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Review
. 2018 Jan 31;11(1):14.
doi: 10.1186/s13045-017-0551-7.

Novel agents for pancreatic ductal adenocarcinoma: emerging therapeutics and future directions

Yiyin Zhang  1   2   3   4 , Chao Yang  1   2   3   4 , He Cheng  1   2   3   4 , Zhiyao Fan  1   2   3   4 , Qiuyi Huang  1   2   3   4 , Yu Lu  1   2   3   4 , Kun Fan  1   2   3   4 , Guopei Luo  1   2   3   4 , Kaizhou Jin  1   2   3   4 , Zhengshi Wang  1   2   3   4 , Chen Liu  5   6   7   8 , Xianjun Yu  9   10   11   12
Affiliations
Review

Novel agents for pancreatic ductal adenocarcinoma: emerging therapeutics and future directions

Yiyin Zhang et al. J Hematol Oncol. .

Abstract

A poor prognosis of pancreatic ductal adenocarcinoma (PDAC) associated with chemoresistance has not changed for the past three decades. A multidisciplinary diagnosis followed by surgery and chemo(radiation)therapy is the main treatment approach. However, gemcitabine- and 5-fluorouracil-based therapies did not present satisfying outcomes. Novel regimens targeting pancreatic cancer cells, the tumor microenvironment, and immunosuppression are emerging. Biomarkers concerning the treatment outcome and patient selection are being discovered in preclinical or clinical studies. Combination therapies of classic chemotherapeutic drugs and novel agents or novel therapeutic combinations might bring hope to the dismal prognosis for PDAC patients.

Keywords: Biomarkers; Combination therapies; Novel regimens; Pancreatic ductal adenocarcinoma.

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The authors declare that they have no competing interests.

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Figures

Fig. 1
Fig. 1
Novel therapies targeting different elements involved in PDAC development. Therapeutics targeting signaling pathways participating in tumorigenesis and progression, the tumor microenvironment, inflammatory and immune responses, and angiogenesis. It also contains future possible therapeutic targets and specific biomarkers for the evaluation of efficacy
Fig. 2
Fig. 2
Mechanism of action of different therapeutic strategies for PDAC. They include cytotoxic agents, PARP inhibitors, CDK inhibitors, MEK/ERK inhibitors, PI3K/AKT/mTOR inhibitors, Hedgehog inhibitors, Notch inhibitors, STAT 3 inhibitors, VEGFR inhibitors, monoclonal antibodies, GVAX/CRS-207, anti-PD-1/PD-L1 antibodies, and CAR-T cell therapy
See this image and copyright information in PMC

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References

    1. Gillen S, Schuster T, Meyer Zum Buschenfelde C, Friess H, Kleeff J. Preoperative/neoadjuvant therapy in pancreatic cancer: a systematic review and meta-analysis of response and resection percentages. PLoS Med. 2010;7(4):e1000267. doi: 10.1371/journal.pmed.1000267. - DOI - PMC - PubMed
    1. Hezel AF, Kimmelman AC, Stanger BZ, Bardeesy N, Depinho RA. Genetics and biology of pancreatic ductal adenocarcinoma. Genes Dev. 2006;20(10):1218–1249. doi: 10.1101/gad.1415606. - DOI - PubMed
    1. Jones S, Zhang X, Parsons DW, Lin JC, Leary RJ, Angenendt P, Mankoo P, Carter H, Kamiyama H, Jimeno A, Hong SM, Fu B, Lin MT, Calhoun ES, Kamiyama M, Walter K, Nikolskaya T, Nikolsky Y, Hartigan J, Smith DR, Hidalgo M, Leach SD, Klein AP, Jaffee EM, Goggins M, Maitra A, Iacobuzio-Donahue C, Eshleman JR, Kern SE, Hruban RH, et al. Core signaling pathways in human pancreatic cancers revealed by global genomic analyses. Science. 2008;321(5897):1801–1806. doi: 10.1126/science.1164368. - DOI - PMC - PubMed
    1. Bailey P, Chang DK, Nones K, Johns AL, Patch AM, Gingras MC, Miller DK, Christ AN, Bruxner TJ, Quinn MC, Nourse C, Murtaugh LC, Harliwong I, Idrisoglu S, Manning S, Nourbakhsh E, Wani S, Fink L, Holmes O, Chin V, Anderson MJ, Kazakoff S, Leonard C, Newell F, Waddell N, Wood S, Xu Q, Wilson PJ, Cloonan N, Kassahn KS, et al. Genomic analyses identify molecular subtypes of pancreatic cancer. Nature. 2016;531(7592):47–52. doi: 10.1038/nature16965. - DOI - PubMed
    1. Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, et al. A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns. Nature. 2016;538(7625):378–382. doi: 10.1038/nature19823. - DOI - PMC - PubMed

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