Cited by 201Telomeres, Telomerase, and SenescenceCancer-related Molecular PathwaysGenetics, Aging, and Longevity in Model Organisms

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Murine fibroblasts lacking p21 undergo senescence and are resistant to transformation by oncogenic Ras.

Pantoja, Cristina, Serrano, Manuel·1999·Oncogene

DOI 10.1038/sj.onc.1202880

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Abstract

The cell-cycle inhibitor p21 is upregulated during senescence and upon induction of senescence-like arrest by oncogenic Ras. We have used primary fibroblasts derived from p21-null mice to evaluate the role of p21 in these processes. We find that primary p21-/- cells enter senescence and have a lifespan similar to wild-type cells. Upon immortalization, most wild-type and p21-/- cultures acquire alterations in either p53 or p16INK4a, further indicating that p21-deficiency is not sufficient by itself to allow immortalization. Primary p21-/- cells, like wild-type cells, respond to oncogenic Ras by accumulating p53 and p16INK4a, and by decreasing their proliferation rate. In agreement with this, p21-/- cells are refractory to neoplasic transformation by oncogenic Ras when compared to p53-/- cells. We conclude that, in murine fibroblasts, p21 is not essential neither for senescence nor for preventing neoplasic transformation by oncogenic Ras.

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WAF1, a potential mediator of p53 tumor suppression
El-Deiry, W. S., Tokino, T., Velculescu, V. E., Levy, D. B., Parsons, R., Trent, J. M., Lin, D., Mercer, W. E., Kinzler, K. W., & Vogelstein, B. (1993) · Cell · doi:10.1016/0092-8674(93)90500-p · Cited by 8,321
The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases.
Wade Harper, J. (1993) · Cell · doi:10.1016/0092-8674(93)90499-g · Cited by 5,651
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 14×
“Accordingly, rodent cells de®cient in p53 or p16 are e ciently transformed by oncogenic Ras (Serrano et al., 1997; Lloyd et al., 1997; Zhu et al., 1998; Lin et al., 1998).”
BackgroundMethodResultInfluential
Extension of Life-Span by Introduction of Telomerase into Normal Human Cells
Bodnar, A. G., Ouellette, M., Frolkis, M., Holt, S. E., Chiu, C.-P., Morin, G. B., Harley, C. B., Shay, J. W., Lichtsteiner, S., & Wright, W. E. (1998) · Science · doi:10.1126/science.279.5349.349 · Cited by 4,975
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A. (1992) · Nature · doi:10.1038/356215a0 · Cited by 4,649
p21 is a universal inhibitor of cyclin kinases
Xiong, Y., Hannon, G., Zhang, H., Casso, D., Kobayashi, R., & Beach, D. (1993) · Nature · doi:10.1038/366701a0 · Cited by 3,691
Inhibitors of mammalian G1 cyclin-dependent kinases.Preprint
Sherr, C. J., & Roberts, J. M. (1995) · Genes & Development · doi:10.1101/gad.9.10.1149 · Cited by 3,242
QUANTITATIVE STUDIES OF THE GROWTH OF MOUSE EMBRYO CELLS IN CULTURE AND THEIR DEVELOPMENT INTO ESTABLISHED LINES
Todaro, G. J., & Green, H. (1963) · The Journal of Cell Biology · doi:10.1083/jcb.17.2.299 · Cited by 2,747
Production of high-titer helper-free retroviruses by transient transfection.
Pear, W. S., Nolan, G. P., Scott, M. L., & Baltimore, D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.18.8392 · Cited by 2,267
Mice Lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control
Deng, C., Zhang, P., Wade Harper, J., Elledge, S. J., & Leder, P. (1995) · Cell · doi:10.1016/0092-8674(95)90039-x · Cited by 2,113
Telomere Shortening and Tumor Formation by Mouse Cells Lacking Telomerase RNA
Blasco, M. A., Lee, H.-W., Hande, M. P., Samper, E., Lansdorp, P. M., DePinho, R. A., & Greider, C. W. (1997) · Cell · doi:10.1016/s0092-8674(01)80006-4 · Cited by 2,108
Advanced mammalian gene transfer: high titre retroviral vectors with multiple drug selection markers and a complementary helper-free packaging cell line
Morgenstern, J. P., & Land, H. (1990) · Nucleic Acids Research · doi:10.1093/nar/18.12.3587 · Cited by 2,099
Tumor spectrum analysis in p53-mutant mice
Jacks, T., Remington, L., Williams, B. O., Schmitt, E. M., Halachmi, S., Bronson, R. T., & Weinberg, R. A. (1994) · Current Biology · doi:10.1016/s0960-9822(00)00002-6 · Cited by 2,051
ARF promotes MDM2 degradation and stabilizes p53: ARF-INK4a locus deletion impairs both the Rb and p53 tumor suppression pathways
Zhang, Y., Xiong, Y., & Yarbrough, W. G. (1998) · Cell · doi:10.1016/s0092-8674(00)81401-4 · Cited by 1,626
Role of the INK4a Locus in Tumor Suppression and Cell Mortality
Serrano, M., Lee, H.-W., Chin, L., Cordon-Cardo, C., Beach, D., & DePinho, R. A. (1996) · Cell · doi:10.1016/s0092-8674(00)81079-x · Cited by 1,585
Tumor Suppression at the Mouse INK4a Locus Mediated by the Alternative Reading Frame Product p19
Kamijo, T., Zindy, F., Roussel, M. F., Quelle, D. E., Downing, J. R., Ashmun, R. A., Grosveld, G., & Sherr, C. J. (1997) · Cell · doi:10.1016/s0092-8674(00)80452-3 · Cited by 1,566
The Ink4a tumor suppressor gene product, p19Arf, interacts with MDM2 and neutralizes MDM2’s inhibition of p53
Pomerantz, J., Schreiber-Agus, N., Liégeois, N. J., Silverman, A., Alland, L., Chin, L., Potes, J., Chen, K., Orlow, I., Lee, H.-W., et al. (1998) · Cell · doi:10.1016/s0092-8674(00)81400-2 · Cited by 1,521
Cloning of senescent cell-derived inhibitors of DNA synthesis using an expression screen
Noda, A., Ning, Y., Venable, S. F., Pereira-Smith, O. M., & Smith, J. R. (1994) · Experimental Cell Research · doi:10.1006/excr.1994.1063 · Cited by 1,351
The complexity of p53 modulation: emerging patterns from divergent signalsPreprint
Giaccia, A. J., & Kastan, M. B. (1998) · Genes & Development · doi:10.1101/gad.12.19.2973 · Cited by 1,315
Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization
Zindy, F., Eischen, C. M., Randle, D. H., Kamijo, T., Cleveland, J. L., Sherr, C. J., & Roussel, M. F. (1998) · Genes & Development · doi:10.1101/gad.12.15.2424 · Cited by 1,245
Radiation-induced cell cycle arrest compromised by p21 deficiency
Brugarolas, J., Chandrasekaran, C., Gordon, J. I., Beach, D., Jacks, T., & Hannon, G. J. (1995) · Nature · doi:10.1038/377552a0 · Cited by 1,242 · cited 3×
“In response to g-radiation, p21 is strongly upregulated in a p53-dependent manner (see El-Deiry et al., 1993; Di Leonardo et al., 1994), and cells derived from p21-null mice arrest ine ciently upon g-radiation (Brugarolas et al., 1995; Deng et al., 1995).”
BackgroundMethodInfluential
DNA damage triggers a prolonged p53-dependent G1 arrest and long-term induction of Cip1 in normal human fibroblasts.
Di Leonardo, A., Linke, S. P., Clarkin, K., & Wahl, G. M. (1994) · Genes & Development · doi:10.1101/gad.8.21.2540 · Cited by 1,215
Both Rb/p16INK4a inactivation and telomerase activity are required to immortalize human epithelial cells
Kiyono, T., Foster, S. A., Koop, J. I., McDougall, J. K., Galloway, D. A., & Klingelhutz, A. J. (1998) · Nature · doi:10.1038/23962 · Cited by 1,206 · cited 1×
“In human cells, telomere attrition is directly implicated in triggering senescence (see for example Bodnar et al., 1998; Kiyono et al., 1998); but in rodent cells, senescence is independent of telomere shortening (Blasco et al., 1997; Carman et al., 1998; Russo et al., 1998).”
Background
The alternative product from the human CDKN2A locus, p14ARF, participates in a regulatory feedback loop with p53 and MDM2
Stott, F. J., Bates, S., James, M. C., McConnell, B. B., Starborg, M., Brookes, S., Palmero, I., Ryan, K. M., Hara, E., Vousden, K. H., et al. (1998) · The EMBO Journal · doi:10.1093/emboj/17.17.5001 · Cited by 1,178
Correlation of Terminal Cell Cycle Arrest of Skeletal Muscle with Induction of p21 by MyoD
Halevy, O., Novitch, B. G., Spicer, D. B., Skapek, S. X., Rhee, J., Hannon, G. J., Beach, D., & Lassar, A. B. (1995) · Science · doi:10.1126/science.7863327 · Cited by 1,139
p53-dependent and independent expression of p21 during cell growth, differentiation, and DNA damage.Preprint
Macleod, K. F., Sherry, N., Hannon, G. J., Beach, D., Tokino, T., Kinzler, K. W., Vogelstein, B., & Jacks, T. (1995) · Genes & Development · doi:10.1101/gad.9.8.935 · Cited by 1,126
Involvement of the cyclin-dependent kinase inhibitor p16 (INK4a) in replicative senescence of normal human fibroblasts
Alcorta, D. A., Xiong, Y., Phelps, D., Hannon, G., Beach, D., & Barrett, J. C. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.24.13742 · Cited by 1,008 · cited 1×
“In senescent human ®broblasts, the levels of p21 are increased (Noda et al., 1994; Tahara et al., 1995; Alcorta et al., 1996), together with those of other p53 transcriptional targets, such as IGFBP-3 (Goldstein et al., 1991; Buckbinder et al., 1995).”
Background
Transforming growth factor beta induces the cyclin-dependent kinase inhibitor p21 through a p53-independent mechanism.
Datto, M., Li, Y., Panus, J. F., Howe, D. J., Xiong, Y., & Wang, X. F. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.12.5545 · Cited by 945
Premature senescence involving p53 and p16 is activated in response to constitutive MEK/MAPK mitogenic signaling
Lin, A. W., Barradas, M., Stone, J. C., van Aelst, L., Serrano, M., & Lowe, S. W. (1998) · Genes & Development · doi:10.1101/gad.12.19.3008 · Cited by 945
p14ARF links the tumour suppressors RB and p53
Bates, S., Phillips, A. C., Clark, P. A., Stott, F., Peters, G., Ludwig, R. L., & Vousden, K. H. (1998) · Nature · doi:10.1038/25867 · Cited by 918
Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2
Kamijo, T., Weber, J. D., Zambetti, G., Zindy, F., Roussel, M. F., & Sherr, C. J. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.14.8292 · Cited by 899
Induction of the growth inhibitor IGF-binding protein 3 by p53
Buckbinder, L., Talbott, R. L., Velasco-Miguel, S., Takenaka, I. M., Faha, B., Seizinger, B. R., & Kley, N. (1995) · Nature · doi:10.1038/377646a0 · Cited by 869
Senescence of human fibroblasts induced by oncogenic Raf
Zhu, J., Woods, D., McMahon, M., & Bishop, J. M. (1998) · Genes & Development · doi:10.1101/gad.12.19.2997 · Cited by 826
Bypass of Senescence After Disruption of p21 CIP1/WAF1 Gene in Normal Diploid Human Fibroblasts
Brown, J. P., Wei, W., & Sedivy, J. M. (1997) · Science · doi:10.1126/science.277.5327.831 · Cited by 804
Tumor surveillance via the ARF–p53 pathwayPreprint
Sherr, C. J. (1998) · Genes & Development · doi:10.1101/gad.12.19.2984 · Cited by 718
Raf-Induced Proliferation or Cell Cycle Arrest Is Determined by the Level of Raf Activity with Arrest Mediated by p21Cip1
Woods, D. B., Parry, D., Cherwinski, H. M., Bosch, E., Lees, E. M., & McMahon, M. (1997) · Molecular and Cellular Biology · doi:10.1128/mcb.17.9.5598 · Cited by 639
Signaling to p53
Prives, C. (1998) · Cell · doi:10.1016/s0092-8674(00)81774-2 · Cited by 623
p19ARF links the tumour suppressor p53 to Ras
Palmero, I., Pantoja, C., & Serrano, M. (1998) · Nature · doi:10.1038/25870 · Cited by 619
E1A signaling to p53 involves the p19ARFtumor suppressorPreprint
de Stanchina, E., McCurrach, M. E., Zindy, F., Shieh, S.-Y., Ferbeyre, G., Samuelson, A. V., Prives, C. L., Roussel, M. F., Sherr, C. J., & Lowe, S. W. (1998) · Genes & Development · doi:10.1101/gad.12.15.2434 · Cited by 611
Expression of the p16INK4a tumor suppressor versus other INK4 family members during mouse development and aging
Zindy, F., Quelle, D. E., Roussel, M. F., & Sherr, C. J. (1997) · Oncogene · doi:10.1038/sj.onc.1201178 · Cited by 574
Cellular commitment to oncogene-induced transformation or apoptosis is dependent on the transcription factor IRF-1
Tanaka, N., Ishihara, M., Kitagawa, M., Harada, H., Kimura, T., Matsuyama, T., Lamphier, M. S., Aizawa, S., Mak, T. W., & Taniguchi, T. (1994) · Cell · doi:10.1016/0092-8674(94)90132-5 · Cited by 491
Signals from Ras and Rho GTPases interact to regulate expression of p21Waf1/Cip1
Olson, M. F., Paterson, H. F., & Marshall, C. J. (1998) · Nature · doi:10.1038/28425 · Cited by 461
High-Intensity Raf Signal Causes Cell Cycle Arrest Mediated by p21 Cip1
Sewing, A., Wiseman, B. S., Lloyd, A. C., & Land, H. (1997) · Molecular and Cellular Biology · doi:10.1128/mcb.17.9.5588 · Cited by 457
p53 alteration is a common event in the spontaneous immortalization of primary BALB/c murine embryo fibroblasts.
Harvey, D. M., & Levine, A. J. (1991) · Genes & Development · doi:10.1101/gad.5.12b.2375 · Cited by 453
Cell cycle arrest mediated by the MEK/mitogen-activated protein kinase pathway
Pumiglia, K. M., & Decker, S. J. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.2.448 · Cited by 357
The absence of p21Cip1/WAF1 alters keratinocyte growth and differentiation and promotes ras-tumor progression.Preprint
Missero, C., Cunto, F. D., Kiyokawa, H., Koff, A., & Dotto, G. P. (1996) · Genes & Development · doi:10.1101/gad.10.23.3065 · Cited by 311
Increased activity of p53 in senescing fibroblasts
Atadja, P., Wong, H., Garkavtsev, I., Veillette, C., & Riabowol, K. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.18.8348 · Cited by 308
Increased p16 expression with first senescence arrest in human mammary epithelial cells and extended growth capacity with p16 inactivation
Brenner, A. J., Stampfer, M. R., & Aldaz, C. M. (1998) · Oncogene · doi:10.1038/sj.onc.1201919 · Cited by 272 · cited 1×
“In addition to ®broblasts, the induction of p21 at senescence has been also observed in vascular endothelial cells (Watanabe et al., 1997), but not in T-lymphocytes or epithelial cells from several tissues (Rezniko et al., 1996; Foster et al., 1998; Brenner et al., 1998; Erickson et al., 1998).”
Background
Alterations in p53 and p16 INK4 Expression and Telomere Length during Spontaneous Immortalization of Li-Fraumeni Syndrome Fibroblasts
Rogan, E. M., Bryan, T. M., Hukku, B., Maclean, K. N., Chang, A. C.-M., Moy, E. L., Englezou, A., Warneford, S., Dalla‐Pozza, L., & Reddel, R. R. (1995) · Molecular and Cellular Biology · doi:10.1128/mcb.15.9.4745 · Cited by 250
Expression of cell cycle-dependent genes in young and senescent WI-38 fibroblasts.
Rittling, S. R., Brooks, K. M., Cristofalo, V. J., & Baserga, R. (1986) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.83.10.3316 · Cited by 241
Inactivation of p16 in Human Mammary Epithelial Cells by CpG Island Methylation
Foster, S. A., Wong, D. J., Barrett, M. T., & Galloway, D. A. (1998) · Molecular and Cellular Biology · doi:10.1128/mcb.18.4.1793 · Cited by 228
Cooperating oncogenes converge to regulate cyclin/cdk complexes.Preprint
Lloyd, A. C., Obermüller, F., Staddon, S., Barth, C. F., McMahon, M., & Land, H. (1997) · Genes & Development · doi:10.1101/gad.11.5.663 · Cited by 224
Untitled work
(1996) · PubMed · Cited by 180
Loss of p 21 increases sensitivity to ionizing radiation and delays the onset of lymphoma in atm -deficient mice
Wang, Y., Elson, A., & Leder, P. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.26.14590 · Cited by 170
Reinitiation of DNA Synthesis and Cell Division in Senescent Human Fibroblasts by Microinjection of Anti-p53 Antibodies
Gire, V., & Wynford-Thomas, D. (1998) · Molecular and Cellular Biology · doi:10.1128/mcb.18.3.1611 · Cited by 161
p21 Is a Critical CDK2 Regulator Essential for Proliferation Control in Rb-deficient Cells
Brugarolas, J., Bronson, R. T., & Jacks, T. (1998) · The Journal of Cell Biology · doi:10.1083/jcb.141.2.503 · Cited by 153
Splicing into Senescence: The Curious Case of p16 and p19ARF
Haber, D. A. (1997) · Cell · doi:10.1016/s0092-8674(00)80441-9 · Cited by 144
Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) delays and induces escape from senescence in human dermal microvascular endothelial cells
Watanabe, Y., Lee, S. W., Detmar, M. J., Ajioka, I., & Dvorak, H. F. (1997) · Oncogene · doi:10.1038/sj.onc.1201033 · Cited by 141
The Cat and Mouse Games That Genes, Viruses, and Cells Play
Weinberg, R. A. (1997) · Cell · doi:10.1016/s0092-8674(00)81897-8 · Cited by 138
Origins of G1 arrest in senescent human fibroblasts
Stein, G. H., & Dulić, V. (1995) · BioEssays · doi:10.1002/bies.950170610 · Cited by 135
Involvement of the Ink4 proteins p16 and p15 in T-lymphocyte senescence
Erickson, S., Sangfelt, O., Heyman, M. M., Castro, J., Einhorn, S., & Grandér, D. (1998) · Oncogene · doi:10.1038/sj.onc.1201965 · Cited by 125
Accumulation of p16INK4a in mouse fibroblasts as a function of replicative senescence and not of retinoblastoma gene status
Palmero, I., McConnell, B. B., Parry, D., Brookes, S., Hara, E., Bates, S., Jat, P., & Peters, G. G. (1997) · Oncogene · doi:10.1038/sj.onc.1201212 · Cited by 123
Absence of p53 allows direct immortalization of hematopoietic cells by the myc and raf oncogenes
Metz, T. M., Harris, A. W., & Adams, J. M. (1995) · Cell · doi:10.1016/0092-8674(95)90049-7 · Cited by 122
Insulin-like growth factor binding protein 3 accumulates to high levels in culture medium of senescent and quiescent human fibroblasts.
Goldstein, S., Moerman, E. J., Jones, R. A., & Baxter, R. C. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.21.9680 · Cited by 104
Involvement of p53 and p21 in Cellular Defects and Tumorigenesis in Atm−/− Mice
Xu, Y., Yang, E. M., Brugarolas, J., Jacks, T., & Baltimore, D. (1998) · Molecular and Cellular Biology · doi:10.1128/mcb.18.7.4385 · Cited by 103
Investigation of the role of G1/S cell cycle mediators in cellular senescence
Afshari, C. A., Vojta, P. J., Annab, L. A., Futreal, P. A., Willard, T. B., & Barrett, J. C. (1993) · Experimental Cell Research · doi:10.1006/excr.1993.1306 · Cited by 100
The tumorigenic potential and cell growth characteristics of p53-deficient cells are equivalent in the presence or absence of Mdm2
Jones, S. N., Sands, A., Hancock, A. R., Vogel, H. S., Donehower, L. A., Linke, S. P., Wahl, G. M., & Bradley, A. (1996) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.93.24.14106 · Cited by 87
Genetic analysis of cellular senescence
Vojta, P. J., & Barrett, J. C. (1995) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/0304-419x(95)00002-w · Cited by 80
Expression of p21 is not required for senescence of human fibroblasts.
Medcalf, A. S. C., Klein-Szanto, A. J., & Cristofalo, V. J. (1996) · PubMed · Cited by 54
A telomere-independent senescence mechanism is the sole barrier to Syrian hamster cell immortalization
Russo, I., Silver, A. R., Cuthbert, A. P., Griffin, D. K., Trott, D. A., & Newbold, R. F. (1998) · Oncogene · doi:10.1038/sj.onc.1202261 · Cited by 47
Cellular Senescence in Telomerase-Expressing Syrian Hamster Embryo Cells
Carman, T. A., Afshari, C. A., & Barrett, J. C. (1998) · Experimental Cell Research · doi:10.1006/excr.1998.4207 · Cited by 38
Molecular Aspects of the Relationship between Cancer and Aging: Tumor Suppressor Activity During Cellular Senescence
Garkavtsev, I., Hull, C. M., & Riabowol, K. T. (1998) · Experimental Gerontology · doi:10.1016/s0531-5565(97)00086-7 · Cited by 29
Adenovirus type 12 early region 1B 54K protein significantly extends the life span of normal mammalian cells in culture
Gallimore, P. H., Lecane, P. S., Roberts, S., Rookes, S. M., Grand, R. J. A., & Parkhill, J. (1997) · Journal of Virology · doi:10.1128/jvi.71.9.6629-6640.1997 · Cited by 23
Loss of p21CIP1/WAF1 does not recapitulate accelerated malignant conversion caused by p53 loss in experimental skin carcinogenesis
Weinberg, W. C., Montano, N. E., & Deng, C. (1997) · Oncogene · doi:10.1038/sj.onc.1201230 · Cited by 20
Clonal Nature of Spontaneously Immortalized 3T3 Cells
Rittling, S. R. (1996) · Experimental Cell Research · doi:10.1006/excr.1996.0337 · Cited by 18
Expression of p24, a novel p21 Waf1/Cip1/Sdi1 -related protein, correlates with measurement of the finite proliferative potential of rodent embryo fibroblasts
Mazars, G. R., & Jat, P. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.1.151 · Cited by 18
Age-dependent alterations of c-fos and growth regulation in human fibroblasts expressing the HPV16 E6 protein.
Yan, Y., Ouellette, M. M., Shay, J. W., & Wright, W. E. (1996) · Molecular Biology of the Cell · doi:10.1091/mbc.7.6.975 · Cited by 9

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The RB and p53 pathways in cancer
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“However, cells lacking Cip1 are not immortal and undergo efficient p19Arf-induced arrest (Pantoja and Serrano, 1999; Modestou et al. 2001).”
Background
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Ben-Porath, I., & Weinberg, R. A. (2005) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2004.10.013 · Cited by 1,046
The INK4a/ARF network in tumour suppression
Sherr, C. J. (2001) · Nature Reviews Molecular Cell Biology · doi:10.1038/35096061 · Cited by 1,001
Endogenous oncogenic K-rasG12D stimulates proliferation and widespread neoplastic and developmental defects
Tuveson, D. A., Shaw, A. T., Willis, N. A., Silver, D. P., Jackson, E. L., Chang, S., Mercer, K. L., Grochow, R., Hock, H., Crowley, D., et al. (2004) · Cancer Cell · doi:10.1016/s1535-6108(04)00085-6 · Cited by 798

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Authors: Pantoja, C., & Serrano, M.
Affiliations: Consejo Superior de Investigaciones Científicas (ES)
ORCID: Pantoja, Cristina
Serrano, Manuel
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 1999-09-02
Volume: 18
Issue: 35
Pages: 4974-4982
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/sj.onc.1202880
OpenAlex: W2081779271
Cited by: 201
References: 78
Citations by year: 2025: 3 · 2023: 6 · 2022: 4 · 2021: 1 · 2020: 4 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 6 · 2015: 7 · 2014: 7 · 2013: 11 · 2012: 6
FWCI: 8.20
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Oncogene (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords: p21, cellular senescence, oncogenic Ras, oncogenic transformation, p53, p16INK4a, cell cycle inhibitors, fibroblasts, cell immortalization
MeSH terms: Animals, Cell Cycle, Cell Division, Cell Line, Transformed, Cell Transformation, Neoplastic, Cells, Cultured, Doxorubicin, Fibroblasts, Serial Passage, Transduction, Genetic, Oncogene Protein p21(ras), Gene Expression, Tumor Suppressor Protein p53, Cyclins, 3T3 Cells, Cellular Senescence, Gene Deletion, Mice, Knockout, Cyclin-Dependent Kinase Inhibitor p16, Cyclin-Dependent Kinase Inhibitor p21, Mice

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Murine fibroblasts lacking p21 undergo senescence and are resistant to transformation by oncogenic Ras.

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