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-supp11.xlsx › Appendix_1-table_11
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
The LOVD3 platform: efficient genome-wide sharing of genetic variants.
Fokkema IFAC et al.
European Journal of Human Genetics : Ejhg, 2021
34521998 (PubMed )
Supplement: 41431_2021_959_MOESM4_ESM.pdf
Pancreatic cancer as a sentinel for hereditary cancer predisposition.
Young EL et al.
Bmc Cancer, 2018
29945567 (PubMed )
Supplement: 12885_2018_4573_MOESM1_ESM.xlsx › Supplemental_Table_2
Recurrent patterns of dual RB and p53 pathway inactivation in melanoma.
Yang G et al.
The Journal of Investigative Dermatology, 2005
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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