbilt-Ingram Cancer Center; Huntsman Cancer Institute at the University of Utah; The Ohio State University Comprehensive Cancer Center - James Cancer Hospital and Solove Research Institute; Massachusetts General Hospital Cancer Center; University of Alabama at Birmingham Comprehensive Cancer Center; Fred & Pamela Buffett Cancer Center at The Nebraska Medical Center; University of Colorado Cancer Center; The University of Texas MD Anderson Cancer Center; Dana-Farber/Brigham and Women's Cancer Center; and National Comprehensive Cancer Network. ·J Natl Compr Canc Netw · Pubmed #25099441.

ABSTRACT: The NCCN Guidelines for Pancreatic Adenocarcinoma discuss the diagnosis and management of adenocarcinomas of the exocrine pancreas and are intended to assist with clinical decision-making. These NCCN Guidelines Insights summarize major discussion points from the 2014 NCCN Pancreatic Adenocarcinoma Panel meeting. The panel discussion focused mainly on the management of borderline resectable and locally advanced disease. In particular, the panel discussed the definition of borderline resectable disease, role of neoadjuvant therapy in borderline disease, role of chemoradiation in locally advanced disease, and potential role of newer, more active chemotherapy regimens in both settings.