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: Journal of Materials in Civil Engineering Volume 38, Issue 5 Get full access to this article View all available purchase options and get full access to this article. Data Availability Statement Some or all data, models, or code that support the findings of this study are available from the corresponding author upon reasonable request.
1 INTRODUCTION Biliary tract cancer (BTC) is an invasive adenocarcinoma that includes cholangiocarcinoma (cancers originating in the intrahepatic, perihilar, or distal biliary tree) and gallbladder carcinoma.1 Despite varying prognoses and molecular characteristics between tumor sites, previous drug trials have often grouped all BTC subtypes together.
Abstract Spindle assembly checkpoint (SAC) plays an essential part in facilitating normal cell division. However, the clinicopathological and biological significance of mitotic arrest deficient 2 like 1 (MAD2/MAD2L1), a highly conserved member of SAC in cholangiocarcinoma (CCA) remain unclear. We aim to determine the role and mechanism of MAD2 in CCA progression.
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