Structural integrity of the cyclin-dependent kinase inhibitor genes, p15, p16 and p18 in myeloid leukaemias.
作者： Tsuyoshi Nakamaki , Norihiko Kawamata , Juurg Schwaller , Andreas Tobler , Martin Fey
DOI: 10.1111/J.1365-2141.1995.TB05259.X
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摘要: Summary The cyclin-dependent kinase inhibitors known as p15, p16 and p18 have been suggested candidates for tumour suppressor genes. We examined these genes their alterations in 46 myeloid leukaemias 15 leukaemia cell lines, mRNA expression was studied 41 leukaemias. p15 were either deleted or mutated lines at a high frequency [6/15 (40%) p15; 8/15 (53%) p16] but primary are much less frequent [2/46 (4%) 3/46 (6%) p16]. Alterations of not found any the samples. 13 samples had negligible levels mRNA. In summary, deletions identified probably occurred during vitro immortalization. pl6 pl5 gene only acute that mixed myeloid/ lymphoid lineage (CD19/CD20-positive [AML], CD2/CD19-positive AML, blastic crisis chronic leukaemia). Further studies required to determine if absence results from inactivation gene.
sci-hub.se 参考文章(51)
R. A. Kratzke, F. J. Kaye, Young Whan Kim, A. Coxon, G. A. Otterson, Absence of p16INK4 protein is restricted to the subset of lung cancer lines that retains wildtype RB. Oncogene. ,vol. 9, pp. 3375- 3378 ,(1994)
A Chase, P de Fabritiis, T Hughes, S Bi, J M Goldman, J M Goldman, J Bungey, p53 in chronic myeloid leukemia cell lines. Leukemia. ,vol. 6, pp. 839- 842 ,(1992)
J Hebert, JM Cayuela, J Berkeley, F Sigaux, Candidate tumor-suppressor genes MTS1 (p16INK4A) and MTS2 (p15INK4B) display frequent homozygous deletions in primary cells from T- but not from B-cell lineage acute lymphoblastic leukemias. Blood. ,vol. 84, pp. 4038- 4044 ,(1994) , 10.1182/BLOOD.V84.12.4038.BLOODJOURNAL84124038
Tetsuro Nishihira, Shozo Mori, Koh Miura, Yusuke Nakamura, Takahisa Aoki, Takahiro Mori, Frequent somatic mutation of the MTS1/CDK4I (multiple tumor suppressor/cyclin-dependent kinase 4 inhibitor) gene in esophageal squamous cell carcinoma. Cancer Research. ,vol. 54, pp. 3396- 3397 ,(1994)
B Quesnel, C Preudhomme, N Philippe, M Vanrumbeke, I Dervite, JL Lai, F Bauters, E Wattel, P Fenaux, p16 gene homozygous deletions in acute lymphoblastic leukemia Blood. ,vol. 85, pp. 657- 663 ,(1995) , 10.1182/BLOOD.V85.3.657.BLOODJOURNAL853657
S Ogawa, N Hirano, N Sato, T Takahashi, A Hangaishi, K Tanaka, M Kurokawa, T Tanaka, K Mitani, Y Yazaki, Homozygous loss of the cyclin-dependent kinase 4-inhibitor (p16) gene in human leukemias Blood. ,vol. 84, pp. 2431- 2435 ,(1994) , 10.1182/BLOOD.V84.8.2431.2431
K Sugimoto, H Toyoshima, R Sakai, K Miyagawa, K Hagiwara, F Ishikawa, F Takaku, Y Yazaki, H Hirai, Frequent mutations in the p53 gene in human myeloid leukemia cell lines. Blood. ,vol. 79, pp. 2378- 2383 ,(1992) , 10.1182/BLOOD.V79.9.2378.2378
Michele Pagano, Jerry W. Shay, Sun W. Tam, Differential Expression and Cell Cycle Regulation of the Cyclin-dependent Kinase 4 Inhibitor p16Ink4 Cancer Research. ,vol. 54, pp. 5816- 5820 ,(1994)
M. Serrano, H. P. Koeffler, Rong Yang, A. F. Gombart, Mutational Effects on the p16INK4a Tumor Suppressor Protein Cancer Research. ,vol. 55, pp. 2503- 2506 ,(1995)
P Ponte, P Gunning, H Blau, L Kedes, Human actin genes are single copy for alpha-skeletal and alpha-cardiac actin but multicopy for beta- and gamma-cytoskeletal genes: 3' untranslated regions are isotype specific but are conserved in evolution. Molecular and Cellular Biology. ,vol. 3, pp. 1783- 1791 ,(1983) , 10.1128/MCB.3.10.1783