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Review
. 2024 May 23;25(11):5661.
doi: 10.3390/ijms25115661.

Pancreatic Cancer and Venous Thromboembolism

Affiliations
Review

Pancreatic Cancer and Venous Thromboembolism

Teagan Prouse et al. Int J Mol Sci. .

Abstract

Pancreatic ductal adenocarcinoma (PDAC) accounts for more than 90% of all pancreatic cancers and is the most fatal of all cancers. The treatment response from combination chemotherapies is far from satisfactory and surgery remains the mainstay of curative strategies. These challenges warrant identifying effective treatments for combating this deadly cancer. PDAC tumor progression is associated with the robust activation of the coagulation system. Notably, cancer-associated thrombosis (CAT) is a significant risk factor in PDAC. CAT is a concept whereby cancer cells promote thromboembolism, primarily venous thromboembolism (VTE). Of all cancer types, PDAC is associated with the highest risk of developing VTE. Hypoxia in a PDAC tumor microenvironment also elevates thrombotic risk. Direct oral anticoagulants (DOACs) or low-molecular-weight heparin (LMWH) are used only as thromboprophylaxis in PDAC. However, a precision medicine approach is recommended to determine the precise dose and duration of thromboprophylaxis in clinical setting.

Keywords: pancreatic ductal adenocarcinoma (PDAC); protein S (PS) 1; thrombosis.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Factors that increase VTE risk in PDAC patients (created using BioRender.com).
Figure 2
Figure 2
Summary of PDAC and VTE (created using BioRender.com).

References

    1. Siegel R.L., Miller K.D., Wagle N.S., Jemal A. Cancer statistics, 2023. CA Cancer J. Clin. 2023;73:17–48. doi: 10.3322/caac.21763. - DOI - PubMed
    1. Hartupee C., Nagalo B.M., Chabu C.Y., Tesfay M.Z., Coleman-Barnett J., West J.T., Moaven O. Pancreatic cancer tumor microenvironment is a major therapeutic barrier and target. Front. Immunol. 2024;15:1287459. doi: 10.3389/fimmu.2024.1287459. - DOI - PMC - PubMed
    1. Rahib L., Smith B.D., Aizenberg R., Rosenzweig A.B., Fleshman J.M., Matrisian L.M. Projecting cancer incidence and deaths to 2030: The unexpected burden of thyroid, liver, and pancreas cancers in the United States. Cancer Res. 2014;74:2913–2921. doi: 10.1158/0008-5472.CAN-14-0155. - DOI - PubMed
    1. Kothari A., Flick M.J. Coagulation Signaling through PAR1 as a Therapeutic Target in Pancreatic Ductal Adenocarcinoma. Int. J. Mol. Sci. 2021;22:5138. doi: 10.3390/ijms22105138. - DOI - PMC - PubMed
    1. Faille D., Bourrienne M.C., de Raucourt E., de Chaisemartin L., Granger V., Lacroix R., Panicot-Dubois L., Hammel P., Levy P., Ruszniewski P., et al. Biomarkers for the risk of thrombosis in pancreatic adenocarcinoma are related to cancer process. Oncotarget. 2018;9:26453–26465. doi: 10.18632/oncotarget.25458. - DOI - PMC - PubMed

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