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pancreatic cancer metabolism

Yuan Seng Wu, Ivy Chung, Won Fen Wong, Atsushi Masamune, Maw Shin Sim, Chung Yeng Looi
BACKGROUND: We previously showed that pancreatic stellate cells (PSC) secreted interleukin (IL)-6 and promoted pancreatic ductal adenocarcinoma (PDAC) cell proliferation via nuclear factor erythroid 2 (Nrf2)-mediated metabolic reprogramming. Epithelial-mesenchymal transition (EMT) is a key process for the metastatic cascade. To study the mechanism of PDAC progression to metastasis, we investigated the role of PSC-secreted IL-6 in activating EMT and the involvement of Nrf2 in this process...
October 14, 2016: Biochimica et Biophysica Acta
James J Farrell, Jennifer Moughan, Jonathan L Wong, William F Regine, Paul Schaefer, Al B Benson, John S Macdonald, Xiyong Liu, Yun Yen, Raymond Lai, Zhong Zheng, Gerold Bepler, Chandan Guha, Hany Elsaleh
OBJECTIVES: There is a need for validated predictive markers of gemcitabine response to guide precision medicine treatment in pancreatic cancer. We previously validated human equilibrative nucleoside transporter 1 as a predictive marker of gemcitabine treatment response using Radiation Therapy Oncology Group 9704. Controversy exists about the predictive value of gemcitabine metabolism pathway biomarkers: deoxycytidine kinase (DCK), ribonucleotide reductase 1 (RRM1), RRM2, and p53R2. METHODS: Radiation Therapy Oncology Group 9704 prospectively randomized 538 patients after pancreatic resection to receive either 5-fluorouracil or gemcitabine...
November 2016: Pancreas
Jessica Brandi, Ilaria Dando, Elisa Dalla Pozza, Giulia Biondani, Rosalind Jenkins, Victoria Elliott, Kevin Park, Giuseppina Fanelli, Lello Zolla, Eithne Costello, Aldo Scarpa, Daniela Cecconi, Marta Palmieri
: Recently, we have shown that the secretome of pancreatic cancer stem cells (CSCs) is characterized by proteins that participate in cancer differentiation, invasion, and metastasis. However, the differentially expressed intracellular proteins that lead to the specific characteristics of pancreatic CSCs have not yet been identified, and as a consequence the deranged metabolic pathways are yet to be elucidated. To identify the modulated proteins of pancreatic CSCs, iTRAQ-based proteomic analysis was performed to compare the proteome of Panc1 CSCs and Panc1 parental cells, identifying 230 modulated proteins...
October 13, 2016: Journal of Proteomics
Jingtao Luo, Yun Hong, Xiaoan Tao, Xi Wei, Lun Zhang, Qiang Li
Unlike normal cells, cancer cells are recently identified to rely on aerobic glycolysis for energy production called the Warburg effect. Several attempts are being made to target this metabolic reprogramming pathway in treating cancers; however, the successful rate is very limited. In this study, we investigated the functional roles of fatty acid oxidation key enzyme carnitine palmitoyl transferase 1a (CPT-1a), during the metabolic programming of pancreatic ductal adenocarcinoma (PDAC) cells induced by glucose deprivation...
October 13, 2016: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
Yu I Patyutko, N E Kudashkin, A G Kotel'nikov, O V Chistyakova
AIM: to determine the indications and to evaluate early and long-term outcomes of total pancreatectomy for pancreatic cancer. MATERIAL AND METHODS: Treatment of 29 patients who underwent one- and two-stage pancreatectomy for different malignancies was analyzed. RESULTS: Median of surgery duration and intraoperative blood loss was 280 min and 2200 ml respectively. Postoperative complications were observed in 9 (31%) patients. There were 2 (6...
2016: Khirurgiia
Yi-Jen Liao, Tzong-Shyuan Lee, Yuh-Ching Twu, Shih-Ming Hsu, Ching-Ping Yang, Chung-Kwe Wang, Yu-Chih Liang, Yi-Ming Arthur Chen
BACKGROUND: Glycine N-methyltransferase (GNMT) is abundantly expressed in the normal liver but is down-regulated in liver cancer tissues. GNMT knockout (Gnmt-/-) mice can spontaneously develop chronic hepatitis, fatty liver, and liver cancer. We previously demonstrated that hepatic GNMT is decreased in high-fat-diet-induced type 2 diabetes mellitus, but its contribution to metabolic syndrome is unclear. Here we show that GNMT modulates key aspects of metabolic syndrome in mice. METHODS: Eleven-week-old Gnmt-/- and wild-type (WT) mice with a C57BL/6 genetic background were used in this study...
October 4, 2016: Journal of Biomedical Science
Jiong Hu, Hai Hu, Jun Jie Hang, Hai Yan Yang, Zhi Yong Wang, Lei Wang, Dong Hui Chen, Li Wei Wang
Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with few therapeutic options. Recently, insight into cancer biology suggested abnormal lipid metabolism to be a risk factor for human malignancies. As a key enzyme implicated in lipid metabolism, PLD1 was elevated in various human cancer associating with malignant phenotypes. However, little was known about its expression and function in PDAC. We showed that PLD1 was elevated in both the cell lines and clinical samples of PDAC, and it positively correlated with vascular invasion (p = 0...
October 4, 2016: Oncotarget
Roberto Catanzaro, Biagio Cuffari, Angelo Italia, Francesco Marotta
After the first description of fatty pancreas in 1933, the effects of pancreatic steatosis have been poorly investigated, compared with that of the liver. However, the interest of research is increasing. Fat accumulation, associated with obesity and the metabolic syndrome (MetS), has been defined as "fatty infiltration" or "nonalcoholic fatty pancreas disease" (NAFPD). The term "fatty replacement" describes a distinct phenomenon characterized by death of acinar cells and replacement by adipose tissue. Risk factors for developing NAFPD include obesity, increasing age, male sex, hypertension, dyslipidemia, alcohol and hyperferritinemia...
September 14, 2016: World Journal of Gastroenterology: WJG
W Jin, E A Mellon, S E Hoffe, J M Frakes, G M Springett, B A Centeno, R Kim, A Mahipal, J M Pimiento, M P Malafa, K Latifi
No abstract text is available yet for this article.
October 1, 2016: International Journal of Radiation Oncology, Biology, Physics
Hui-Yi Feng, Yang-Chao Chen
The role of bile acids in colorectal cancer has been well documented, but their role in pancreatic cancer remains unclear. In this review, we examined the risk factors of pancreatic cancer. We found that bile acids are associated with most of these factors. Alcohol intake, smoking, and a high-fat diet all lead to high secretion of bile acids, and bile acid metabolic dysfunction is a causal factor of gallstones. An increase in secretion of bile acids, in addition to a long common channel, may result in bile acid reflux into the pancreatic duct and to the epithelial cells or acinar cells, from which pancreatic adenocarcinoma is derived...
September 7, 2016: World Journal of Gastroenterology: WJG
Hayato Kaida, Koichi Azuma, Akihiko Kawahara, Masafumi Yasunaga, Yuhei Kitasato, Satoshi Hattori, Tomoki Taira, Hiroki Ureshino, Masayoshi Kage, Kazunari Ishii, Takamichi Murakami, Masatoshi Ishibashi
PURPOSE: We examined whether fluorine-18 fluorodeoxyglucose (FDG) uptake is related to the mammalian target of rapamycin (mTOR) signal pathway and its related proteins in pancreatic cancer patients. METHODS: We retrospectively studied 53 pancreatic cancer patients who underwent FDG positron emission tomography (PET) or FDG PET/CT, and complete curative surgical resection. The SUV max, the tumor to nontumor activity of pancreas [T/N (P)] ratio and the T/N of liver [T/N (L)] ratio were calculated...
October 2016: European Journal of Radiology
Yinnong Jia, Wenting Zhang, Wei Fan, Susan Brusnahan, Jered Garrison
The neurotensin receptor 1 (NTR1) has been shown to be a promising target, due to its increased level of expression relative to normal tissue, for pancreatic and colon cancers. This has prompted the development of a variety of NTR1-targeted radiopharmaceuticals, based on the neurotensin (NT) peptide, for diagnostic and radiotherapeutic applications. A major obstacle for the clinical translation of NTR1-targeted radiotherapeutics would likely be nephrotoxicity due to the high levels of kidney retention. It is well-known that for many peptide-based agents, renal uptake is influenced by the overall molecular charge...
October 21, 2016: Bioconjugate Chemistry
Chen Liang, Yi Qin, Bo Zhang, Shunrong Ji, Si Shi, Wenyan Xu, Jiang Liu, Jinfeng Xiang, Dingkong Liang, Qiangsheng Hu, Liang Liu, Chen Liu, Guopei Luo, Quanxing Ni, Jin Xu, Xianjun Yu
Metabolic reprogramming is one of the emerging hallmarks of cancers. As a highly malignant tumor, pancreatic ductal adenocarcinoma (PDA) is not only a metabolic disease but also a heterogeneous disease. Heterogeneity induces PDA dependence on distinct nutritive substrates, thereby inducing different metabolic phenotypes. We stratified PDA into four phenotypes with distinct types of energy metabolism, including a Warburg phenotype, a reverse Warburg phenotype, a glutaminolysis phenotype, and a lipid-dependent phenotype...
September 20, 2016: Acta Biochimica et Biophysica Sinica
Samuel N Rodman, Jacquelyn M Spence, Tyler J Ronnfeldt, Yueming Zhu, Shane R Solst, Rebecca A O'Neill, Bryan G Allen, Xiangming Guan, Douglas R Spitz, Melissa A Fath
The goal of this study was to determine if depletion of glutathione (GSH) and inhibition of thioredoxin (Trx) reductase (TrxR) activity could enhance radiation responses in human breast cancer stem cells by a mechanism involving thiol-dependent oxidative stress. The following were used to inhibit GSH and Trx metabolism: buthionine sulfoximine (BSO), a GSH synthesis inhibitor; sulfasalazine (SSZ), an inhibitor of xc(-) cysteine/glutamate antiporter; auranofin (Au), a thioredoxin reductase inhibitor; or 2-AAPA, a GSH-reductase inhibitor...
September 19, 2016: Radiation Research
Koji Nishi, Kenta Suzuki, Junpei Sawamoto, Yuma Tokizawa, Yumiko Iwase, Nagahiko Yumita, Toshihiko Ikeda
Cancer cells tend to have a high requirement for lipids, including fatty acids, cholesterol and triglyceride, because of their rapid proliferative rate compared to normal cells. In this study, we investigated the effects of inhibition of lipid synthesis on the proliferation and viability of human pancreatic cancer cells. Of the inhibitors of lipid synthesis that were tested, 5-(tetradecyloxy)-2-furoic acid (TOFA), which is an inhibitor of acetyl-CoA carboxylase, and the fatty acid synthase (FAS) inhibitors cerulenin and irgasan, significantly suppressed the proliferation of MiaPaCa-2 and AsPC-1 cells...
September 2016: Anticancer Research
Erik S Knudsen, Uthra Balaji, Elizaveta Freinkman, Peter McCue, Agnieszka K Witkiewicz
Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis. The aggressiveness and therapeutic recalcitrance of this malignancy has been attributed to multiple factors including the influence of an active desmoplastic stroma. How the stromal microenvironment of PDAC contributes to the fatal nature of this disease is not well defined. In the analysis of clinical specimens, we observed diverse expression of the hypoxic marker carbonic anhydrase IX and the lactate transporter MCT4 in the stromal compartment...
September 7, 2016: Oncotarget
Kevin A Meyer, Christopher K Neeley, Nicki A Baker, Alexandra R Washabaugh, Carmen G Flesher, Barbara S Nelson, Timothy L Frankel, Carey N Lumeng, Costas A Lyssiotis, Michelle L Wynn, Andrew D Rhim, Robert W O'Rourke
Adipocytes promote progression of multiple cancers, but their role in pancreatic intraepithelial neoplasia (PanIN) and ductal adenocarcinoma (PDAC) is poorly defined. Nutrient transfer is a mechanism underlying stromal cell-cancer crosstalk. We studied the role of adipocytes in regulating in vitro PanIN and PDAC cell proliferation with a focus on glutamine metabolism. Murine 3T3L1 adipocytes were used to model adipocytes. Cell lines derived from PKCY mice were used to model PanIN and PDAC. Co-culture was used to study the effect of adipocytes on PanIN and PDAC cell proliferation in response to manipulation of glutamine metabolism...
September 2016: Biochemistry and Biophysics Reports
Mohit P Mathew, Elaine Tan, Christopher T Saeui, Patawut Bovonratwet, Samuel Sklar, Rahul Bhattacharya, Kevin J Yarema
In prior work we reported that advanced stage, drug-resistant pancreatic cancer cells (the SW1990 line) can be sensitized to the EGFR-targeting tyrosine kinase inhibitors (TKIs) erlotinib and gefitinib by treatment with 1,3,4-O-Bu3ManNAc (Bioorg. Med. Chem. Lett. (2015) 25(6):1223-7). Here we provide mechanistic insights into how this compound inhibits EGFR activity and provides synergy with TKI drugs. First, we showed that the sialylation of the EGFR receptor was at most only modestly enhanced (by ~20 to 30%) compared to overall ~2-fold increase in cell surface levels of this sugar...
August 24, 2016: Oncotarget
Jared R Mayers, Margaret E Torrence, Laura V Danai, Thales Papagiannakopoulos, Shawn M Davidson, Matthew R Bauer, Allison N Lau, Brian W Ji, Purushottam D Dixit, Aaron M Hosios, Alexander Muir, Christopher R Chin, Elizaveta Freinkman, Tyler Jacks, Brian M Wolpin, Dennis Vitkup, Matthew G Vander Heiden
Tumor genetics guides patient selection for many new therapies, and cell culture studies have demonstrated that specific mutations can promote metabolic phenotypes. However, whether tissue context defines cancer dependence on specific metabolic pathways is unknown. Kras activation and Trp53 deletion in the pancreas or the lung result in pancreatic ductal adenocarinoma (PDAC) or non-small cell lung carcinoma (NSCLC), respectively, but despite the same initiating events, these tumors use branched-chain amino acids (BCAAs) differently...
September 9, 2016: Science
Marco Del Chiaro, Elena Rangelova, Ralf Segersvärd, Urban Arnelo
Total pancreatectomy is associated with short- and long-term high complication rate and without evidence of oncologic advantages. Several metabolic consequences are co-related with the apancreatic state. The unstable diabetes related to the total resection of the pancreas expose the patients to short- and long-term life-threatening complications. Severe hypoglycemia is a short-term dangerous complication that can also cause patients' death. Chronic complications of severe diabetes (cardiac and vascular diseases, neuropathy, nephropathy, and retinopathy) are also cause of morbidity, mortality and worsening of quality of life...
September 7, 2016: Updates in Surgery
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