The p16INK4a/CDKN2A tumor suppressor and its relatives.

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[30]  P. Kleihues,et al.  Hemizygous or homozygous deletion of the chromosomal region containing the p16INK4a gene is associated with amplification of the EGF receptor gene in glioblastomas , 1997, International journal of cancer.

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[32]  G. Peters,et al.  Accumulation of p16INK4a in mouse fibroblasts as a function of replicative senescence and not of retinoblastoma gene status , 1997, Oncogene.

[33]  G. Mann,et al.  Differential expression of p16INK4a and p16β transcripts in B-lymphoblastoid cells from members of hereditary melanoma families without CDKN2A exon mutations , 1997, Oncogene.

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[37]  H. Koeffler,et al.  The p19INK4D Cyclin dependent kinase inhibitor gene is altered in osteosarcoma , 1997, Oncogene.

[38]  G. Thomas,et al.  Loss of heterozygosity on chromosome 9 and p16 (MTS1, CDKN2) gene mutations in esophageal cancers , 1997, International journal of cancer.

[39]  N. Hayward,et al.  Restoration of CDKN2A into melanoma cells induces morphologic changes and reduction in growth rate but not anchorage-independent growth reversal. , 1997, The Journal of investigative dermatology.

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[41]  W. Farrell,et al.  Chromosome 9p deletions in invasive and noninvasive nonfunctional pituitary adenomas: the deleted region involves markers outside of the MTS1 and MTS2 genes. , 1997, Cancer research.

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[139]  V P Collins,et al.  Human glioblastomas with no alterations of the CDKN2A (p16INK4A, MTS1) and CDK4 genes have frequent mutations of the retinoblastoma gene. , 1996, Oncogene.

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[155]  F. Dammacco,et al.  p16 gene analysis in multiple myeloma (MM). , 1996, Leukemia.

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[167]  Ciro Mercurio,et al.  Biochemical Characterization of p16INK4- and p18-containing Complexes in Human Cell Lines* , 1996, The Journal of Biological Chemistry.

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