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  • 1
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    A p16INK4a-insensitive CDK4 mutant targeted by cytolytic T lymphocytes in a human melanoma (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-01
    Description: A mutated cyclin-dependent kinase 4 (CDK4) was identified as a tumor-specific antigen recognized by HLA-A2. 1-restricted autologous cytolytic T lymphocytes (CTLs) in a human melanoma. The mutated CDK4 allele was present in autologous cultured melanoma cells and metastasis tissue, but not in the patient's lymphocytes. The mutation, an arginine-to-cysteine exchange at residue 24, was part of the CDK4 peptide recognized by CTLs and prevented binding of the CDK4 inhibitor p16INK4a, but not of p21 or of p27KIP1. The same mutation was found in one additional melanoma among 28 melanomas analyzed. These results suggest that mutation of CDK4 can create a tumor-specific antigen and can disrupt the cell-cycle regulation exerted by the tumor suppressor p16INK4a.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wolfel, T -- Hauer, M -- Schneider, J -- Serrano, M -- Wolfel, C -- Klehmann-Hieb, E -- De Plaen, E -- Hankeln, T -- Meyer zum Buschenfelde, K H -- Beach, D -- New York, N.Y. -- Science. 1995 Sep 1;269(5228):1281-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medizinische Klinik und Poliklinik, Johannes Gutenberg-Universitat, Mainz, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7652577" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins/metabolism/*pharmacology ; *Cell Cycle Proteins ; Cell Line ; Cloning, Molecular ; Cyclin-Dependent Kinase 4 ; Cyclin-Dependent Kinase Inhibitor p15 ; Cyclin-Dependent Kinase Inhibitor p16 ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p27 ; *Cyclin-Dependent Kinases ; Cyclins/metabolism/pharmacology ; HLA-A2 Antigen/immunology ; Humans ; Melanoma/enzymology/*immunology ; Microtubule-Associated Proteins/metabolism/pharmacology ; Molecular Sequence Data ; Point Mutation ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases/antagonists & ; inhibitors/genetics/*immunology/metabolism ; *Proto-Oncogene Proteins ; T-Lymphocytes, Cytotoxic/*immunology ; Transfection ; Tumor Cells, Cultured ; *Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    CDC25 phosphatases as potential human oncogenes (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-09-15
    Description: Cyclin-dependent kinases (CDKs) are activated by CDC25 phosphatases, which remove inhibitory phosphate from tyrosine and threonine residues. In human cells, CDC25 proteins are encoded by a multigene family, consisting of CDC25A, CDC25B, and CDC25C. In rodent cells, human CDC25A or CDC25B but not CDC25C phosphatases cooperate with either Ha-RASG12V or loss of RB1 in oncogenic focus formation. Such transformants were highly aneuploid, grew in soft agar, and formed high-grade tumors in nude mice. Overexpression of CDC25B was detected in 32 percent of human primary breast cancers tested. The CDC25 phosphatases may contribute to the development of human cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galaktionov, K -- Lee, A K -- Eckstein, J -- Draetta, G -- Meckler, J -- Loda, M -- Beach, D -- New York, N.Y. -- Science. 1995 Sep 15;269(5230):1575-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7667636" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/genetics ; Cell Cycle Proteins/*genetics ; Cell Division ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Gene Expression ; Genes, Retinoblastoma ; Genes, p53 ; Genes, ras ; Humans ; In Situ Hybridization ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; *Multigene Family ; Neoplasm Transplantation ; *Oncogenes ; Phosphoprotein Phosphatases/*genetics ; Prognosis ; Transfection ; Tumor Cells, Cultured ; cdc25 Phosphatases
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Inhibition of ras-induced proliferation and cellular transformation by p16INK4 (1995)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1995-01-13
    Description: The cyclin-dependent kinase 4 (CDK4) regulates progression through the G1 phase of the cell cycle. The activity of CDK4 is controlled by the opposing effects of the D-type cyclin, an activating subunit, and p16INK4, an inhibitory subunit. Ectopic expression of p16INK4 blocked entry into S phase of the cell cycle induced by oncogenic Ha-Ras, and this block was relieved by coexpression of a catalytically inactive CDK4 mutant. Expression of p16INK4 suppressed cellular transformation of primary rat embryo fibroblasts by oncogenic Ha-Ras and Myc, but not by Ha-Ras and E1a. Together, these observations provide direct evidence that p16INK4 can inhibit cell growth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Serrano, M -- Gomez-Lahoz, E -- DePinho, R A -- Beach, D -- Bar-Sagi, D -- CA55360/CA/NCI NIH HHS/ -- EY09300-01/EY/NEI NIH HHS/ -- HD28317-02/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1995 Jan 13;267(5195):249-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, NY 11724.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7809631" target="_blank"〉PubMed〈/a〉
    Keywords: Adenovirus E1A Proteins/genetics/physiology ; Animals ; Carrier Proteins/genetics/*physiology ; *Cell Division ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Cyclin-Dependent Kinase 4 ; Cyclin-Dependent Kinase Inhibitor p16 ; *Cyclin-Dependent Kinases ; Genes, Reporter ; Genes, Retinoblastoma ; Genes, myc ; Genes, ras ; Plasmids ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; *Proto-Oncogene Proteins ; Rats ; Retinoblastoma Protein/physiology ; S Phase ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; ras Proteins/genetics/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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