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of outstanding interest. Hypoxia, which is found in poorly vascularized parts of tumors, is demonstrated to induce p53-dependent apoptosis. Highly apoptotic regions in tumors were found to correlate with both hypoxia and wild-type p53. The authors propose that hypoxia provides a physiological selective pressure in tumors such that cells containing mutant p53 escape apoptosis and have a proliferative advantage that contributes to tumor expansion.
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Nature
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Graeber, T.G.1
Osmanian, C.2
Jacks, T.3
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Lowe, S.W.6
Giaccia, A.J.7
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15
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P53 mediated tumor cell response to chemotherapeutic DNA damage: A preliminary study in matched pairs of breast cancer biopsies
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No germline TP53 mutations detected in familial and bilateral testicular cancer
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0025951144
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P53 mutations in human lymphoid malignancies: Association with Burkitt lymphoma and chronic lymphocytic leukemia
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Apoptotic death of tumor cells correlates with chemosensitivity, independent of p53 of Bcl-2
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of special interest. A study demonstrating that cells responding well to lethal doses of chemotherapeutic drugs do so independently of a p53-mediated response or the Bcl-2 : Bax ratios present in the cell. The authors suggest that although p53 status may be a determining factor in some cell types, a more consistent predictor of chemosensitivity is the in vitro measurement of induction of apoptosis.
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Wu GS, El-Deiry WS. Apoptotic death of tumor cells correlates with chemosensitivity, independent of p53 of Bcl-2. of special interest Clin Cancer Res. 2:1996;623-633 A study demonstrating that cells responding well to lethal doses of chemotherapeutic drugs do so independently of a p53-mediated response or the Bcl-2 : Bax ratios present in the cell. The authors suggest that although p53 status may be a determining factor in some cell types, a more consistent predictor of chemosensitivity is the in vitro measurement of induction of apoptosis.
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Wu, G.S.1
El-Deiry, W.S.2
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0011821868
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P53 alterations in ovarian cancer as a determinant of response to carboplatin
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Al-Azraqi A, Chapman C, Challen C, Sigalas J, Aswaad S, Sinha D, Calvert AH, Lunec J. p53 alterations in ovarian cancer as a determinant of response to carboplatin. Br J Cancer. 69:1994;7-15.
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Al-Azraqi, A.1
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Aswaad, S.5
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Calvert, A.H.7
Lunec, J.8
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20
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0030026934
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Loss of normal p53 function confers sensitization to Taxol by increasing G2/M arrest and apoptosis
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Wahl AF, Donaldson KL, Fairchild C, Lee FY, Foster SA, Demers GW, Galloway DA. Loss of normal p53 function confers sensitization to Taxol by increasing G2/M arrest and apoptosis. Nat Med. 2:1996;72-79.
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Wahl, A.F.1
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Galloway, D.A.7
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0028849274
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Waldman T, Kinzler KW, Vogelstein B. p21 is necessary for the p53-mediated G1 arrest in human cancer cells. of outstanding interest Cancer Res. 55:1995;5187-5190 See annotation [23].
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Waldman, T.1
Kinzler, K.W.2
Vogelstein, B.3
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23
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0030011128
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Uncoupling of S phase and mitosis induced by anticancer agents in cells lacking p21
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waf1,cip1 is involved in the normal coupling of S and M phases of the cell cycle.
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waf1,cip1 is involved in the normal coupling of S and M phases of the cell cycle.
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Nature
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Waldman, T.1
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24
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cip1/waf1 undergo normal development but are defective in, G1 checkpoint control. Cell. 82:1995;675-684.
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25
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Characterization of p21cip1/waf1 peptide domains required for cyclin E/Cdk2 and PCNA interaction
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of special interest. See annotation [27].
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Chen IT, Akamatsu M, Smith ML, Lung F-DT, Duba D, Roller PP, Fornace AJ, O'Conner PM. Characterization of p21cip1/waf1 peptide domains required for cyclin E/Cdk2 and PCNA interaction. of special interest Oncogene. 12:1996;595-607 See annotation [27].
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Chen, I.T.1
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Roller, P.P.6
Fornace, A.J.7
O'Conner, P.M.8
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26
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0029948612
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P21 contains independent binding sites for cyclin and cdk2: Both sites are required to inhibit cdk2 kinase activity
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of special interest. See annotation [27].
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Fotedar R, Fitzgerald P, Rousselle T, Cannella D, Doree M, Messier H, Fotedar A. p21 contains independent binding sites for cyclin and cdk2: both sites are required to inhibit cdk2 kinase activity. of special interest Oncogene. 12:1996;2155-2164 See annotation [27].
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Fotedar, R.1
Fitzgerald, P.2
Rousselle, T.3
Cannella, D.4
Doree, M.5
Messier, H.6
Fotedar, A.7
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27
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0029257341
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A small peptide inhibitor of DNA replication defines the site of interaction between the cyclin-dependent kinase inhibitor p21WAF1 and proliferating cell nuclear antigen
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waf1,cip1 are required to bind in inhibit cyclin-dependent kinase: the first domain (amino acids 15-40) binds cyclin E-CDK2 and inhibits kinase, whereas the second domain (amino acids 58-77) binds cyclin E-CDK2 but does not inhibit kinase. A third domain, approximately amino acids 139-164, binds PCNA.
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waf1,cip1 are required to bind in inhibit cyclin-dependent kinase: the first domain (amino acids 15-40) binds cyclin E-CDK2 and inhibits kinase, whereas the second domain (amino acids 58-77) binds cyclin E-CDK2 but does not inhibit kinase. A third domain, approximately amino acids 139-164, binds PCNA.
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Warbrick, E.1
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Prelich, G.1
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Li, R.1
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31
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0029881977
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Abnormal centrosome amplification in the absence of p53
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of outstanding interest. Mouse embryo fibroblasts lacking p53 are shown to contain multiple copies of functionally competent centrosomes. Although there was no apparent increase in centrosome number in early versus late passage p53-/- cells, (possibly due to selection gainst cells with more than three centrosomes), serum stimulation of cells previously growth-arrested showed a 40% decline in the number of cells containing a single centrosome (with a corresponding increase in cells containing two or more centrosomes), compared to p53+/+ cells which showed only a 10% decrease in cells containing a single centrosome. Thus, it is proposed that p53 maintains genomic stability through regulation of centrosome duplication.
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Fukasawa K, Choi T, Kuriyama R, Rulong S, Vande Woude GF. Abnormal centrosome amplification in the absence of p53. of outstanding interest Science. 271:1996;1744-1747 Mouse embryo fibroblasts lacking p53 are shown to contain multiple copies of functionally competent centrosomes. Although there was no apparent increase in centrosome number in early versus late passage p53-/- cells, (possibly due to selection gainst cells with more than three centrosomes), serum stimulation of cells previously growth-arrested showed a 40% decline in the number of cells containing a single centrosome (with a corresponding increase in cells containing two or more centrosomes), compared to p53+/+ cells which showed only a 10% decrease in cells containing a single centrosome. Thus, it is proposed that p53 maintains genomic stability through regulation of centrosome duplication.
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Science
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Fukasawa, K.1
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Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo
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Miyashita T, Krajewski S, Krajewska M, Wang HG, Lin HK, Liebermann DA, Hoffman B, Reed JC. Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo. Oncogene. 9:1996;1799-1805.
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Miyashita, T.1
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Liebermann, D.A.6
Hoffman, B.7
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Miyashita T, Reed JC. Tumor suppressor p53 is a direct transcriptional activator of the human bax gene. Cell. 80:1995;293-299.
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Miyashita, T.1
Reed, J.C.2
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0029003501
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Wildtype human p53 and a temperature-sensitive mutant induce Fas/APO-1 expression
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Owen-Schaub LB, Zhang W, Cusack JC, Angelo LS, Santee SM, Fujiwara T, Roth JA, Deisseroth AB, Zhang WW, Kruzel E. Wildtype human p53 and a temperature-sensitive mutant induce Fas/APO-1 expression. Mol Cell Biol. 15:1995;3032-3040.
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Owen-Schaub, L.B.1
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Cusack, J.C.3
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Fujiwara, T.6
Roth, J.A.7
Deisseroth, A.B.8
Zhang, W.W.9
Kruzel, E.10
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0028277934
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The p53-associated protein MDM2 contains a newly characterized zinc-binding domain called the RING finger
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Boddy MN, Freemont PS, Borden KLB. The p53-associated protein MDM2 contains a newly characterized zinc-binding domain called the RING finger. Trends Biochem Sci. 19:1994;10-11.
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Amplification of a gene encoding a p53-associated protein in human sarcomas
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Oliner JD, Kinzler KW, Melzers PS, George D, Vogelstein B. Amplification of a gene encoding a p53-associated protein in human sarcomas. Nature. 358:1992;80-83.
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George, D.4
Vogelstein, B.5
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0027325132
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Oncoprotein MDM2 conceals the activation domain of tumour suppressor p53
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Oliner JD, Pietenpol JA, Thiagalingam S, Gyuris J, Kinzler KW, Vogelstein B. Oncoprotein MDM2 conceals the activation domain of tumour suppressor p53. Nature. 362:1993;857-860.
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Nature
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Oliner, J.D.1
Pietenpol, J.A.2
Thiagalingam, S.3
Gyuris, J.4
Kinzler, K.W.5
Vogelstein, B.6
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39
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0027196974
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Amplification and overexpression of the MDM2 gene in a subset of human malignant gliomas without p53 mutation
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Reifenberger G, Liu L, Ichimur K, Schmidt EE, Collins VP. Amplification and overexpression of the MDM2 gene in a subset of human malignant gliomas without p53 mutation. Cancer Res. 53:1993;2736-2739.
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Reifenberger, G.1
Liu, L.2
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Schmidt, E.E.4
Collins, V.P.5
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0029985647
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Cell type-specific inhibition of p53-mediated apoptosis by MDM2
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of outstanding interest. See annotation [43].
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Haupt Y, Barak Y, Oren M. Cell type-specific inhibition of p53-mediated apoptosis by MDM2. of outstanding interest EMBO J. 15:1996;1596-1606 See annotation [43].
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Haupt, Y.1
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Oren, M.3
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0029913730
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Mdm-2 inhibits the G1 arrest and apoptosis functions of the p53 tumor suppressor protein
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of outstanding interest. See annotation [43].
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Chen J, Wu X, Lin J, Levine AJ. Mdm-2 inhibits the G1 arrest and apoptosis functions of the p53 tumor suppressor protein. of outstanding interest Mol Cell Biol. 16:1996;2445-2452 See annotation [43].
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Chen, J.1
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42
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0028834902
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Rescue of embryonic lethality in Mdm2-deficient mice by absence of p53
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of outstanding interest. See annotation [43].
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Jones SN, Roe AE, Donehower LA, Bradley A. Rescue of embryonic lethality in Mdm2-deficient mice by absence of p53. of outstanding interest Nature. 378:1995;206-208 See annotation [43].
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Jones, S.N.1
Roe, A.E.2
Donehower, L.A.3
Bradley, A.4
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43
-
-
0028823020
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Rescue of early embryonic lethality in mdm2-deficient mice by deletion of p53
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