Reference Citation Analysis: Find an Article, Find a Category, Find a Journal, Find a Scholar

For: Trajkovic-Arsic M, Kalideris E, Siveke JT. The role of insulin and IGF system in pancreatic cancer. J Mol Endocrinol 2013;50:R67-74. [PMID: 23493758 DOI: 10.1530/jme-12-0259] [Citation(s) in RCA: 63] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]

For:	Trajkovic-Arsic M, Kalideris E, Siveke JT. The role of insulin and IGF system in pancreatic cancer. J Mol Endocrinol 2013;50:R67-74. [PMID: 23493758 DOI: 10.1530/jme-12-0259] [Citation(s) in RCA: 63] [Impact Index Per Article: 5.3] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]

Number

Cited by Other Article(s)

Gupta T, Murtaza M. Advancing targeted therapies in pancreatic cancer: Leveraging molecular abberrations for therapeutic success. PROGRESS IN BIOPHYSICS AND MOLECULAR BIOLOGY 2025;196:19-32. [PMID: 39988056 DOI: 10.1016/j.pbiomolbio.2025.02.003] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 11/10/2024] [Revised: 02/03/2025] [Accepted: 02/20/2025] [Indexed: 02/25/2025]

Zhou K, Liu Y, Tang C, Zhu H. Pancreatic Cancer: Pathogenesis and Clinical Studies. MedComm (Beijing) 2025;6:e70162. [PMID: 40182139 PMCID: PMC11965705 DOI: 10.1002/mco2.70162] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/24/2024] [Revised: 03/08/2025] [Accepted: 03/12/2025] [Indexed: 04/05/2025] Open

Hu C, Chen Y, Yin X, Xu R, Yin C, Wang C, Zhao Y. Pancreatic endocrine and exocrine signaling and crosstalk in physiological and pathological status. Signal Transduct Target Ther 2025;10:39. [PMID: 39948335 PMCID: PMC11825823 DOI: 10.1038/s41392-024-02098-3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/20/2024] [Revised: 10/20/2024] [Accepted: 12/03/2024] [Indexed: 02/16/2025] Open

Affiliation(s)

Chenglin Hu Department of General Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, PR China Key Laboratory of Research in Pancreatic Tumor, Chinese Academy of Medical Sciences, Beijing, PR China State Key Laboratory of Complex, Severe, and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, PR China
Yuan Chen Department of General Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, PR China Key Laboratory of Research in Pancreatic Tumor, Chinese Academy of Medical Sciences, Beijing, PR China State Key Laboratory of Complex, Severe, and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, PR China
Xinpeng Yin Department of General Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, PR China Key Laboratory of Research in Pancreatic Tumor, Chinese Academy of Medical Sciences, Beijing, PR China State Key Laboratory of Complex, Severe, and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, PR China
Ruiyuan Xu Department of General Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, PR China Key Laboratory of Research in Pancreatic Tumor, Chinese Academy of Medical Sciences, Beijing, PR China State Key Laboratory of Complex, Severe, and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, PR China
Chenxue Yin Department of General Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, PR China Key Laboratory of Research in Pancreatic Tumor, Chinese Academy of Medical Sciences, Beijing, PR China State Key Laboratory of Complex, Severe, and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, PR China
Chengcheng Wang Key Laboratory of Research in Pancreatic Tumor, Chinese Academy of Medical Sciences, Beijing, PR China. State Key Laboratory of Complex, Severe, and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, PR China. National Infrastructures for Translational Medicine, Peking Union Medical College Hospital, Beijing, PR China. Institute of Clinical Medicine, Peking Union Medical College Hospital, Beijing, PR China.
Yupei Zhao Department of General Surgery, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, PR China. Key Laboratory of Research in Pancreatic Tumor, Chinese Academy of Medical Sciences, Beijing, PR China. State Key Laboratory of Complex, Severe, and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, PR China. National Infrastructures for Translational Medicine, Peking Union Medical College Hospital, Beijing, PR China.

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Ding L, Qian J, Dai R, Zhang H, Miao J, Wang J, Yu M, Tan X, Li Y. The hidden impact: social isolation and inflammation's role in pancreatic cancer risk among those with diabetes. BMC Cancer 2025;25:58. [PMID: 39794805 PMCID: PMC11720300 DOI: 10.1186/s12885-025-13470-z] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/26/2024] [Accepted: 01/07/2025] [Indexed: 01/13/2025] Open

Asiri A, Al Qarni A, Bakillah A. The Interlinking Metabolic Association between Type 2 Diabetes Mellitus and Cancer: Molecular Mechanisms and Therapeutic Insights. Diagnostics (Basel) 2024;14:2132. [PMID: 39410536 PMCID: PMC11475808 DOI: 10.3390/diagnostics14192132] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/25/2024] [Revised: 09/15/2024] [Accepted: 09/16/2024] [Indexed: 10/20/2024] Open

García-Montero C, Fraile-Martinez O, Cobo-Prieto D, De Leon-Oliva D, Boaru DL, De Castro-Martinez P, Pekarek L, Gragera R, Hernández-Fernández M, Guijarro LG, Toledo-Lobo MDV, López-González L, Díaz-Pedrero R, Monserrat J, Álvarez-Mon M, Saez MA, Ortega MA. Abnormal Histopathological Expression of Klotho, Ferroptosis, and Circadian Clock Regulators in Pancreatic Ductal Adenocarcinoma: Prognostic Implications and Correlation Analyses. Biomolecules 2024;14:947. [PMID: 39199335 PMCID: PMC11353028 DOI: 10.3390/biom14080947] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/07/2024] [Revised: 07/27/2024] [Accepted: 07/29/2024] [Indexed: 09/01/2024] Open

Affiliation(s)

Cielo García-Montero Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.)
Oscar Fraile-Martinez Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.)
David Cobo-Prieto Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Immune System Diseases-Rheumatology Service, Central University Hospital of Defence-UAH Madrid, 28801 Alcala de Henares, Spain
Diego De Leon-Oliva Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.)
Diego Liviu Boaru Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.)
Patricia De Castro-Martinez Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.)
Leonel Pekarek Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.)
Raquel Gragera Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.)
Mauricio Hernández-Fernández Department of Surgery, Medical and Social Sciences, Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain;
Luis G. Guijarro Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.) Unit of Biochemistry and Molecular Biology, Department of System Biology (CIBEREHD), University of Alcalá, 28801 Alcala de Henares, Spain
María Del Val Toledo-Lobo Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.) Department of Biomedicine and Biotechnology, Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain
Laura López-González Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.) Department of Surgery, Medical and Social Sciences, Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain;
Raul Díaz-Pedrero Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.) Department of Surgery, Medical and Social Sciences, Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain;
Jorge Monserrat Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.)
Melchor Álvarez-Mon Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.) Immune System Diseases-Rheumatology and Internal Medicine Service, University Hospital Prince of Asturias, Networking Research Center on for Liver and Digestive Diseases (CIBEREHD), 28806 Alcala de Henares, Spain
Miguel A. Saez Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.) Pathological Anatomy Service, University Hospital Gómez-Ulla, 28806 Alcala de Henares, Spain
Miguel A. Ortega Department of Medicine and Medical Specialities (CIBEREHD), Faculty of Medicine and Health Sciences, University of Alcalá, 28801 Alcala de Henares, Spain; (C.G.-M.); (O.F.-M.); (D.C.-P.); (D.D.L.-O.); (D.L.B.); (P.D.C.-M.); (L.P.); (R.G.); (J.M.); (M.Á.-M.); (M.A.S.) Ramón y Cajal Institute of Sanitary Research (IRYCIS), 28034 Madrid, Spain; (L.G.G.); (M.D.V.T.-L.); (L.L.-G.); (R.D.-P.)

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Song Y, Jiang L, Han Y, Zhang S, Li S. Triglyceride-glucose index and glycemic dynamics in pancreatic ductal adenocarcinoma: implications for disease progression and prognosis. J Transl Med 2024;22:708. [PMID: 39080703 PMCID: PMC11290143 DOI: 10.1186/s12967-024-05524-w] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/22/2024] [Accepted: 07/20/2024] [Indexed: 08/02/2024] Open

Mustafa M, Abbas K, Alam M, Habib S, Zulfareen, Hasan GM, Islam S, Shamsi A, Hassan I. Investigating underlying molecular mechanisms, signaling pathways, emerging therapeutic approaches in pancreatic cancer. Front Oncol 2024;14:1427802. [PMID: 39087024 PMCID: PMC11288929 DOI: 10.3389/fonc.2024.1427802] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/04/2024] [Accepted: 07/01/2024] [Indexed: 08/02/2024] Open

Zhou Y, He Z, Li T, Choppavarapu L, Hu X, Cao R, Leone GW, Kahn M, Jin VX. 3D Chromatin Alteration by Disrupting β-Catenin/CBP Interaction Is Enriched with Insulin Signaling in Pancreatic Cancer. Cancers (Basel) 2024;16:2202. [PMID: 38927910 PMCID: PMC11201718 DOI: 10.3390/cancers16122202] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/28/2024] [Revised: 06/02/2024] [Accepted: 06/08/2024] [Indexed: 06/28/2024] Open

Yun HY. Leucine rich repeat LGI family member 3: Integrative analyses support its prognostic association with pancreatic adenocarcinoma. Medicine (Baltimore) 2024;103:e37183. [PMID: 38394487 PMCID: PMC11309673 DOI: 10.1097/md.0000000000037183] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/12/2023] [Accepted: 01/17/2024] [Indexed: 02/25/2024] Open

Abstract

Leucine rich repeat LGI family member 3 (LGI3) is a member of the LGI protein family. Previous studies of our group have reported that LGI3 is expressed in adipose tissue, skin and brain, and serves as a multifunctional cytokine. LGI3 may also be involved in cytokine networks in various cancers. This study aimed to analyze differentially expressed genes in pancreatic adenocarcinoma (PAC) tissues and PAC cohort data in order to evaluate the prognostic role of LGI3. The expression microarray and the PAC cohort data were analyzed by bioinformatic methods for differential expression, protein-protein interactions, functional enrichment and pathway analyses, gene co-expression network analysis, and prognostic association analysis. Results showed that LGI3 expression was significantly reduced in PAC tissues. Nineteen upregulated genes and 31 downregulated genes in PAC tissues were identified as LGI3-regulated genes. Protein-protein interaction network analysis demonstrated that 92% (46/50) of the LGI3-regulated genes that were altered in PACs belonged to a protein-protein interaction network cluster. Functional enrichment and gene co-expression network analyses demonstrated that these genes in the network cluster were associated with various processes including inflammatory and immune responses, metabolic processes, cell differentiation, and angiogenesis. PAC cohort analyses revealed that low expression levels of LGI3 were significantly associated with poor PAC prognosis. Analysis of favorable or unfavorable prognostic gene products in PAC showed that 93 LGI3-regulated genes were differentially associated with PAC prognosis. LGI3 expression was correlated with the tumor-infiltration levels of various immune cells. Taken together, these results suggested that LGI3 may be a potential prognostic marker of PAC.

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Darrigrand JF, Salowka A, Torres-Cano A, Tapia-Rojo R, Zhu T, Garcia-Manyes S, Spagnoli FM. Acinar-ductal cell rearrangement drives branching morphogenesis of the murine pancreas in an IGF/PI3K-dependent manner. Dev Cell 2024;59:326-338.e5. [PMID: 38237591 PMCID: PMC11805742 DOI: 10.1016/j.devcel.2023.12.011] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/20/2023] [Revised: 10/24/2023] [Accepted: 12/20/2023] [Indexed: 02/08/2024]

Miao X, Shen S, Koch G, Wang X, Li J, Shen X, Qu J, Straubinger RM, Jusko WJ. Systems Pharmacodynamic Model of Combined Gemcitabine and Trabectedin in Pancreatic Cancer Cells. Part I: Effects on Signal Transduction Pathways Related to Tumor Growth. J Pharm Sci 2024;113:214-227. [PMID: 38498417 PMCID: PMC11017371 DOI: 10.1016/j.xphs.2023.10.030] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/30/2023] [Revised: 10/22/2023] [Accepted: 10/22/2023] [Indexed: 03/20/2024]

Zhou Y, Li T, He Z, Choppavarapu L, Hu X, Cao R, Leone GW, Kahn M, Jin VX. Reprogramming of 3D chromatin domains by antagonizing the β-catenin/CBP interaction attenuates insulin signaling in pancreatic cancer. BIORXIV : THE PREPRINT SERVER FOR BIOLOGY 2023:2023.11.10.566585. [PMID: 38013997 PMCID: PMC10680786 DOI: 10.1101/2023.11.10.566585] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/29/2023]

Zhang W, Peng Y, Kang X, Wang C, Chen F, He Y, Li W. Healthy and Unhealthy Plant-Based Diets and Glioma in the Chinese Population. Brain Sci 2023;13:1401. [PMID: 37891770 PMCID: PMC10605677 DOI: 10.3390/brainsci13101401] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/04/2023] [Revised: 09/22/2023] [Accepted: 09/29/2023] [Indexed: 10/29/2023] Open

Mukhtar S, Moradi A, Kodali A, Okoye C, Klein D, Mohamoud I, Olanisa OO, Parab P, Chaudhary P, Hamid P. On the Menu: Analyzing the Macronutrients, Micronutrients, Beverages, Dietary Patterns, and Pancreatic Cancer Risk. Cureus 2023;15:e45259. [PMID: 37842365 PMCID: PMC10576649 DOI: 10.7759/cureus.45259] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/26/2023] [Accepted: 09/13/2023] [Indexed: 10/17/2023] Open

Fan H, Mao Q, Zhang W, Fang Q, Zou Q, Gong J. The Impact of Bariatric Surgery on Pancreatic Cancer Risk: a Systematic Review and Meta-Analysis. Obes Surg 2023:10.1007/s11695-023-06570-x. [PMID: 37020161 DOI: 10.1007/s11695-023-06570-x] [Citation(s) in RCA: 4] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/16/2023] [Revised: 03/26/2023] [Accepted: 03/28/2023] [Indexed: 04/07/2023]

Dya GA, Klychnikov OI, Adasheva DA, Vladychenskaya EA, Katrukha AG, Serebryanaya DV. IGF-Binding Proteins and Their Proteolysis as a Mechanism of Regulated IGF Release in the Nervous Tissue. BIOCHEMISTRY (MOSCOW) 2023;88:S105-S122. [PMID: 37069117 DOI: 10.1134/s0006297923140079] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/22/2023]

Prinz C, Fehring L, Frese R. MicroRNAs as Indicators of Malignancy in Pancreatic Ductal Adenocarcinoma (PDAC) and Cystic Pancreatic Lesions. Cells 2022;11:cells11152374. [PMID: 35954223 PMCID: PMC9368175 DOI: 10.3390/cells11152374] [Citation(s) in RCA: 10] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/08/2022] [Revised: 07/25/2022] [Accepted: 07/30/2022] [Indexed: 12/04/2022] Open

Abstract

The dysregulation of microRNAs has recently been associated with cancer development and progression in pancreatic ductal adenocarcinoma (PDAC) and cystic pancreatic lesions. In solid pancreatic tumor tissue, the dysregulation of miR-146, miR-196a/b, miR-198, miR-217, miR-409, and miR-490, as well as miR-1290 has been investigated in tumor biopsies of patients with PDAC and was reported to predict cancer presence. However, the value of the predictive biomarkers may further be increased during clinical conditions suggesting cancer development such as hyperinsulinemia or onset of diabetes. In this specific context, the dysregulation of miR-486 and miR-196 in tumors has been observed in the tumor tissue of PDAC patients with newly diagnosed diabetes mellitus. Moreover, miR-1256 is dysregulated in pancreatic cancer, possibly due to the interaction with long non-coding RNA molecules that seem to affect cell-cycle control and diabetes manifestation in PDAC patients, and, thus, these three markers may be of special or “sentinel value”. In blood samples, Next-generation sequencing (NGS) has also identified a set of microRNAs (miR-20a, miR-31-5p, miR-24, miR-25, miR-99a, miR-185, and miR-191) that seem to differentiate patients with pancreatic cancer remarkably from healthy controls, but limited data exist in this context regarding the prediction of cancer presences and outcomes. In contrast to solid pancreatic tumors, in cystic pancreatic cancer lesions, as well as premalignant lesions (such as intraductal papillary neoplasia (IPMN) or mucinous-cystic adenomatous cysts (MCAC)), the dysregulation of a completely different expression panel of miR-31-5p, miR-483-5p, miR-99a-5p, and miR-375 has been found to be of high clinical value in differentiating benign from malignant lesions. Interestingly, signal transduction pathways associated with miR-dysregulation seem to be entirely different in patients with pancreatic cysts when compared to PDAC. Overall, the determination of these different dysregulation “panels” in solid tumors, pancreatic cysts, obtained via fine-needle aspirate biopsies and/or in blood samples at the onset or during the treatment of pancreatic diseases, seems to be a reasonable candidate approach for predicting cancer presence, cancer development, and even therapy responses.

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Yang R, Gao Y, Ouyang Z, Shi X, Shen M. Gold nanostar‐based complexes applied for cancer theranostics. VIEW 2022;3. [DOI: 10.1002/viw.20200171] [Citation(s) in RCA: 21] [Impact Index Per Article: 7.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/18/2021] [Accepted: 09/25/2021] [Indexed: 01/06/2025] Open

Wang S, Wang YX, Sandoval-Insausti H, Farland LV, Shifren JL, Zhang D, Manson JE, Birmann BM, Willett WC, Giovannucci EL, Missmer SA, Chavarro JE. Menstrual cycle characteristics and incident cancer: a prospective cohort study. Hum Reprod 2022;37:341-351. [PMID: 34893843 PMCID: PMC8804333 DOI: 10.1093/humrep/deab251] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/02/2021] [Revised: 10/06/2021] [Indexed: 12/30/2022] Open

Abstract

STUDY QUESTION

Are menstrual cycle characteristics throughout the reproductive lifespan associated with cancer risk?

SUMMARY ANSWER

Irregular and long menstrual cycles throughout the reproductive lifespan were associated with increased risk of total invasive cancer, especially obesity-related cancers.

WHAT IS KNOWN ALREADY

Long and irregular menstrual cycles have been associated with lower risk of pre-menopausal breast cancer and higher risk of endometrial cancer, but associations with other malignancies are less clear.

STUDY DESIGN, SIZE, DURATION

Prospective cohort study. Prospective follow-up of 78 943 women participating in the Nurses' Health Study II between 1989 and 2015.

PARTICIPANTS/MATERIALS, SETTING, METHODS

We followed 78 943 pre-menopausal women without cancer history who reported the usual length and regularity of their menstrual cycles at different ages (14-17, 18-22 and 29-46 years). Cancer diagnosis was confirmed through medical record review and classified as obesity-related (colorectal, gallbladder, kidney, multiple myeloma, thyroid, pancreatic, esophageal, gastric, liver, endometrial, ovarian and post-menopausal breast) or non-obesity-related. We fitted Cox proportional hazards models to estimate hazard ratios (HRs) and 95% CIs of the association between menstrual cycle characteristics and cancer incidence.

MAIN RESULTS AND THE ROLE OF CHANCE

We documented 5794 incident cancer cases during 1 646 789 person-years of follow-up. After adjusting for BMI and other potential confounders, women reporting irregular cycles at age 29-46 years had an 11% (95% CI: 2-21%) higher risk of total invasive cancer than women reporting very regular cycles at the same age. This association was limited to obesity-related cancers, with a 23% (95% CI: 9-39%) higher risk and was strongest for endometrial cancer (HR = 1.39; 95% CI: 1.09-1.77). Findings were comparable for cycle characteristics earlier in life and for menstrual cycle length. Very irregular cycles at age 14-17 years were associated with significant increase in risk of colorectal cancer (HR = 1.36; 95% CI: 1.02-1.81).

LIMITATIONS, REASONS FOR CAUTION

Our study might be subject to recall bias for findings pertaining to cycle characteristics in adolescence and early adulthood, as these were retrospectively reported. Generalizability to non-White women may be limited, as 96% of participants were White.

WIDER IMPLICATIONS OF THE FINDINGS

Women with irregular or long menstrual cycles in mid-adulthood had a statistically significantly higher risk of developing cancer, especially obesity-related cancers. This association was not limited to gynecological cancers. Obesity-related cancers may need to be added to the spectrum of long-term health consequences of long or irregular cycles, possibly warranting targeted screening among women who experience long or irregular cycles in mid-adulthood.

STUDY FUNDING/COMPETING INTEREST

This work was supported by grants U01 CA176726, U01 HL145386 and R01 HD096033 from the National Institutes of Health. The authors have no conflicts of interest to declare.

TRIAL REGISTRATION NUMBER

N/A.

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Affiliation(s)

Siwen Wang Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China
Yi-Xin Wang Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA
Helena Sandoval-Insausti Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA
Leslie V Farland Department of Epidemiology and Biostatistics, Mel and Enid Zuckerman University of Arizona College of Public Health, University of Arizona, Tucson, AZ, USA
Jan L Shifren Department of Obstetrics and Gynecology, Midlife Women's Health Center, Massachusetts General Hospital, Boston, MA, USA
Dan Zhang Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China
JoAnn E Manson Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
Brenda M Birmann Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
Walter C Willett Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
Edward L Giovannucci Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
Stacey A Missmer Department of Obstetrics, Gynecology and Reproductive Biology, Michigan State University College of Human Medicine, East Lansing, MI, USA
Jorge E Chavarro Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA

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Mai S, Inkielewicz-Stepniak I. Pancreatic Cancer and Platelets Crosstalk: A Potential Biomarker and Target. Front Cell Dev Biol 2021;9:749689. [PMID: 34858977 PMCID: PMC8631477 DOI: 10.3389/fcell.2021.749689] [Citation(s) in RCA: 15] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/29/2021] [Accepted: 10/04/2021] [Indexed: 12/12/2022] Open

Roy A, Sahoo J, Kamalanathan S, Naik D, Mohan P, Kalayarasan R. Diabetes and pancreatic cancer: Exploring the two-way traffic. World J Gastroenterol 2021;27:4939-4962. [PMID: 34497428 PMCID: PMC8384733 DOI: 10.3748/wjg.v27.i30.4939] [Citation(s) in RCA: 37] [Impact Index Per Article: 9.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/28/2021] [Revised: 06/16/2021] [Accepted: 07/07/2021] [Indexed: 02/06/2023] Open

Hu L, Xu X, Li Q, Chen X, Yuan X, Qiu S, Yao C, Zhang D, Wang F. Caveolin-1 increases glycolysis in pancreatic cancer cells and triggers cachectic states. FASEB J 2021;35:e21826. [PMID: 34320244 DOI: 10.1096/fj.202100121rrr] [Citation(s) in RCA: 15] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/21/2021] [Revised: 07/13/2021] [Accepted: 07/15/2021] [Indexed: 12/24/2022]

Alhakamy NA, Ahmed OAA, Fahmy UA, Md S. Apamin-Conjugated Alendronate Sodium Nanocomplex for Management of Pancreatic Cancer. Pharmaceuticals (Basel) 2021;14:ph14080729. [PMID: 34451826 PMCID: PMC8398389 DOI: 10.3390/ph14080729] [Citation(s) in RCA: 16] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/17/2021] [Revised: 07/23/2021] [Accepted: 07/24/2021] [Indexed: 01/10/2023] Open

Abstract

Pancreatic cancer has a low survival rate and has limited therapeutic options due to the peculiarity of the tumor tissue. Cancer nanotechnology provides several opportunities to resolve such difficulties as a result of the high surface-to-volume ratio of nanostructures. Peptide-drug nanocomplexes have proved to have immense potential in anticancer activity against pancreatic cancer cells. Thus, in the present study apamin (APA) and alendronate sodium (ALS) were combined to form nanocomplexes (APA-ALS-NC) against pancreatic cancer cells. Optimization of ALS, incubation time, and sonication time in terms of particle size of the nanocomplex was carried out. The optimized formulation was evaluated for anticancer activities in pancreatic cancer cells (PANC-1 cells). A Box-Behnken design using ALS, incubation time, and sonication time as independent factors and particle size as the response was chosen to optimize the APA-ALS-NC formulation. The optimized APA-ALS-NC had a particle size of 161.52 ± 8.4 nm. The evaluation of APA-ALS-NC in PANC-1 cells was carried out using various in vitro tests. The IC₅₀ values were determined by MTT assay and found to be 37.6 ± 1.65, 13.4 ± 0.59, and 1.01 ± 0.04 µg/mL for ALS, APA, and APA-ALS-NC, respectively. The higher cytotoxicity activity of APA-ALS-NC was confirmed from the higher percentage of cells in the necrosis phase (apoptosis study) and the G2-M phase (cell cycle study) compared to that of ALS and APA. While the loss of mitochondrial membrane potential was less for APA-ALS-NC, the levels of IL-1β, TNF-α, caspase-3, ROS, IL-6, and NF-kB showed that APA-ALS-NC can significantly enhance apoptosis and cytotoxicity in PANC-1 cells. Moreover, Bax (10.87 ± 1.36), Bcl-2 (0.27 ± 0.02), and p53 (9.16 ± 1.22) gene expressions confirmed that APA-ALS-NC had a significant apoptotic effect compared to ALS and APA. In summary, the APA-ALS-NC had a more significant cytotoxic effect than ALS and APA. The results of the present study are promising for further evaluation in pre-clinical and clinical trials for arriving at a successful therapeutic strategy against pancreatic cancer.

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Heckl SM, Mau F, Senftleben A, Daunke T, Beckinger S, Abdullazade S, Schreiber S, Röcken C, Sebens S, Schäfer H. Programmed Death-Ligand 1 (PD-L1) Expression Is Induced by Insulin in Pancreatic Ductal Adenocarcinoma Cells Pointing to Its Role in Immune Checkpoint Control. Med Sci (Basel) 2021;9:48. [PMID: 34202040 PMCID: PMC8293454 DOI: 10.3390/medsci9030048] [Citation(s) in RCA: 15] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/24/2021] [Revised: 06/19/2021] [Accepted: 06/22/2021] [Indexed: 02/06/2023] Open

Affiliation(s)

Steffen M. Heckl Department of Internal Medicine I, UKSH Campus Kiel, Arnold-Heller-Str. 3, Bldg. K3, 24105 Kiel, Germany; (S.M.H.); (S.S.) Department of Internal Medicine II, UKSH Campus Kiel, university, Arnold-Heller-Str. 3, Bldg. E, 24105 Kiel, Germany
Franziska Mau Institute of Experimental Cancer Research, UKSH Campus Kiel & Christian-Albrechts-University Kiel, Arnold-Heller-Str. 3, Bldg. U30, 24105 Kiel, Germany; (F.M.); (A.S.); (T.D.); (S.B.); (S.S.)
Anke Senftleben Institute of Experimental Cancer Research, UKSH Campus Kiel & Christian-Albrechts-University Kiel, Arnold-Heller-Str. 3, Bldg. U30, 24105 Kiel, Germany; (F.M.); (A.S.); (T.D.); (S.B.); (S.S.)
Tina Daunke Institute of Experimental Cancer Research, UKSH Campus Kiel & Christian-Albrechts-University Kiel, Arnold-Heller-Str. 3, Bldg. U30, 24105 Kiel, Germany; (F.M.); (A.S.); (T.D.); (S.B.); (S.S.)
Silje Beckinger Institute of Experimental Cancer Research, UKSH Campus Kiel & Christian-Albrechts-University Kiel, Arnold-Heller-Str. 3, Bldg. U30, 24105 Kiel, Germany; (F.M.); (A.S.); (T.D.); (S.B.); (S.S.)
Samir Abdullazade Department of Pathology, Christian-Albrechts-University Kiel, Arnold-Heller-Str. 3, Bldg. U33, 24105 Kiel, Germany; (S.A.); (C.R.)
Stefan Schreiber Department of Internal Medicine I, UKSH Campus Kiel, Arnold-Heller-Str. 3, Bldg. K3, 24105 Kiel, Germany; (S.M.H.); (S.S.)
Christoph Röcken Department of Pathology, Christian-Albrechts-University Kiel, Arnold-Heller-Str. 3, Bldg. U33, 24105 Kiel, Germany; (S.A.); (C.R.)
Susanne Sebens Institute of Experimental Cancer Research, UKSH Campus Kiel & Christian-Albrechts-University Kiel, Arnold-Heller-Str. 3, Bldg. U30, 24105 Kiel, Germany; (F.M.); (A.S.); (T.D.); (S.B.); (S.S.)
Heiner Schäfer Department of Internal Medicine I, UKSH Campus Kiel, Arnold-Heller-Str. 3, Bldg. K3, 24105 Kiel, Germany; (S.M.H.); (S.S.) Institute of Experimental Cancer Research, UKSH Campus Kiel & Christian-Albrechts-University Kiel, Arnold-Heller-Str. 3, Bldg. U30, 24105 Kiel, Germany; (F.M.); (A.S.); (T.D.); (S.B.); (S.S.)

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Eibl G, Rozengurt E. Metformin: review of epidemiology and mechanisms of action in pancreatic cancer. Cancer Metastasis Rev 2021;40:865-878. [PMID: 34142285 DOI: 10.1007/s10555-021-09977-z] [Citation(s) in RCA: 30] [Impact Index Per Article: 7.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/26/2021] [Accepted: 05/27/2021] [Indexed: 12/15/2022]

Nikulin S, Zakharova G, Poloznikov A, Raigorodskaya M, Wicklein D, Schumacher U, Nersisyan S, Bergquist J, Bakalkin G, Astakhova L, Tonevitsky A. Effect of the Expression of ELOVL5 and IGFBP6 Genes on the Metastatic Potential of Breast Cancer Cells. Front Genet 2021;12:662843. [PMID: 34149804 PMCID: PMC8206645 DOI: 10.3389/fgene.2021.662843] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/17/2021] [Accepted: 04/20/2021] [Indexed: 12/09/2022] Open

Loss of ZNF215 imprinting is associated with poor five-year survival in patients with cytogenetically abnormal-acute myeloid leukemia. Blood Cells Mol Dis 2021;90:102577. [PMID: 34091126 DOI: 10.1016/j.bcmd.2021.102577] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/01/2021] [Revised: 05/23/2021] [Accepted: 05/23/2021] [Indexed: 01/05/2023]

Zhang AM, Wellberg EA, Kopp JL, Johnson JD. Hyperinsulinemia in Obesity, Inflammation, and Cancer. Diabetes Metab J 2021;45:285-311. [PMID: 33775061 PMCID: PMC8164941 DOI: 10.4093/dmj.2020.0250] [Citation(s) in RCA: 118] [Impact Index Per Article: 29.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/20/2020] [Accepted: 12/23/2020] [Indexed: 12/13/2022] Open

Luo Y, Li X, Ma J, Abbruzzese JL, Lu W. Pancreatic Tumorigenesis: Oncogenic KRAS and the Vulnerability of the Pancreas to Obesity. Cancers (Basel) 2021;13:cancers13040778. [PMID: 33668583 PMCID: PMC7918840 DOI: 10.3390/cancers13040778] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/17/2021] [Revised: 02/08/2021] [Accepted: 02/10/2021] [Indexed: 12/17/2022] Open

Abstract

Simple Summary

Pancreatic cancer is a devastating disease with a poor survival rate, and oncogenic mutant KRAS is a major driver of its initiation and progression; however, effective strategies/drugs targeting major forms of mutant KRAS have not been forthcoming. Of note, obesity is known to worsen mutant KRAS-mediated pathologies, leading to PDAC with high penetrance; however, the mechanistic link between obesity and pancreatic cancer remains elusive. The recent discovery of FGF21 as an anti-obesity and anti-inflammation factor and as a downstream target of KRAS has shed new light on the problem.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies and KRAS (Kirsten rat sarcoma 2 viral oncogene homolog) mutations have been considered a critical driver of PDAC initiation and progression. However, the effects of mutant KRAS alone do not recapitulate the full spectrum of pancreatic pathologies associated with PDAC development in adults. Historically, mutant KRAS was regarded as constitutively active; however, recent studies have shown that endogenous levels of mutant KRAS are not constitutively fully active and its activity is still subject to up-regulation by upstream stimuli. Obesity is a metabolic disease that induces a chronic, low-grade inflammation called meta-inflammation and has long been recognized clinically as a major modifiable risk factor for pancreatic cancer. It has been shown in different animal models that obesogenic high-fat diet (HFD) and pancreatic inflammation promote the rapid development of mutant KRAS-mediated PDAC with high penetrance. However, it is not clear why the pancreas with endogenous levels of mutant KRAS is vulnerable to chronic HFD and inflammatory challenges. Recently, the discovery of fibroblast growth factor 21 (FGF21) as a novel anti-obesity and anti-inflammatory factor and as a downstream target of mutant KRAS has shed new light on this problem. This review is intended to provide an update on our knowledge of the vulnerability of the pancreas to KRAS-mediated invasive PDAC in the context of challenges engendered by obesity and associated inflammation.

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Takenaga K, Akimoto M, Koshikawa N, Nagase H. Obesity reduces the anticancer effect of AdipoRon against orthotopic pancreatic cancer in diet-induced obese mice. Sci Rep 2021;11:2923. [PMID: 33536560 PMCID: PMC7859201 DOI: 10.1038/s41598-021-82617-2] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/07/2020] [Accepted: 01/12/2021] [Indexed: 02/07/2023] Open

Vujasinovic M, Dugic A, Maisonneuve P, Aljic A, Berggren R, Panic N, Valente R, Pozzi Mucelli R, Waldthaler A, Ghorbani P, Kordes M, Hagström H, Löhr JM. Risk of Developing Pancreatic Cancer in Patients with Chronic Pancreatitis. J Clin Med 2020;9:3720. [PMID: 33228173 PMCID: PMC7699479 DOI: 10.3390/jcm9113720] [Citation(s) in RCA: 36] [Impact Index Per Article: 7.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/20/2020] [Revised: 11/16/2020] [Accepted: 11/17/2020] [Indexed: 12/24/2022] Open

Abstract

Background: Patients with chronic pancreatitis (CP) have an increased risk of developing pancreatic ductal adenocarcinoma (PDAC). We present data on PDAC in one of the most extensive European single-centre cohort studies of patients with CP. Methods: Retrospective analysis of prospectively collected data of patients with CP was performed. Aetiology of CP was determined according to the M-ANNHEIM classification system and only patients with definite CP > 18 years at data analysis were included. The final dataset included 581 patients with definite CP diagnosed between 2003 and 2018. Results: At CP diagnosis, there were 371 (63.9%) males and 210 (36.1%) females (median age 57 years, range 2-86). During 3423 person-years of observation, six pancreatic cancers were diagnosed (0.2% year). The mean time between diagnosis of CP and the occurrence of PDAC was 5.0 years (range 2.7-8.6). None of the cancer patients had a family history of PDAC. Diabetes mellitus (DM) was present in five of six (83.3%) patients with PDAC: in three patients before and in two after CP diagnosis. Clinical/laboratory signs of pancreatic exocrine insufficiency (PEI) were present in five of six (83.3%) patients with PDAC: in two at diagnosis of CP and in three after diagnosis. The mean survival time was 4 months after the diagnosis of PDAC (range 0.5-13). PDAC occurred significantly more often (p < 0.001) in two groups of patients without previous acute pancreatitis (AP): 2 of 20 patients (10%) with low body mass index (BMI) and PEI and in 3 of 10 (30%) patients with high BMI and DM at diagnosis of CP. Conclusions: Patients with CP have a high risk of developing PDAC, although risk is low in absolute terms. Our data suggest the possibility of defining subgroups of patients with a particularly elevated risk of PDAC. Such a possibility would open a path to personalised decision making on initiation of PDAC surveillance of patients with no previous episode of AP, (i) with low BMI and PEI, or (ii) elevated BMI and DM.

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Affiliation(s)

Miroslav Vujasinovic Department of Upper Abdominal Diseases, Karolinska University Hospital, 14186 Stockholm, Sweden; (N.P.); (A.W.); (P.G.); (M.K.); (H.H.); (J.-M.L.) Department of Medicine, Huddinge, Karolinska Institutet, 14186 Stockholm, Sweden; (A.D.); (A.A.); (R.B.); (R.V.)
Ana Dugic Department of Medicine, Huddinge, Karolinska Institutet, 14186 Stockholm, Sweden; (A.D.); (A.A.); (R.B.); (R.V.)
Patrick Maisonneuve Division of Epidemiology and Biostatistics, IEO, European Institute of Oncology IRCCS, 20141 Milan, Italy;
Amer Aljic Department of Medicine, Huddinge, Karolinska Institutet, 14186 Stockholm, Sweden; (A.D.); (A.A.); (R.B.); (R.V.)
Robin Berggren Department of Medicine, Huddinge, Karolinska Institutet, 14186 Stockholm, Sweden; (A.D.); (A.A.); (R.B.); (R.V.)
Nikola Panic Department of Upper Abdominal Diseases, Karolinska University Hospital, 14186 Stockholm, Sweden; (N.P.); (A.W.); (P.G.); (M.K.); (H.H.); (J.-M.L.)
Roberto Valente Department of Medicine, Huddinge, Karolinska Institutet, 14186 Stockholm, Sweden; (A.D.); (A.A.); (R.B.); (R.V.)
Raffaella Pozzi Mucelli Department of Clinical Science, Intervention, and Technology (CLINTEC), Karolinska Institutet, 14186 Stockholm, Sweden; Department of Abdominal Radiology, Karolinska University Hospital, 14186 Stockholm, Sweden
Alexander Waldthaler Department of Upper Abdominal Diseases, Karolinska University Hospital, 14186 Stockholm, Sweden; (N.P.); (A.W.); (P.G.); (M.K.); (H.H.); (J.-M.L.) Department of Medicine, Huddinge, Karolinska Institutet, 14186 Stockholm, Sweden; (A.D.); (A.A.); (R.B.); (R.V.)
Poya Ghorbani Department of Upper Abdominal Diseases, Karolinska University Hospital, 14186 Stockholm, Sweden; (N.P.); (A.W.); (P.G.); (M.K.); (H.H.); (J.-M.L.) Department of Clinical Science, Intervention, and Technology (CLINTEC), Karolinska Institutet, 14186 Stockholm, Sweden;
Maximilian Kordes Department of Upper Abdominal Diseases, Karolinska University Hospital, 14186 Stockholm, Sweden; (N.P.); (A.W.); (P.G.); (M.K.); (H.H.); (J.-M.L.) Department of Clinical Science, Intervention, and Technology (CLINTEC), Karolinska Institutet, 14186 Stockholm, Sweden;
Hannes Hagström Department of Upper Abdominal Diseases, Karolinska University Hospital, 14186 Stockholm, Sweden; (N.P.); (A.W.); (P.G.); (M.K.); (H.H.); (J.-M.L.) Department of Medicine, Huddinge, Karolinska Institutet, 14186 Stockholm, Sweden; (A.D.); (A.A.); (R.B.); (R.V.) Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, 17177 Stockholm, Sweden
Johannes-Matthias Löhr Department of Upper Abdominal Diseases, Karolinska University Hospital, 14186 Stockholm, Sweden; (N.P.); (A.W.); (P.G.); (M.K.); (H.H.); (J.-M.L.) Department of Clinical Science, Intervention, and Technology (CLINTEC), Karolinska Institutet, 14186 Stockholm, Sweden;

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Xia B, He Q, Pan Y, Gao F, Liu A, Tang Y, Chong C, Teoh AYB, Li F, He Y, Zhang C, Yuan J. Metabolic syndrome and risk of pancreatic cancer: A population‐based prospective cohort study. Int J Cancer 2020;147:3384-3393. [PMID: 32580250 DOI: 10.1002/ijc.33172] [Citation(s) in RCA: 31] [Impact Index Per Article: 6.2] [Reference Citation Analysis] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/06/2020] [Revised: 06/05/2020] [Accepted: 06/08/2020] [Indexed: 12/12/2022]

Affiliation(s)

Bin Xia Clinical Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China Scientific Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China Center for Digestive Disease, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China
Qiangsheng He Clinical Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China Scientific Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China Center for Digestive Disease, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China
Yihang Pan Precision Medicine Center. Scientific Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China
Fang Gao Perioperative, Critical Care and Trauma Trials Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK
Anran Liu Center for Digestive Disease, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China Department of Nutriology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China
Yan Tang Clinical Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China Scientific Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China
Charing Chong Department of Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong SAR, China
Anthony Y B Teoh Department of Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong SAR, China
Fangping Li Department of Endocrinology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China
Yulong He Center for Digestive Disease, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China
Changhua Zhang Center for Digestive Disease, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China
Jinqiu Yuan Clinical Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China Scientific Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China Center for Digestive Disease, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China Precision Medicine Center. Scientific Research Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China

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Nweke EE, Brand M. Downregulation of the let-7 family of microRNAs may promote insulin receptor/insulin-like growth factor signalling pathways in pancreatic ductal adenocarcinoma. Oncol Lett 2020;20:2613-2620. [PMID: 32782579 PMCID: PMC7400736 DOI: 10.3892/ol.2020.11854] [Citation(s) in RCA: 13] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/18/2019] [Accepted: 05/27/2020] [Indexed: 02/07/2023] Open

The Role of Dysfunctional Adipose Tissue in Pancreatic Cancer: A Molecular Perspective. Cancers (Basel) 2020;12:cancers12071849. [PMID: 32659999 PMCID: PMC7408631 DOI: 10.3390/cancers12071849] [Citation(s) in RCA: 14] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/31/2020] [Revised: 07/04/2020] [Accepted: 07/06/2020] [Indexed: 12/24/2022] Open

Hu L, Chen X, Qiu S, Yang J, Liu H, Zhang J, Zhang D, Wang F. Intra-Pancreatic Insulin Nourishes Cancer Cells: Do Insulin-Receptor Antagonists such as PGG and EGCG Play a Role? THE AMERICAN JOURNAL OF CHINESE MEDICINE 2020;48:1005-1019. [PMID: 32468825 DOI: 10.1142/s0192415x20500482] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/25/2022]

Abstract

Harboring insulin-producing cells, the pancreas has more interstitial insulin than any other organ. In vitro, insulin activates both insulin receptor (IR) and insulin-like growth factor-1 receptor (IGF1R) to stimulate pancreatic cancer cells. Whether intra-pancreatic insulin nourishes pancreatic cancer cells in vivo remains uncertain. In the present studies, we transplanted human pancreatic cancer cells orthotopically in euglycemic athymic mice whose intra-pancreatic insulin was intact or was decreased following pretreatment with streptozotocin (STZ). In the next eight weeks, the tumor carriers were treated with one of the IR/IGF1R antagonists penta-O-galloyl-[Formula: see text]-D-glucose (PGG) and epigallocatechin gallate (EGCG) or treated with vehicle. When pancreatic tumors were examined, their fraction occupied with living cells was decreased following STZ pretreatment and/or IR/IGF1R antagonism. Using Western blot, we examined tumor grafts for IR/IGF1R expression and activity. We also determined proteins that were downstream to IR/IGF1R and responsible for signal transduction, glycolysis, angiogenesis, and apoptosis. We demonstrated that STZ-induced decrease in intra-pancreatic insulin reduced IR/IGF1R expression and activity, decreased the proteins that promoted cell survival, and increased the proteins that promoted apoptosis. These suggest that intra-pancreatic insulin supported local cancer cells. When tumor carriers were treated with PGG or EGCG, the results were similar to those seen following STZ pretreatment. Thus, the biggest changes in examined proteins were usually seen when STZ pretreatment and PGG/EGCG treatment concurred. This suggests that intra-pancreatic insulin normally combated pharmacologic effects of PGG and EGCG. In conclusion, intra-pancreatic insulin nourishes pancreatic cancer cells and helps the cells resist IR/IGF1R antagonism.

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Barreto SG, Michael MZ, Keating DJ. Islets and pancreatic ductal adenocarcinoma - An opportunity for translational research from the 'Bench to the Bedside'. Pancreatology 2020;20:385-390. [PMID: 32057682 DOI: 10.1016/j.pan.2020.02.001] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/22/2019] [Revised: 01/15/2020] [Accepted: 02/01/2020] [Indexed: 02/06/2023]

Nepstad I, Hatfield KJ, Grønningsæter IS, Aasebø E, Hernandez-Valladares M, Hagen KM, Rye KP, Berven FS, Selheim F, Reikvam H, Bruserud Ø. Effects of insulin and pathway inhibitors on the PI3K-Akt-mTOR phosphorylation profile in acute myeloid leukemia cells. Signal Transduct Target Ther 2019;4:20. [PMID: 31240133 PMCID: PMC6582141 DOI: 10.1038/s41392-019-0050-0] [Citation(s) in RCA: 52] [Impact Index Per Article: 8.7] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/12/2018] [Revised: 02/05/2019] [Accepted: 04/04/2019] [Indexed: 12/17/2022] Open

Abstract

The phosphatidylinositol 3-kinase (PI3K)-Akt-mechanistic target of rapamycin (mTOR) pathway is constitutively activated in human acute myeloid leukemia (AML) cells and is regarded as a possible therapeutic target. Insulin is an agonist of this pathway and a growth factor for AML cells. We characterized the effect of insulin on the phosphorylation of 10 mediators in the main track of the PI3K-Akt-mTOR pathway in AML cells from 76 consecutive patients. The overall results showed that insulin significantly increased the phosphorylation of all investigated mediators. However, insulin effects on the pathway activation profile varied among patients, and increased phosphorylation in all mediators was observed only in a minority of patients; in other patients, insulin had divergent effects. Global gene expression profiling and proteomic/phosphoproteomic comparisons suggested that AML cells from these two patient subsets differed with regard to AML cell differentiation, transcriptional regulation, RNA metabolism, and cellular metabolism. Strong insulin-induced phosphorylation was associated with weakened antiproliferative effects of metabolic inhibitors. PI3K, Akt, and mTOR inhibitors also caused divergent effects on the overall pathway phosphorylation profile in the presence of insulin, although PI3K and Akt inhibition caused a general reduction in Akt pT308 and 4EBP1 pT36/pT45 phosphorylation. For Akt inhibition, the phosphorylation of upstream mediators was generally increased or unaltered. In contrast, mTOR inhibition reduced mTOR pS2448 and S6 pS244 phosphorylation but increased Akt pT308 phosphorylation. In conclusion, the effects of both insulin and PI3K-Akt-mTOR inhibitors differ between AML patient subsets, and differences in insulin responsiveness are associated with differential susceptibility to metabolic targeting.

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Yang J, Wang F, Chen X, Qiu S, Cui L, Hu L. β-Pentagalloyl-Glucose Sabotages Pancreatic Cancer Cells and Ameliorates Cachexia in Tumor-Bearing Mice. THE AMERICAN JOURNAL OF CHINESE MEDICINE 2019;47:675-689. [PMID: 30966770 DOI: 10.1142/s0192415x19500356] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]

Abstract

Pancreatic cancer cells overexpress the insulin receptor (IR) and the insulin-like growth factor-1 receptor (IGF1R). Activating these receptors, insulin and insulin-like growth factor-1 increase the growth and glycolysis of pancreatic cancer cells. The high glycolysis in pancreatic cancer cells increases whole-body energy expenditure and is therefore involved in the pathogenesis of cancer cachexia. The antagonism of IR and IGF1R may sabotage pancreatic cancer cells and attenuate cancer cachexia. Previous studies have shown that the intracellular regulating system of IR/IGF1R may be functionally interrelated to another intracellular system whose master regulator is hypoxia-inducible factor-1 (HIF-1). In this study, we investigated how the IR/IGF1R and HIF-1 systems are interrelated in pancreatic cancer cells. We also investigated whether a phytochemical, penta-O-galloyl- β -D-glucose ( β -PGG), antagonizes IR/IGF1R, sabotages pancreatic cancer cells and alleviates cancer cachexia. We found in MiaPaCa2 pancreatic cancer cells that IR/IGF1R activation increased both the α -subunit of HIF-1 and caveolin-1. This result suggests that IR/IGF1R, HIF-1 α , and caveolin-1 may constitute a feed-forward loop to mediate the effect of IR/IGF1R activation. β -PGG inhibited IR/IGF1R activity and decreased glycolytic enzymes in MiaPaCa2 and Panc-1 pancreatic cancer cells. When MiaPaCa2 cells were transplanted in athymic mice, their growth was inhibited by β -PGG or by a HIF-1 α inhibitor, rhein. β -PGG and rhein also decreased glycolytic enzymes in the tumor grafts and reduced liver gluconeogenesis, skeletal-muscle proteolysis and fat lipolysis in the tumor carriers. Cancer-induced body-weight loss, however, was prevented by β -PGG but not rhein. In conclusion, β -PGG combats pancreatic cancer cells and cures cancer cachexia.

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Activation of IGF/IGF-IR signaling pathway fails to induce epithelial-mesenchymal transition in pancreatic cancer cells. Pancreatology 2019;19:390-396. [PMID: 30799278 DOI: 10.1016/j.pan.2019.01.010] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/10/2018] [Revised: 12/16/2018] [Accepted: 01/14/2019] [Indexed: 12/11/2022]

Koulouris AI, Luben R, Banim P, Hart AR. Dietary Fiber and the Risk of Pancreatic Cancer. Pancreas 2019;48:121-125. [PMID: 30489447 DOI: 10.1097/mpa.0000000000001191] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]

The role of some ADAM-proteins and activation of the insulin growth factor-related pathway in colorectal cancer. Cent Eur J Immunol 2018;43:109-113. [PMID: 29731694 PMCID: PMC5927180 DOI: 10.5114/ceji.2018.74881] [Citation(s) in RCA: 14] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/05/2017] [Accepted: 02/14/2017] [Indexed: 12/13/2022] Open

Marchetti C, Zyner KG, Ohnmacht SA, Robson M, Haider SM, Morton JP, Marsico G, Vo T, Laughlin-Toth S, Ahmed AA, Di Vita G, Pazitna I, Gunaratnam M, Besser RJ, Andrade ACG, Diocou S, Pike JA, Tannahill D, Pedley RB, Evans TRJ, Wilson WD, Balasubramanian S, Neidle S. Targeting Multiple Effector Pathways in Pancreatic Ductal Adenocarcinoma with a G-Quadruplex-Binding Small Molecule. J Med Chem 2018;61:2500-2517. [PMID: 29356532 PMCID: PMC5867665 DOI: 10.1021/acs.jmedchem.7b01781] [Citation(s) in RCA: 113] [Impact Index Per Article: 16.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/07/2017] [Indexed: 12/11/2022]

Affiliation(s)

Chiara Marchetti UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, U.K.
Katherine G. Zyner Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, U.K.
Stephan A. Ohnmacht UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, U.K.
Mathew Robson Cancer Research UK Cancer Centre, UCL Cancer Institute, University College London, London WC1E 6BT, U.K.
Shozeb M. Haider UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, U.K.
Jennifer P. Morton Cancer Research UK, Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD U.K. Institute of Cancer Sciences. University of Glasgow, Glasgow G12 8QQ, U.K.
Giovanni Marsico Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, U.K.
Tam Vo Department of Chemistry and Center for Biotechnology and Drug Design, Georgia State University, Atlanta, Georgia 30303-3083, United States
Sarah Laughlin-Toth Department of Chemistry and Center for Biotechnology and Drug Design, Georgia State University, Atlanta, Georgia 30303-3083, United States
Ahmed A. Ahmed UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, U.K.
Gloria Di Vita UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, U.K.
Ingrida Pazitna UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, U.K.
Mekala Gunaratnam UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, U.K.
Rachael J. Besser UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, U.K.
Ana C. G. Andrade UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, U.K.
Seckou Diocou UCL Cancer Institute, University College London, London WC1E 6BT, U.K.
Jeremy A. Pike Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, U.K.
David Tannahill Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, U.K.
R. Barbara Pedley UCL Cancer Institute, University College London, London WC1E 6BT, U.K.
T. R. Jeffry Evans Cancer Research UK, Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD U.K. Institute of Cancer Sciences. University of Glasgow, Glasgow G12 8QQ, U.K.
W. David Wilson Department of Chemistry and Center for Biotechnology and Drug Design, Georgia State University, Atlanta, Georgia 30303-3083, United States
Shankar Balasubramanian Cancer Research UK, Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 0RE, U.K. Department of Chemistry, University of Cambridge, Cambridge CB2 1EW, U.K. The School of Clinical Medicine, University of Cambridge, Cambridge CB2 0SP, U.K.
Stephen Neidle UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, U.K.

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Mutgan AC, Besikcioglu HE, Wang S, Friess H, Ceyhan GO, Demir IE. Insulin/IGF-driven cancer cell-stroma crosstalk as a novel therapeutic target in pancreatic cancer. Mol Cancer 2018;17:66. [PMID: 29475434 PMCID: PMC5824531 DOI: 10.1186/s12943-018-0806-0] [Citation(s) in RCA: 82] [Impact Index Per Article: 11.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/22/2017] [Accepted: 02/01/2018] [Indexed: 12/15/2022] Open

Amanam I, Chung V. Targeted Therapies for Pancreatic Cancer. Cancers (Basel) 2018;10:E36. [PMID: 29382159 PMCID: PMC5836068 DOI: 10.3390/cancers10020036] [Citation(s) in RCA: 59] [Impact Index Per Article: 8.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/22/2017] [Revised: 01/15/2018] [Accepted: 01/23/2018] [Indexed: 12/15/2022] Open

Shi H, Fang W, Liu M, Fu D. Complement component 1, q subcomponent binding protein (C1QBP) in lipid rafts mediates hepatic metastasis of pancreatic cancer by regulating IGF-1/IGF-1R signaling. Int J Cancer 2017;141:1389-1401. [PMID: 28608366 DOI: 10.1002/ijc.30831] [Citation(s) in RCA: 28] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/28/2017] [Revised: 04/03/2017] [Accepted: 05/24/2017] [Indexed: 12/19/2022]

Lev A, Lulla AR, Wagner J, Ralff MD, Kiehl JB, Zhou Y, Benes CH, Prabhu VV, Oster W, Astsaturov I, Dicker DT, El-Deiry WS. Anti-pancreatic cancer activity of ONC212 involves the unfolded protein response (UPR) and is reduced by IGF1-R and GRP78/BIP. Oncotarget 2017;8:81776-81793. [PMID: 29137221 PMCID: PMC5669847 DOI: 10.18632/oncotarget.20819] [Citation(s) in RCA: 33] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/25/2017] [Accepted: 08/17/2017] [Indexed: 02/07/2023] Open

Sun Y, He W, Luo M, Zhou Y, Chang G, Ren W, Wu K, Li X, Shen J, Zhao X, Hu Y. Role of transgelin-2 in diabetes-associated pancreatic ductal adenocarcinoma. Oncotarget 2017;8:49592-49604. [PMID: 28521289 PMCID: PMC5564790 DOI: 10.18632/oncotarget.17519] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/29/2016] [Accepted: 03/29/2017] [Indexed: 01/23/2023] Open

Ottaiano A, Capozzi M, De Divitiis C, De Stefano A, Botti G, Avallone A, Tafuto S. Gemcitabine mono-therapy versus gemcitabine plus targeted therapy in advanced pancreatic cancer: a meta-analysis of randomized phase III trials. Acta Oncol 2017;56:377-383. [PMID: 28256961 DOI: 10.1080/0284186x.2017.1288922] [Citation(s) in RCA: 46] [Impact Index Per Article: 5.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/31/2022]

La Paglia L, Listì A, Caruso S, Amodeo V, Passiglia F, Bazan V, Fanale D. Potential Role of ANGPTL4 in the Cross Talk between Metabolism and Cancer through PPAR Signaling Pathway. PPAR Res 2017;2017:8187235. [PMID: 28182091 PMCID: PMC5274667 DOI: 10.1155/2017/8187235] [Citation(s) in RCA: 121] [Impact Index Per Article: 15.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/20/2016] [Accepted: 12/19/2016] [Indexed: 02/07/2023] Open