|
1
|
Molenaar JJ, Ebus ME, Geerts D, et al:
Inactivation of CDK2 is synthetically lethal to MYCN
over-expressing cancer cells. Proc Natl Acad Sci USA.
106:12968–12973. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
2
|
Canaani D: Methodological approaches in
application of synthetic lethality screening towards anticancer
therapy. Br J Cancer. 100:1213–1218. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
3
|
Kaelin WG Jr: The concept of synthetic
lethality in the context of anticancer therapy. Nat Rev Cancer.
5:689–698. 2005. View
Article : Google Scholar : PubMed/NCBI
|
|
4
|
Bandyopadhyay N, Ranka S and Kahveci T:
Sslpred: predicting synthetic sickness lethality. Pac Symp
Biocomput. 7–18. 2012.
|
|
5
|
Luo J, Emanuele MJ, Li D, et al: A
genome-wide RNAi screen identifies multiple synthetic lethal
interactions with the Ras oncogene. Cell. 137:835–848. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
6
|
Scholl C, Fröhling S, Dunn IF, et al:
Synthetic lethal interaction between oncogenic KRAS dependency and
STK33 suppression in human cancer cells. Cell. 137:821–834. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
7
|
Farmer H, McCabe N, Lord CJ, et al:
Targeting the DNA repair defect in BRCA mutant cells as a
therapeutic strategy. Nature. 434:917–921. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
8
|
Kaye SB, Lubinski J, Matulonis U, et al:
Phase II, open-label, randomized, multicenter study comparing the
efficacy and safety of olaparib, a poly (ADP-ribose) polymerase
inhibitor, and pegylated liposomal doxorubicin in patients with
BRCA1 or BRCA2 mutations and recurrent ovarian cancer. J Clin
Oncol. 30:372–379. 2012. View Article : Google Scholar
|
|
9
|
Hollstein M, Sidransky D, Vogelstein B and
Harris CC: p53 mutations in human cancers. Science. 253:49–53.
1991. View Article : Google Scholar : PubMed/NCBI
|
|
10
|
Levine AJ: p53, the cellular gatekeeper
for growth and division. Cell. 88:323–331. 1997. View Article : Google Scholar : PubMed/NCBI
|
|
11
|
Lill NL, Grossman SR, Ginsberg D, DeCaprio
J and Livingston DM: Binding and modulation of p53 by p300/CBP
coactivators. Nature. 387:823–827. 1997. View Article : Google Scholar : PubMed/NCBI
|
|
12
|
Sakaguchi K, Herrera JE, Saito S, et al:
DNA damage activates p53 through a phosphorylation-acetylation
cascade. Genes Dev. 12:2831–2841. 1998. View Article : Google Scholar : PubMed/NCBI
|
|
13
|
Soussi T, Dehouche K and Béroud C: p53
website and analysis of p53 gene mutations in human cancer: forging
a link between epidemiology and carcinogenesis. Hum Mutat.
15:105–113. 2000. View Article : Google Scholar : PubMed/NCBI
|
|
14
|
Olivier M, Eeles R, Hollstein M, Khan MA,
Harris CC and Hainaut P: The IARC TP53 database: new online
mutation analysis and recommendations to users. Hum Mutat.
19:607–614. 2002. View Article : Google Scholar : PubMed/NCBI
|
|
15
|
Soussi T, Ishioka C, Claustres M and
Béroud C: Locus-specific mutation databases: pitfalls and good
practice based on the p53 experience. Nat Rev Cancer. 6:83–90.
2006. View
Article : Google Scholar : PubMed/NCBI
|
|
16
|
Kato S, Han SY, Liu W, et al:
Understanding the function-structure and function-mutation
relationships of p53 tumor suppressor protein by high-resolution
missense mutation analysis. Proc Natl Acad Sci USA. 100:8424–8429.
2003. View Article : Google Scholar : PubMed/NCBI
|
|
17
|
Olive KP, Tuveson DA, Ruhe ZC, et al:
Mutant p53 gain of function in two mouse models of Li-Fraumeni
syndrome. Cell. 119:847–860. 2004. View Article : Google Scholar : PubMed/NCBI
|
|
18
|
Lang GA, Iwakuma T, Suh YA, et al: Gain of
function of a p53 hot spot mutation in a mouse model of Li-Fraumeni
syndrome. Cell. 119:861–872. 2004. View Article : Google Scholar : PubMed/NCBI
|
|
19
|
Song H, Hollstein M and Xu Y: p53
gain-of-function cancer mutants induce genetic instability by
inactivating ATM. Nat Cell Biol. 9:573–580. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
20
|
Liu G, McDonnell TJ, Montes de Oca Luna R,
et al: High metastatic potential in mice inheriting a targeted p53
missense mutation. Proc Natl Acad Sci USA. 97:4174–4179. 2000.
View Article : Google Scholar : PubMed/NCBI
|
|
21
|
Watanabe G, Kato S, Nakata H, Ishida T,
Ohuchi N and Ishioka C: αB-crystallin: a novel p53-target gene
required for p53-dependent apoptosis. Cancer Sci. 100:2368–2375.
2009.
|
|
22
|
Shiraishi K, Kato S, Han SY, et al:
Isolation of temperature-sensitive p53 mutations from a
comprehensive missense mutation library. J Biol Chem. 279:348–355.
2004. View Article : Google Scholar : PubMed/NCBI
|
|
23
|
Dong Z, Wei F, Zhou C, et al: Silencing
Id-1 inhibits lymphangiogenesis through down-regulation of VEGF-C
in oral squamous cell carcinoma. Oral Oncol. 47:27–32. 2011.
View Article : Google Scholar : PubMed/NCBI
|
|
24
|
Kakudo Y, Shibata H, Otsuka K, Kato S and
Ishioka C: Lack of correlation between p53-dependent
transcriptional activity and the ability to induce apoptosis among
179 mutant p53s. Cancer Res. 65:2108–2114. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
25
|
Ling MT, Wang X, Zhang X and Wong YC: The
multiple roles of Id-1 in cancer progression. Differentiation.
74:481–487. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
26
|
Benezra R, Davis RL, Lockshon D, Turner DL
and Weintraub H: The protein Id: a negative regulator of
helix-loop-helix DNA binding proteins. Cell. 61:49–59. 1990.
View Article : Google Scholar : PubMed/NCBI
|
|
27
|
Sun XH: Constitutive expression of the Id1
gene impairs mouse B cell development. Cell. 79:893–900. 1994.
View Article : Google Scholar : PubMed/NCBI
|
|
28
|
Jen Y, Weintraub H and Benezra R:
Overexpression of Id protein inhibits the muscle differentiation
program: in vivo association of Id with E2A proteins. Genes Dev.
6:1466–1479. 1992. View Article : Google Scholar : PubMed/NCBI
|
|
29
|
Kreider BL, Benezra R, Rovera G and
Kadesch T: Inhibition of myeloid differentiation by the
helix-loop-helix protein Id. Science. 255:1700–1702. 1992.
View Article : Google Scholar : PubMed/NCBI
|
|
30
|
Rothschild SI, Kappeler A, Rastchiller D,
et al: The stem cell gene ‘inhibitor of differentiation 1’ (ID1) is
frequently expressed in non-small cell lung cancer. Lung Cancer.
71:306–311. 2011.
|
|
31
|
Ling MT, Wang X, Ouyang XS, Xu K, Tsao SW
and Wong YC: Id-1 expression promotes cell survival through
activation of NF-κB signalling pathway in prostate cancer cells.
Oncogene. 22:4498–4508. 2003.PubMed/NCBI
|
|
32
|
Brosh R and Rotter V: When mutants gain
new powers: news from the mutant p53 field. Nat Rev Cancer.
9:701–713. 2009.PubMed/NCBI
|
|
33
|
Roger L, Jullien L, Gire V and Roux P:
Gain of oncogenic function of p53 mutants regulates E-cadherin
expression uncoupled from cell invasion in colon cancer cells. J
Cell Sci. 123:1295–1305. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
34
|
Yan W and Chen X: Identification of GRO1
as a critical determinant for mutant p53 gain of function. J Biol
Chem. 284:12178–12187. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
35
|
Liu DP, Song H and Xu Y: A common gain of
function of p53 cancer mutants in inducing genetic instability.
Oncogene. 29:949–956. 2010. View Article : Google Scholar : PubMed/NCBI
|
