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Pancreatic Neoplasms: HELP
Articles by Charles H. Cha
Based on 5 articles published since 2009
(Why 5 articles?)
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Between 2009 and 2019, Charles Cha wrote the following 5 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 Resection of oligometastatic lung cancer to the pancreas may yield a survival benefit in select patients--a systematic review. 2015

DeLuzio, Matthew R / Moores, Craig / Dhamija, Ankit / Wang, Zuoheng / Cha, Charles / Boffa, Daniel J / Detterbeck, Frank C / Kim, Anthony W. ·Department of Surgery, Yale-New Haven Hospital, New Haven, CT 06520, USA. · Department of Surgery, Morristown Medical Center, Morristown, NJ 07960, USA. · Division of Biostatistics, Yale School of Public Health, New Haven, CT 06520, USA. · Section of Surgical Oncology, Yale School of Medicine, New Haven, CT 06520, USA. · Section of Thoracic Surgery, Yale School of Medicine, New Haven, CT 06520, USA. · Section of Thoracic Surgery, Yale School of Medicine, New Haven, CT 06520, USA. Electronic address: anthony.kim@yale.edu. ·Pancreatology · Pubmed #25900320.

ABSTRACT: OBJECTIVES: To conduct a systematic review of the existing literature regarding surgical therapy for oligometastatic lung cancer to the pancreas. METHODS: Data was collected on patients with singular pancreatic metastases from lung cancer from papers published between January 1970 and June 2014. This was performed following the Preferred Reporting Items for Systematic reviews and Meta-analysis (PRISMA) guidelines. Kaplan-Meier and Cox Regression analyses were then used to determine and compare survival. RESULTS: There were 27 papers that fulfilled the search criteria, from which data on 32 patients was collected. Non-small cell lung cancer (NSCLC) was the most prevalent type of primary lung malignancy, and metachronous presentations of metastases were most common. Lesions were most frequently located in the pancreatic head and consequently the most common curative intent metastasectomy was pancreaticoduodenectomy. There was a statistically significant survival benefit for patients whose metastasis were discovered incidentally by surveillance CT as opposed to those whose metastasis were discovered during a work up for new somatic complaints (p = 0.024). The overall median survival for patients undergoing curative intent resection was 29 months, with 2-year and 5-year survivals of 65% and 21% respectively. Palliative surgery or medical only management was associated with a median survival of 8 months and 2-year and 5-year survivals of 25% and 8% respectively. CONCLUSIONS: Curative intent resection of isolated pancreatic metastasis from lung cancer may be beneficial in a select group of patients.

3 Clinical Trial Final analysis of a phase II study of modified FOLFIRINOX in locally advanced and metastatic pancreatic cancer. 2016

Stein, Stacey M / James, Edward S / Deng, Yanhong / Cong, Xiangyu / Kortmansky, Jeremy S / Li, Jia / Staugaard, Carol / Indukala, Doddamane / Boustani, Ann Marie / Patel, Vatsal / Cha, Charles H / Salem, Ronald R / Chang, Bryan / Hochster, Howard S / Lacy, Jill. ·Department of Medicine, Section of Medical Oncology, Yale School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA. · Yale School of Public Health, 300 George Street, New Haven, CT 06510, USA. · VA Connecticut Healthcare System, 950 Campbell Avenue, West Haven, CT 06516, USA. · Department of Diagnostic Radiology, Yale School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA. · Department of Surgery, Yale School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA. · Department of Therapeutic Radiology, Yale School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA. ·Br J Cancer · Pubmed #27022826.

ABSTRACT: BACKGROUND: Modifications of FOLFIRINOX are widely used despite the absence of prospective data validating efficacy in metastatic disease (metastatic pancreatic cancer (MPC)) or locally advanced pancreatic cancer (LAPC). We conducted a multicentre phase II study of modified FOLFIRINOX in advanced pancreatic cancer to assess the impact of dose attenuation in MPC and efficacy in LAPC. METHODS: Patients with untreated MPC or LAPC received modified FOLFIRINOX (irinotecan and bolus 5-fluorouracil reduced by 25%). Adverse events (AEs) were compared with full-dose FOLFIRINOX. Response rate (RR), median progression-free survival (PFS) and median overall survival (OS) were determined. RESULTS: In total, 31 and 44 patients with LAPC and MPC were enrolled, respectively. In MPC, efficacy of modified FOLFIRINOX was comparable with FOLFIRINOX with RR 35.1%, OS 10.2 months (95% CI 7.65-14.32) and PFS 6.1 months (95% CI 5.19-8.31). In LAPC, efficacy was notable with RR 17.2%, resection rate 41.9%, PFS 17.8 months (95% CI 11.0-23.9) and OS 26.6 months (95% CI 16.7, NA). Neutropenia (P<0.0001), vomiting (P<0.001) and fatigue (P=0.01) were significantly decreased. [(18)F]-Fluorodeoxyglucose positron emission tomography imaging response did not correlate with PFS or OS. CONCLUSIONS: In this first prospective study of modified FOLFIRINOX in MPC and LAPC, we observed decreased AEs compared with historical control patients. In MPC, the efficacy appears comparable with FOLFIRINOX. In LAPC, PFS and OS were prolonged and support the continued use of FOLFIRINOX in this setting.

4 Article Inhibition of renalase expression and signaling has antitumor activity in pancreatic cancer. 2016

Guo, Xiaojia / Hollander, Lindsay / MacPherson, Douglas / Wang, Ling / Velazquez, Heino / Chang, John / Safirstein, Robert / Cha, Charles / Gorelick, Fred / Desir, Gary V. ·Department of Medicine, VACHS, Yale University School of Medicine, New Haven, CT 06520, USA. · Department of Surgery, University of Connecticut, Farmington, CT 06032, USA. · Renal Division, Renji hospital, Shanghai Jiaotong Univ School of Medicine, Shanghai, China. · Department of Surgery, VACHS, Yale University, New Haven, CT 06520, USA. ·Sci Rep · Pubmed #26972355.

ABSTRACT: An essential feature of cancer is dysregulation of cell senescence and death. Renalase, a recently discovered secreted flavoprotein, provides cytoprotection against ischemic and toxic cellular injury by signaling through the PI3K-AKT and MAPK pathways. Here we show that renalase expression is increased in pancreatic cancer tissue and that it functions as a growth factor. In a cohort of patients with pancreatic ductal adenocarcinoma, overall survival was inversely correlated with renalase expression in the tumor mass, suggesting a pathogenic role for renalase. Inhibition of renalase signaling using siRNA or inhibitory anti-renalase antibodies decreased the viability of cultured pancreatic ductal adenocarcinoma cells. In two xenograft mouse models, either the renalase monoclonal antibody m28-RNLS or shRNA knockdown of renalase inhibited pancreatic ductal adenocarcinoma growth. Inhibition of renalase caused tumor cell apoptosis and cell cycle arrest. These results reveal a previously unrecognized role for the renalase in cancer: its expression may serve as a prognostic maker and its inhibition may provide an attractive therapeutic target in pancreatic cancer.

5 Article The novel tumor angiogenic factor, adrenomedullin-2, predicts survival in pancreatic adenocarcinoma. 2015

Hollander, Lindsay L / Guo, Xiaojia / Salem, Ronald R / Cha, Charles H. ·Department of Surgery, Yale University School of Medicine, New Haven, Connecticut; Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut. · Department of Surgery, Yale University School of Medicine, New Haven, Connecticut. · Department of Surgery, Yale University School of Medicine, New Haven, Connecticut. Electronic address: Charles.cha@yale.edu. ·J Surg Res · Pubmed #25982376.

ABSTRACT: BACKGROUND: Tumor angiogenesis has been demonstrated to have an important role in the development, progression, and metastasis of pancreas cancer. Adrenomedullin-2 (ADM2) is a calcitonin gene-related peptide that has recently been shown to be a novel tumor angiogenesis factor, acting via mitogen-activated protein kinase/extracellular signal-regulated kinase, phosphoinositide 3-kinase/Akt, and vascular endothelial growth factor/vascular endothelial growth factor-2 signaling pathways. Through the use of tissue microarray (TMA) technology, we hypothesize that ADM2 is an important tumor angiogenesis factor in pancreatic cancer. METHODS: Multiple TMAs were created using tissue from pancreatic cancer patients resected between January 1996 and December 2006. Core tissue samples of formalin-fixed, paraffin-embedded blocks of pancreatic cancer tissue were collected through an institutional review board-approved protocol and linked to available clinicopathologic data. Two TMAs consisting of 112 and 60 patients with pancreatic adenocarcinoma were studied for ADM2 protein expression using a quantitative, automated immunofluorescent microscopy system, a technology that removes potential observer bias in TMA analysis. The results were analyzed using independent Student t-test, chi-square, log-rank regression, and Kaplan-Meier methods. RESULTS: One hundred sixteen patients were identified for complete analysis, and 56 patients had complete survival data. Median follow-up for survivors was 14.5 mo. Total cellular levels of ADM2 were found to be a predictor of survival in pancreatic cancer. Low ADM2 levels were associated with a higher 5-y survival compared with high ADM2 levels (18% versus 6%, P = 0.05). Median survival was also worse in high ADM2 expressers (18.7 versus 8.6 mo). In accordance with prior-published pancreatic cancer data, a worse histologic grade (P = 0.001), tumor (T) stage (P = 0.009), and overall disease stage (P = 0.004), all portended a worse survival. CONCLUSIONS: For the first time, we have demonstrated that high levels of ADM2 expression predict a poorer survival in patients with pancreatic adenocarcinoma. This suggests a possible role of ADM2 in pancreas cancer and as a novel biomarker that predicts poorer survival. Additional study of ADM2 in pancreatic cancer will help reveal its true angiogenic role in pancreas cancer and its potential role as a novel therapeutic target.