Associated Papers
Functional characterization of all CDKN2A missense variants and comparison to in silico models of pathogenicity.
Kimura H et al.
Elife, 2025
40238651 (PubMed )
Supplement: elife-95347-fig2-figsupp3-data1.xlsx › Figure_2-figure_supplement_3A
Functional characterization of all CDKN2A missense variants and comparison to in silico models of pathogenicity.
Kimura H et al.
Biorxiv : the Preprint Server for Biology, 2025
38234851 (PubMed )
Supplement: media-11.pdf
Identification of Potential Genomic Alterations Using Pan-Cancer Cell-Free DNA Next-Generation Sequencing in Patients With Gastric Cancer.
Kim B et al.
Annals of Laboratory Medicine, 2024
37903652 (PubMed )
Supplement: alm-44-2-164-supple1.xlsx › Assay_B
Targeted Next-Generation Sequencing-Based Multiple Gene Mutation Profiling of Patients with Rectal Adenocarcinoma Receiving or Not Receiving Neoadjuvant Chemoradiotherapy.
Chang YK et al.
International Journal of Molecular Sciences, 2022
36142267 (PubMed )
Supplement: ijms-23-10353-s001.zip › ijms-1910530-supplementary.pdf
Enrichment of short mutant cell-free DNA fragments enhanced detection of pancreatic cancer.
Liu X et al.
Ebiomedicine, 2019
30857943 (PubMed )
Supplement: mmc3.xlsx › mutations_detected_in_cfDNA
Point mutations can inactivate in vitro and in vivo activities of p16(INK4a)/CDKN2A in human glioma.
Arap W et al.
Oncogene, 1997
The CDKN2A (p16) gene and human cancer.
Foulkes WD et al.
Molecular Medicine (cambridge, Mass.), 1997
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