Associated Papers
Mutational scanning reveals substrate-assisted autoregulation of the WNT destruction complex.
Padmanarayana M et al.
Biorxiv : the Preprint Server for Biology, 2025
41278994 (PubMed )
Supplement: media-1.xlsx › WNT_DC_CBE_Screen
Clinicopathologic Evaluation of CTNNB1 Mutations in High-Intermediate Risk Endometrial Endometrioid Carcinoma.
Haag JG et al.
International Journal of Gynecological Pathology : Official Journal of the International Society of Gynecological Pathologists, 2023
Ultra Deep Sequencing of Circulating Cell-Free DNA as a Potential Tool for Hepatocellular Carcinoma Management.
Higuera M et al.
Cancers, 2022
36010868 (PubMed )
Supplement: cancers-14-03875-s001.zip › Supplementary_Table_S4_Somatic_mutations.xlsx › HCC_patients_mutations
Oncogenic Serine 45-Deleted β-Catenin Remains Susceptible to Wnt Stimulation and APC Regulation in Human Colonocytes.
Parker TW et al.
Cancers, 2020
32751567 (PubMed )
Supplement: cancers-12-02114-s001.zip › cancers-848197_Supplementary_Data_Files_Parker_Rudeen_Neufeld_11july20.xlsx › Ctnnb1_Mutations
Prospective analysis of 895 patients on a UK Genomics Review Board.
Moore DA et al.
Esmo Open, 2019
Somatic POLE exonuclease domain mutations are early events in sporadic endometrial and colorectal carcinogenesis, determining driver mutational landscape, clonal neoantigen burden and immune response.
Temko D et al.
The Journal of Pathology, 2018
29604063 (PubMed )
Supplement: PATH-245-283-s022.xlsx › CRC.Drivers.Edited
Synchronous endometrioid carcinomas of the uterine corpus and ovary: alterations in the beta-catenin (CTNNB1) pathway are associated with independent primary tumors and favorable prognosis.
Irving JA et al.
Human Pathology, 2005
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