-
1
-
-
84923427009
-
Novel targets in pancreatic cancer research
-
• This paper discusses the key genetic and non-genetic mechanisms responsible for PDA initiation and progression. Based on these mechanisms it suggests novel therapeutic targets in PD
-
G.Kozak, F.F.Blanco, J.R.Brody Novel targets in pancreatic cancer research. Semin Oncol. 2015;42:177–187.• This paper discusses the key genetic and non-genetic mechanisms responsible for PDA initiation and progression. Based on these mechanisms it suggests novel therapeutic targets in PDA.
-
(2015)
Semin Oncol
, vol.42
, pp. 177-187
-
-
Kozak, G.1
Blanco, F.F.2
Brody, J.R.3
-
2
-
-
84927620483
-
Targeting RAS membrane association: back to the future for anti-ras drug discovery?
-
A.D.Cox, C.J.Der, M.R.Philips Targeting RAS membrane association: back to the future for anti-ras drug discovery?. Clin Cancer Res. 2015;21:1819–1827.
-
(2015)
Clin Cancer Res
, vol.21
, pp. 1819-1827
-
-
Cox, A.D.1
Der, C.J.2
Philips, M.R.3
-
3
-
-
84927609396
-
RAS synthetic lethal screens revisited: still seeking the elusive prize?
-
J.Downward. RAS synthetic lethal screens revisited: still seeking the elusive prize?. Clin Cancer Res. 2015;21:1802–1809.
-
(2015)
Clin Cancer Res
, vol.21
, pp. 1802-1809
-
-
Downward, J.1
-
4
-
-
84936930978
-
Pancreatic cancer: optimizing treatment options, new, and emerging targeted therapies
-
E.G.Chiorean, A.L.Coveler. Pancreatic cancer: optimizing treatment options, new, and emerging targeted therapies. Drug Des Devel Ther. 2015;9:3529–3545.
-
(2015)
Drug Des Devel Ther
, vol.9
, pp. 3529-3545
-
-
Chiorean, E.G.1
Coveler, A.L.2
-
5
-
-
84925004122
-
Molecular landscape of pancreatic cancer: implications for current clinical trials
-
G.M.Heestand, R.Kurzrock. Molecular landscape of pancreatic cancer: implications for current clinical trials. Oncotarget. 2015;6:4553–4561.
-
(2015)
Oncotarget
, vol.6
, pp. 4553-4561
-
-
Heestand, G.M.1
Kurzrock, R.2
-
6
-
-
84899992621
-
Not just gRASping at flaws: finding vulnerabilities to develop novel therapies for treating KRAS mutant cancers
-
H.Ebi, A.C.Faber, J.A.Engelman, et al. Not just gRASping at flaws: finding vulnerabilities to develop novel therapies for treating KRAS mutant cancers. Cancer Sci. 2014;105:499–505.
-
(2014)
Cancer Sci
, vol.105
, pp. 499-505
-
-
Ebi, H.1
Faber, A.C.2
Engelman, J.A.3
-
7
-
-
84908491115
-
Drugging the undruggable RAS: Mission possible?
-
• The authors summarize the progress and the promise of five key approaches to target Ras: (1) direct inhibitors of RAS; (2) RAS membrane association; (3) targeting RAS downstream effector signalling; (4) synthetic lethal interactors of mutant RAS; and (5) RAS-mediated changes in cell metabolis
-
A.D.Cox, S.W.Fesik, A.C.Kimmelman, et al. Drugging the undruggable RAS: Mission possible?. Nat Rev Drug Discov. 2014;13:828–851.• The authors summarize the progress and the promise of five key approaches to target Ras: (1) direct inhibitors of RAS; (2) RAS membrane association; (3) targeting RAS downstream effector signalling; (4) synthetic lethal interactors of mutant RAS; and (5) RAS-mediated changes in cell metabolism.
-
(2014)
Nat Rev Drug Discov
, vol.13
, pp. 828-851
-
-
Cox, A.D.1
Fesik, S.W.2
Kimmelman, A.C.3
-
8
-
-
84939893323
-
A method for the second-site screening of K-Ras in the presence of a covalently attached first-site ligand
-
Q.Sun, J.Phan, A.R.Friberg, et al. A method for the second-site screening of K-Ras in the presence of a covalently attached first-site ligand. J Biomol NMR. 2014;60:11–14.
-
(2014)
J Biomol NMR
, vol.60
, pp. 11-14
-
-
Sun, Q.1
Phan, J.2
Friberg, A.R.3
-
9
-
-
84878181372
-
TRAPP: a tool for analysis of transient binding pockets in proteins
-
D.B.Kokh, S.Richter, S.Henrich, et al. TRAPP: a tool for analysis of transient binding pockets in proteins. J Chem Inf Model. 2013;53:1235–1252.
-
(2013)
J Chem Inf Model
, vol.53
, pp. 1235-1252
-
-
Kokh, D.B.1
Richter, S.2
Henrich, S.3
-
10
-
-
84892946966
-
Searching for protein binding sites from Molecular Dynamics simulations and paramagnetic fragment-based NMR studies
-
A.Bernini, L.Henrici De Angelis, E.Morandi, et al Searching for protein binding sites from Molecular Dynamics simulations and paramagnetic fragment-based NMR studies. Biochim Biophys Acta. 2014;1844:561–566.
-
(2014)
Biochim Biophys Acta
, vol.1844
, pp. 561-566
-
-
Bernini, A.1
Henrici De Angelis, L.2
Morandi, E.3
-
11
-
-
84872225145
-
Compound activity prediction using models of binding pockets or ligand properties in 3D
-
I.Kufareva, Y.-C.Chen, A.V.Ilatovskiy, et al. Compound activity prediction using models of binding pockets or ligand properties in 3D. Curr Top Med Chem. 2012;12:1869–1882.
-
(2012)
Curr Top Med Chem
, vol.12
, pp. 1869-1882
-
-
Kufareva, I.1
Chen, Y.-C.2
Ilatovskiy, A.V.3
-
12
-
-
84911921917
-
Allosteric modulation of Ras and the PI3K/AKT/mTOR pathway: emerging therapeutic opportunities
-
• The authors focus on the recent advances and merits of developing allosteric drugs targeting Ras and the PI3K/AKT/mTOR pathway
-
P.A.Hubbard, C.L.Moody, R.Murali. Allosteric modulation of Ras and the PI3K/AKT/mTOR pathway: emerging therapeutic opportunities. Front Physiol. 2014;5:478.• The authors focus on the recent advances and merits of developing allosteric drugs targeting Ras and the PI3K/AKT/mTOR pathway.
-
(2014)
Front Physiol
, vol.5
, pp. 478
-
-
Hubbard, P.A.1
Moody, C.L.2
Murali, R.3
-
13
-
-
84888639050
-
K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions
-
•• Here the authors describe the design of an a covalent allosteric drug to target K-Ras(G12C) to control GTP affinity and effector interactions. This is the first such desig
-
J.M.Ostrem, U.Peters, M.L.Sos, et al. K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions. Nature. 2013;503:548–551.•• Here the authors describe the design of an a covalent allosteric drug to target K-Ras(G12C) to control GTP affinity and effector interactions. This is the first such design.
-
(2013)
Nature
, vol.503
, pp. 548-551
-
-
Ostrem, J.M.1
Peters, U.2
Sos, M.L.3
-
14
-
-
84880169201
-
Targeting mutant KRAS for anticancer therapeutics: a review of novel small molecule modulators
-
Y.Wang, C.E.Kaiser, B.Frett, et al. Targeting mutant KRAS for anticancer therapeutics: a review of novel small molecule modulators. J Med Chem. 2013;56:5219–5230.
-
(2013)
J Med Chem
, vol.56
, pp. 5219-5230
-
-
Wang, Y.1
Kaiser, C.E.2
Frett, B.3
-
15
-
-
84941808747
-
The key role of calmodulin in KRAS-driven adenocarcinomas
-
•• Here the authors propose an explanation for the challenging question of how calmodulin acts to uniquely stimulate oncogenic K-Ras action rather than other Ras isoforms, and do so in mechanistic detail. Based on this mechanistic underpinning they further suggest a drug targe
-
R.Nussinov, S.Muratcioglu, C.-J.Tsai, et al. The key role of calmodulin in KRAS-driven adenocarcinomas. Mol Cancer Res. 2015;13:1265–1273.•• Here the authors propose an explanation for the challenging question of how calmodulin acts to uniquely stimulate oncogenic K-Ras action rather than other Ras isoforms, and do so in mechanistic detail. Based on this mechanistic underpinning they further suggest a drug target.
-
(2015)
Mol Cancer Res
, vol.13
, pp. 1265-1273
-
-
Nussinov, R.1
Muratcioglu, S.2
Tsai, C.-J.3
-
16
-
-
84890574861
-
The many faces of calmodulin in cell proliferation, programmed cell death, autophagy, and cancer
-
•• A very useful review of the action of CaM and CaM-dependent signaling systems in the control of vertebrate cell proliferation, programmed cell death and autophagy. The authors highlight the importance of CaM and interconnected CaM-regulated systems for the physiology of cancer cells including tumor stem cells, and processes required for tumor progression such as growth, tumor-associated angiogenesis and metastasis are highlighted. It also discusses the potential targeting of CaM-dependent signaling processes for therapeutic us
-
M.W.Berchtold, A.Villalobo. The many faces of calmodulin in cell proliferation, programmed cell death, autophagy, and cancer. Biochim Biophys Acta. 2014;1843:398–435.•• A very useful review of the action of CaM and CaM-dependent signaling systems in the control of vertebrate cell proliferation, programmed cell death and autophagy. The authors highlight the importance of CaM and interconnected CaM-regulated systems for the physiology of cancer cells including tumor stem cells, and processes required for tumor progression such as growth, tumor-associated angiogenesis and metastasis are highlighted. It also discusses the potential targeting of CaM-dependent signaling processes for therapeutic use.
-
(2014)
Biochim Biophys Acta
, vol.1843
, pp. 398-435
-
-
Berchtold, M.W.1
Villalobo, A.2
-
17
-
-
84930678799
-
Cell adhesion. Mechanical strain induces E-cadherin-dependent Yap1 and β-catenin activation to drive cell cycle entry
-
•• In this paper the authors showed that mechanical strain applied to quiescent epithelial cells induced rapid cell cycle reentry. Of particular importance, this cell cycle effect was mediated by accumulation and transcriptional activity of Yap1 followed by β-catenin. Inhibition of Yap1- and β-catenin-mediated transcription blocked cell cycle reentry and progression through G1 into S phase, respectively. Maintenance of quiescence, Yap1 nuclear exclusion, and β-catenin transcriptional responses to mechanical strain required E-cadherin extracellular engagemen
-
B.W.Benham-Pyle, B.L.Pruitt, W.J.Nelson. Cell adhesion. Mechanical strain induces E-cadherin-dependent Yap1 and β-catenin activation to drive cell cycle entry. Science. 2015;348:1024–1027.•• In this paper the authors showed that mechanical strain applied to quiescent epithelial cells induced rapid cell cycle reentry. Of particular importance, this cell cycle effect was mediated by accumulation and transcriptional activity of Yap1 followed by β-catenin. Inhibition of Yap1- and β-catenin-mediated transcription blocked cell cycle reentry and progression through G1 into S phase, respectively. Maintenance of quiescence, Yap1 nuclear exclusion, and β-catenin transcriptional responses to mechanical strain required E-cadherin extracellular engagement.
-
(2015)
Science
, vol.348
, pp. 1024-1027
-
-
Benham-Pyle, B.W.1
Pruitt, B.L.2
Nelson, W.J.3
-
18
-
-
84903984143
-
Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer
-
A.Kapoor, W.Yao, H.Ying, et al. Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer. Cell. 2014;158:185–197.
-
(2014)
Cell
, vol.158
, pp. 185-197
-
-
Kapoor, A.1
Yao, W.2
Ying, H.3
-
19
-
-
84886948259
-
‘Pathway drug cocktail’: targeting Ras signaling based on structural pathways
-
R.Nussinov, C.-J.Tsai, C.Mattos. ‘Pathway drug cocktail’: targeting Ras signaling based on structural pathways. Trends Mol Med. 2013;19:695–704.
-
(2013)
Trends Mol Med
, vol.19
, pp. 695-704
-
-
Nussinov, R.1
Tsai, C.-J.2
Mattos, C.3
-
20
-
-
84940893103
-
Flexibility and small pockets at protein-protein interfaces: New insights into druggability
-
H.Jubb, T.L.Blundell, D.B.Ascher. Flexibility and small pockets at protein-protein interfaces: New insights into druggability. Prog Biophys Mol Biol. 2015;119:2–9.
-
(2015)
Prog Biophys Mol Biol
, vol.119
, pp. 2-9
-
-
Jubb, H.1
Blundell, T.L.2
Ascher, D.B.3
-
21
-
-
84893018543
-
Protein-protein interactions as druggable targets: recent technological advances
-
A.P.Higueruelo, H.Jubb, T.L.Blundell. Protein-protein interactions as druggable targets: recent technological advances. Curr Opin Pharmacol. 2013;13:791–796.
-
(2013)
Curr Opin Pharmacol
, vol.13
, pp. 791-796
-
-
Higueruelo, A.P.1
Jubb, H.2
Blundell, T.L.3
-
22
-
-
84899656717
-
Unraveling structural mechanisms of allosteric drug action
-
•• This paper provides a novel mechanistic insight into the mode of action of allosteric drug
-
R.Nussinov, C.-J.Tsai. Unraveling structural mechanisms of allosteric drug action. Trends Pharmacol Sci. 2014;35:256–264.•• This paper provides a novel mechanistic insight into the mode of action of allosteric drugs.
-
(2014)
Trends Pharmacol Sci
, vol.35
, pp. 256-264
-
-
Nussinov, R.1
Tsai, C.-J.2
-
23
-
-
78149473070
-
Allostery and population shift in drug discovery
-
G.Kar, O.Keskin, A.Gursoy, et al. Allostery and population shift in drug discovery. Curr Opin Pharmacol. 2010;10:715–722.
-
(2010)
Curr Opin Pharmacol
, vol.10
, pp. 715-722
-
-
Kar, G.1
Keskin, O.2
Gursoy, A.3
-
24
-
-
84857759143
-
The different ways through which specificity works in orthosteric and allosteric drugs
-
R.Nussinov, C.-J.Tsai. The different ways through which specificity works in orthosteric and allosteric drugs. Curr Pharm Des. 2012;18:1311–1316.
-
(2012)
Curr Pharm Des
, vol.18
, pp. 1311-1316
-
-
Nussinov, R.1
Tsai, C.-J.2
-
25
-
-
84876266689
-
Allostery in disease and in drug discovery
-
R.Nussinov, C.-J.Tsai. Allostery in disease and in drug discovery. Cell. 2013;153:293–305.
-
(2013)
Cell
, vol.153
, pp. 293-305
-
-
Nussinov, R.1
Tsai, C.-J.2
-
27
-
-
84941879580
-
Evading inhibitory constraints - destabilizing p110alpha/p85alpha interactions
-
C.Sheridan. Evading inhibitory constraints - destabilizing p110alpha/p85alpha interactions. Febs J. 2015;282:3525–3527.
-
(2015)
Febs J
, vol.282
, pp. 3525-3527
-
-
Sheridan, C.1
-
28
-
-
0034911881
-
Synthesis and function of 3-phosphorylated inositol lipids
-
B.Vanhaesebroeck, S.J.Leevers, K.Ahmadi, et al Synthesis and function of 3-phosphorylated inositol lipids. Annu Rev Biochem. 2001;70:535–602.
-
(2001)
Annu Rev Biochem
, vol.70
, pp. 535-602
-
-
Vanhaesebroeck, B.1
Leevers, S.J.2
Ahmadi, K.3
-
29
-
-
80054736907
-
Structural basis for activation and inhibition of class I phosphoinositide 3-kinases
-
•• Here the authors provide unique insight into the structural basis for activation and inhibition of class I phosphoinositide 3-kinase
-
O.Vadas, J.E.Burke, X.Zhang, et al. Structural basis for activation and inhibition of class I phosphoinositide 3-kinases. Sci Signal. 2011;4:re2.•• Here the authors provide unique insight into the structural basis for activation and inhibition of class I phosphoinositide 3-kinases.
-
(2011)
Sci Signal
, vol.4
, pp. 2
-
-
Vadas, O.1
Burke, J.E.2
Zhang, X.3
-
30
-
-
0030722224
-
Calmodulin activates phosphatidylinositol 3-kinase
-
J.L.Joyal, D.J.Burks, S.Pons, et al Calmodulin activates phosphatidylinositol 3-kinase. J Biol Chem. 1997;272:28183–28186.
-
(1997)
J Biol Chem
, vol.272
, pp. 28183-28186
-
-
Joyal, J.L.1
Burks, D.J.2
Pons, S.3
-
31
-
-
84901231782
-
Emerging roles of the p38 MAPK and PI3K/AKT/mTOR pathways in oncogene-induced senescence
-
• The authors provide a useful overview of scenesence, focusing on the roles of p38 MAPK and PI3K/AKT/mTOR pathways in oncogene-induced senescenc
-
Y.Xu, N.Li, R.Xiang, et al. Emerging roles of the p38 MAPK and PI3K/AKT/mTOR pathways in oncogene-induced senescence. Trends Biochem Sci. 2014;39:268–276.• The authors provide a useful overview of scenesence, focusing on the roles of p38 MAPK and PI3K/AKT/mTOR pathways in oncogene-induced senescence.
-
(2014)
Trends Biochem Sci
, vol.39
, pp. 268-276
-
-
Xu, Y.1
Li, N.2
Xiang, R.3
-
32
-
-
70350126139
-
A frequent kinase domain mutation that changes the interaction between PI3K alpha and the membrane
-
D.Mandelker, S.B.Gabelli, O.Schmidt-Kittler, et al A frequent kinase domain mutation that changes the interaction between PI3K alpha and the membrane. Proc Natl Acad Sci U S A. 2009;106:16996–17001.
-
(2009)
Proc Natl Acad Sci U S A
, vol.106
, pp. 16996-17001
-
-
Mandelker, D.1
Gabelli, S.B.2
Schmidt-Kittler, O.3
-
33
-
-
84897820841
-
Activation of PI3Kα by physiological effectors and by oncogenic mutations: structural and dynamic effects
-
S.Gabelli, I.Echeverria, M.Alexander, et al. Activation of PI3Kα by physiological effectors and by oncogenic mutations: structural and dynamic effects. Biophys Rev. 2014;6:89–95.
-
(2014)
Biophys Rev
, vol.6
, pp. 89-95
-
-
Gabelli, S.1
Echeverria, I.2
Alexander, M.3
-
34
-
-
84866544615
-
Oncogenic mutations mimic and enhance dynamic events in the natural activation of phosphoinositide 3-kinase p110 alpha (PIK3CA)
-
•• In this paper the authors elucidate a unifying mechanism in which diverse PIK3CA mutations stimulate lipid kinase activity by facilitating allosteric motions required for catalysis on membrane
-
J.E.Burke, O.Perisic, G.R.Masson, et al. Oncogenic mutations mimic and enhance dynamic events in the natural activation of phosphoinositide 3-kinase p110 alpha (PIK3CA). Proc Natl Acad Sci U S A. 2012;109:15259–15264.•• In this paper the authors elucidate a unifying mechanism in which diverse PIK3CA mutations stimulate lipid kinase activity by facilitating allosteric motions required for catalysis on membranes.
-
(2012)
Proc Natl Acad Sci U S A
, vol.109
, pp. 15259-15264
-
-
Burke, J.E.1
Perisic, O.2
Masson, G.R.3
-
35
-
-
79960189344
-
Dynamic allostery: linkers are not merely flexible
-
B.Ma, C.-J.Tsai, T.Haliloglu, et al. Dynamic allostery: linkers are not merely flexible. Structure. 2011;19:907–917.
-
(2011)
Structure
, vol.19
, pp. 907-917
-
-
Ma, B.1
Tsai, C.-J.2
Haliloglu, T.3
-
36
-
-
51849128358
-
Class IPI3K in oncogenic cellular transformation
-
L.Zhao, P.K.Vogt. Class IPI3K in oncogenic cellular transformation. Oncogene. 2008;27:5486–5496.
-
(2008)
Oncogene
, vol.27
, pp. 5486-5496
-
-
Zhao, L.1
Vogt, P.K.2
-
37
-
-
0031936353
-
Ras signalling and apoptosis
-
J.Downward. Ras signalling and apoptosis. Curr Opin Genet Dev. 1998;8:49–54.
-
(1998)
Curr Opin Genet Dev
, vol.8
, pp. 49-54
-
-
Downward, J.1
-
38
-
-
0030880741
-
Increasing complexity of Ras signal transduction: involvement of Rho family proteins
-
R.Khosravi-Far, S.Campbell, K.L.Rossman, et al. Increasing complexity of Ras signal transduction: involvement of Rho family proteins. Adv Cancer Res. 1998;72:57–107.
-
(1998)
Adv Cancer Res
, vol.72
, pp. 57-107
-
-
Khosravi-Far, R.1
Campbell, S.2
Rossman, K.L.3
-
39
-
-
33745265268
-
Germline missense mutations affecting KRAS Isoform B are associated with a severe Noonan syndrome phenotype
-
C.Carta, F.Pantaleoni, G.Bocchinfuso, et al Germline missense mutations affecting KRAS Isoform B are associated with a severe Noonan syndrome phenotype. Am J Hum Genet. 2006;79:129–135.
-
(2006)
Am J Hum Genet
, vol.79
, pp. 129-135
-
-
Carta, C.1
Pantaleoni, F.2
Bocchinfuso, G.3
-
40
-
-
0030718568
-
Developmentally-regulated expression of murine K-ras isoforms
-
S.Pells, M.Divjak, P.Romanowski, et al. Developmentally-regulated expression of murine K-ras isoforms. Oncogene. 1997;15:1781–1786.
-
(1997)
Oncogene
, vol.15
, pp. 1781-1786
-
-
Pells, S.1
Divjak, M.2
Romanowski, P.3
-
41
-
-
0033145517
-
Dominant-negative caveolin inhibits H-Ras function by disrupting cholesterol-rich plasma membrane domains
-
S.Roy, R.Luetterforst, A.Harding, et al. Dominant-negative caveolin inhibits H-Ras function by disrupting cholesterol-rich plasma membrane domains. Nat Cell Biol. 1999;1:98–105.
-
(1999)
Nat Cell Biol
, vol.1
, pp. 98-105
-
-
Roy, S.1
Luetterforst, R.2
Harding, A.3
-
42
-
-
0032508517
-
Ras isoforms vary in their ability to activate Raf-1 and phosphoinositide 3-kinase
-
J.Yan, S.Roy, A.Apolloni, et al. Ras isoforms vary in their ability to activate Raf-1 and phosphoinositide 3-kinase. J Biol Chem. 1998;273:24052–24056.
-
(1998)
J Biol Chem
, vol.273
, pp. 24052-24056
-
-
Yan, J.1
Roy, S.2
Apolloni, A.3
-
43
-
-
0345135149
-
K-ras is an essential gene in the mouse with partial functional overlap with N-ras
-
L.Johnson, D.Greenbaum, K.Cichowski, et al. K-ras is an essential gene in the mouse with partial functional overlap with N-ras. Genes Dev. 1997;11:2468–2481.
-
(1997)
Genes Dev
, vol.11
, pp. 2468-2481
-
-
Johnson, L.1
Greenbaum, D.2
Cichowski, K.3
-
44
-
-
0035136213
-
Targeted genomic disruption of H-ras and N-ras, individually or in combination, reveals the dispensability of both loci for mouse growth and development
-
L.M.Esteban, C.Vicario-Abejon, P.Fernandez-Salguero, et al. Targeted genomic disruption of H-ras and N-ras, individually or in combination, reveals the dispensability of both loci for mouse growth and development. Mol Cell Biol. 2001;21:1444–1452.
-
(2001)
Mol Cell Biol
, vol.21
, pp. 1444-1452
-
-
Esteban, L.M.1
Vicario-Abejon, C.2
Fernandez-Salguero, P.3
-
45
-
-
0028584355
-
Polylysine domain of K-ras 4B protein is crucial for malignant transformation
-
J.H.Jackson, J.W.Li, J.E.Buss, et al. Polylysine domain of K-ras 4B protein is crucial for malignant transformation. Proc Natl Acad Sci U S A. 1994;91:12730–12734.
-
(1994)
Proc Natl Acad Sci U S A
, vol.91
, pp. 12730-12734
-
-
Jackson, J.H.1
Li, J.W.2
Buss, J.E.3
-
46
-
-
33746381948
-
K-ras 4A and 4B are co-expressed widely in human tissues, and their ratio is altered in sporadic colorectal cancer
-
S.J.Plowman, R.L.Berry, S.A.Bader, et al. K-ras 4A and 4B are co-expressed widely in human tissues, and their ratio is altered in sporadic colorectal cancer. J Exp Clin Cancer Res. 2006;25:259–267.
-
(2006)
J Exp Clin Cancer Res
, vol.25
, pp. 259-267
-
-
Plowman, S.J.1
Berry, R.L.2
Bader, S.A.3
-
47
-
-
70450195266
-
Implications for KRAS status and EGFR-targeted therapies in metastatic CRC
-
N.Normanno, S.Tejpar, F.Morgillo, et al. Implications for KRAS status and EGFR-targeted therapies in metastatic CRC. Nat Rev Clin Oncol. 2009;6:519–527.
-
(2009)
Nat Rev Clin Oncol
, vol.6
, pp. 519-527
-
-
Normanno, N.1
Tejpar, S.2
Morgillo, F.3
-
48
-
-
79960044081
-
Regulation and function of the rasgrp family of ras activators in blood cells
-
J.C.Stone. Regulation and function of the rasgrp family of ras activators in blood cells. Genes Cancer. 2011;2:320–334.
-
(2011)
Genes Cancer
, vol.2
, pp. 320-334
-
-
Stone, J.C.1
-
49
-
-
84922287331
-
K-Ras4A splice variant is widely expressed in cancer and uses a hybrid membrane-targeting motif
-
•• Here the authors show that K-Ras4A splice variant is widely expressed and can act in two distinct modes: K-Ras4B- and N-Ras-like. This is the first paper to analyze K-Ras4A in such depth, leading to unique insight into its actio
-
F.D.Tsai, M.S.Lopes, M.Zhou, et al. K-Ras4A splice variant is widely expressed in cancer and uses a hybrid membrane-targeting motif. Proc Natl Acad Sci U S A. 2015;112:779–784.•• Here the authors show that K-Ras4A splice variant is widely expressed and can act in two distinct modes: K-Ras4B- and N-Ras-like. This is the first paper to analyze K-Ras4A in such depth, leading to unique insight into its action.
-
(2015)
Proc Natl Acad Sci U S A
, vol.112
, pp. 779-784
-
-
Tsai, F.D.1
Lopes, M.S.2
Zhou, M.3
-
50
-
-
39649125571
-
Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis
-
C.E.Patek, M.J.Arends, W.A.Wallace, et al. Mutationally activated K-ras 4A and 4B both mediate lung carcinogenesis. Exp Cell Res. 2008;314:1105–1114.
-
(2008)
Exp Cell Res
, vol.314
, pp. 1105-1114
-
-
Patek, C.E.1
Arends, M.J.2
Wallace, W.A.3
-
51
-
-
72249091662
-
Prognostic significance of alterations in KRAS isoforms KRAS-4A/4B and KRAS mutations in colorectal carcinoma
-
J.Abubaker, P.Bavi, W.Al-Haqawi, et al. Prognostic significance of alterations in KRAS isoforms KRAS-4A/4B and KRAS mutations in colorectal carcinoma. J Pathol. 2009;219:435–445.
-
(2009)
J Pathol
, vol.219
, pp. 435-445
-
-
Abubaker, J.1
Bavi, P.2
Al-Haqawi, W.3
-
52
-
-
0033538559
-
Endomembrane trafficking of ras: the CAAX motif targets proteins to the ER and Golgi
-
E.Choy, V.K.Chiu, J.Silletti, et al. Endomembrane trafficking of ras: the CAAX motif targets proteins to the ER and Golgi. Cell. 1999;98:69–80.
-
(1999)
Cell
, vol.98
, pp. 69-80
-
-
Choy, E.1
Chiu, V.K.2
Silletti, J.3
-
53
-
-
0025013547
-
A polybasic domain or palmitoylation is required in addition to the CAAX motif to localize p21ras to the plasma membrane
-
J.F.Hancock, H.Paterson, C.J.Marshall. A polybasic domain or palmitoylation is required in addition to the CAAX motif to localize p21ras to the plasma membrane. Cell. 1990;63:133–139.
-
(1990)
Cell
, vol.63
, pp. 133-139
-
-
Hancock, J.F.1
Paterson, H.2
Marshall, C.J.3
-
55
-
-
79960055459
-
RAS interaction with PI3K: more than just another effector pathway
-
E.Castellano, J.Downward. RAS interaction with PI3K: more than just another effector pathway. Genes Cancer. 2011;2:261–274.
-
(2011)
Genes Cancer
, vol.2
, pp. 261-274
-
-
Castellano, E.1
Downward, J.2
-
57
-
-
79960038169
-
Functional specificity of ras isoforms: so similar but so different
-
E.Castellano, E.Santos. Functional specificity of ras isoforms: so similar but so different. Genes Cancer. 2011;2:216–231.
-
(2011)
Genes Cancer
, vol.2
, pp. 216-231
-
-
Castellano, E.1
Santos, E.2
-
58
-
-
84861147473
-
A comprehensive survey of Ras mutations in cancer
-
I.A.Prior, P.D.Lewis, C.Mattos. A comprehensive survey of Ras mutations in cancer. Cancer Res. 2012;72:2457–2467.
-
(2012)
Cancer Res
, vol.72
, pp. 2457-2467
-
-
Prior, I.A.1
Lewis, P.D.2
Mattos, C.3
-
59
-
-
84915813644
-
Pancreatic adenocarcinoma
-
• A useful overview overview of pancreatic adenocarcinoma from the basic and clinical standpoint
-
D.P.Ryan, T.S.Hong, N.Bardeesy. Pancreatic adenocarcinoma. N Engl J Med. 2014;371:1039–1049.• A useful overview overview of pancreatic adenocarcinoma from the basic and clinical standpoints.
-
(2014)
N Engl J Med
, vol.371
, pp. 1039-1049
-
-
Ryan, D.P.1
Hong, T.S.2
Bardeesy, N.3
-
60
-
-
84892861646
-
KRAS: feeding pancreatic cancer proliferation
-
• The authors provide a comprehensive and coherent description of the central role of oncogenic KRAS in controlling tumor metabolism by orchestrating multiple metabolic changes including stimulation of glucose uptake, differential channeling of glucose intermediates, reprogrammed glutamine metabolism, increased autophagy, and macropinocytosis. They also discuss how these may be applied to develop new PDAC treatment
-
K.L.Bryant, J.D.Mancias, A.C.Kimmelman, et al. KRAS: feeding pancreatic cancer proliferation. Trends Biochem Sci. 2014;39:91–100.• The authors provide a comprehensive and coherent description of the central role of oncogenic KRAS in controlling tumor metabolism by orchestrating multiple metabolic changes including stimulation of glucose uptake, differential channeling of glucose intermediates, reprogrammed glutamine metabolism, increased autophagy, and macropinocytosis. They also discuss how these may be applied to develop new PDAC treatments.
-
(2014)
Trends Biochem Sci
, vol.39
, pp. 91-100
-
-
Bryant, K.L.1
Mancias, J.D.2
Kimmelman, A.C.3
-
61
-
-
33847419143
-
Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice
-
C.Guerra, A.J.Schuhmacher, M.Cañamero, et al. Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice. Cancer Cell. 2007;11:291–302.
-
(2007)
Cancer Cell
, vol.11
, pp. 291-302
-
-
Guerra, C.1
Schuhmacher, A.J.2
Cañamero, M.3
-
62
-
-
9144266295
-
Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse
-
S.R.Hingorani, E.F.Petricoin, A.Maitra, et al Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. Cancer Cell. 2003;4:437–450.
-
(2003)
Cancer Cell
, vol.4
, pp. 437-450
-
-
Hingorani, S.R.1
Petricoin, E.F.2
Maitra, A.3
-
63
-
-
77957150824
-
KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma
-
•• The authors provide a useful review of the roles of Hedgehog and Wnt signaling in K-Ras-driven pancreatic adenocarcinom
-
J.Morris, S.C.Wang, M.Hebrok. KRAS, Hedgehog, Wnt and the twisted developmental biology of pancreatic ductal adenocarcinoma. Nat Rev Cancer. 2010;10:683–695.•• The authors provide a useful review of the roles of Hedgehog and Wnt signaling in K-Ras-driven pancreatic adenocarcinoma.
-
(2010)
Nat Rev Cancer
, vol.10
, pp. 683-695
-
-
Morris, J.1
Wang, S.C.2
Hebrok, M.3
-
64
-
-
79954513296
-
Adult pancreatic acinar cells dedifferentiate to an embryonic progenitor phenotype with concomitant activation of a senescence programme that is present in chronic pancreatitis
-
A.V.Pinho, I.Rooman, M.Reichert, et al. Adult pancreatic acinar cells dedifferentiate to an embryonic progenitor phenotype with concomitant activation of a senescence programme that is present in chronic pancreatitis. Gut. 2011;60:958–966.
-
(2011)
Gut
, vol.60
, pp. 958-966
-
-
Pinho, A.V.1
Rooman, I.2
Reichert, M.3
-
65
-
-
48249128709
-
A Cre-loxP-based mouse model for conditional somatic gene expression and knockdown in vivo by using avian retroviral vectors
-
B.Seidler, A.Schmidt, U.Mayr, et al. A Cre-loxP-based mouse model for conditional somatic gene expression and knockdown in vivo by using avian retroviral vectors. Proc Natl Acad Sci U S A. 2008;105:10137–10142.
-
(2008)
Proc Natl Acad Sci U S A
, vol.105
, pp. 10137-10142
-
-
Seidler, B.1
Schmidt, A.2
Mayr, U.3
-
66
-
-
42649145667
-
Wild-type KRAS is required for panitumumab efficacy in patients with metastatic colorectal cancer
-
R.G.Amado, M.Wolf, M.Peeters, et al. Wild-type KRAS is required for panitumumab efficacy in patients with metastatic colorectal cancer. J Clin Oncol. 2008;26:1626–1634.
-
(2008)
J Clin Oncol
, vol.26
, pp. 1626-1634
-
-
Amado, R.G.1
Wolf, M.2
Peeters, M.3
-
67
-
-
54949085398
-
K-ras mutations and benefit from cetuximab in advanced colorectal cancer
-
C.S.Karapetis, S.Khambata-Ford, D.J.Jonker, et al. K-ras mutations and benefit from cetuximab in advanced colorectal cancer. N Engl J Med. 2008;359:1757–1765.
-
(2008)
N Engl J Med
, vol.359
, pp. 1757-1765
-
-
Karapetis, C.S.1
Khambata-Ford, S.2
Jonker, D.J.3
-
68
-
-
0023748414
-
Genetic alterations during colorectal-tumor development
-
B.Vogelstein, E.R.Fearon, S.R.Hamilton, et al. Genetic alterations during colorectal-tumor development. N Engl J Med. 1988;319:525–532.
-
(1988)
N Engl J Med
, vol.319
, pp. 525-532
-
-
Vogelstein, B.1
Fearon, E.R.2
Hamilton, S.R.3
-
69
-
-
84922083729
-
BYL719, a selective inhibitor of phosphoinositide 3-Kinase alpha, enhances the effect of selumetinib (AZD6244, ARRY-142886) in KRAS-mutant non-small cell lung cancer
-
B.M.Ku, E.H.Jho, Y.H.Bae, et al. BYL719, a selective inhibitor of phosphoinositide 3-Kinase alpha, enhances the effect of selumetinib (AZD6244, ARRY-142886) in KRAS-mutant non-small cell lung cancer. Invest New Drugs. 2015;33:12–21.
-
(2015)
Invest New Drugs
, vol.33
, pp. 12-21
-
-
Ku, B.M.1
Jho, E.H.2
Bae, Y.H.3
-
71
-
-
68849095670
-
The hypervariable region of K-Ras4B is responsible for its specific interactions with calmodulin
-
S.J.Abraham, R.P.Nolet, R.J.Calvert, et al. The hypervariable region of K-Ras4B is responsible for its specific interactions with calmodulin. Biochemistry. 2009;48:7575–7583.
-
(2009)
Biochemistry
, vol.48
, pp. 7575-7583
-
-
Abraham, S.J.1
Nolet, R.P.2
Calvert, R.J.3
-
72
-
-
84930948748
-
ANO1 (TMEM16A) in pancreatic ductal adenocarcinoma (PDAC)
-
D.R.Sauter, I.Novak, S.F.Pedersen, et al. ANO1 (TMEM16A) in pancreatic ductal adenocarcinoma (PDAC). Pflugers Arch. 2015;467:1495–1508.
-
(2015)
Pflugers Arch
, vol.467
, pp. 1495-1508
-
-
Sauter, D.R.1
Novak, I.2
Pedersen, S.F.3
-
73
-
-
33645105705
-
Identification of differently expressed genes in human colorectal adenocarcinoma
-
Y.Chen, Y.Z.Zhang, Z.G.Zhou, et al. Identification of differently expressed genes in human colorectal adenocarcinoma. World J Gastroenterol. 2006;12:1025–1032.
-
(2006)
World J Gastroenterol
, vol.12
, pp. 1025-1032
-
-
Chen, Y.1
Zhang, Y.Z.2
Zhou, Z.G.3
-
74
-
-
0029996388
-
A study on the levels of calmodulin and DNA in human lung cancer cells
-
G.X.Liu, H.F.Sheng, S.Wu. A study on the levels of calmodulin and DNA in human lung cancer cells. Br J Cancer. 1996;73:899–901.
-
(1996)
Br J Cancer
, vol.73
, pp. 899-901
-
-
Liu, G.X.1
Sheng, H.F.2
Wu, S.3
-
76
-
-
4644303140
-
Calmodulin-mediated activation of Akt regulates survival of c-Myc-overexpressing mouse mammary carcinoma cells
-
T.B.Deb, C.M.Coticchia, R.B.Dickson. Calmodulin-mediated activation of Akt regulates survival of c-Myc-overexpressing mouse mammary carcinoma cells. J Biol Chem. 2004;279:38903–38911.
-
(2004)
J Biol Chem
, vol.279
, pp. 38903-38911
-
-
Deb, T.B.1
Coticchia, C.M.2
Dickson, R.B.3
-
77
-
-
83655165720
-
Regulation of calcium signaling in lung cancer
-
H.Yang, Q.Zhang, J.He, et al. Regulation of calcium signaling in lung cancer. J Thorac Dis. 2010;2:52–56.
-
(2010)
J Thorac Dis
, vol.2
, pp. 52-56
-
-
Yang, H.1
Zhang, Q.2
He, J.3
-
78
-
-
79954465036
-
Expression and unique functions of four nuclear factor of activated T cells isoforms in non-small cell lung cancer
-
Z.L.Chen, S.H.Zhao, Z.Wang, et al. Expression and unique functions of four nuclear factor of activated T cells isoforms in non-small cell lung cancer. Chin J Cancer. 2011;30:62–68.
-
(2011)
Chin J Cancer
, vol.30
, pp. 62-68
-
-
Chen, Z.L.1
Zhao, S.H.2
Wang, Z.3
-
79
-
-
84937926994
-
Ca2+/calmodulin-dependent protein kinase IIgamma enhances stem-like traits and tumorigenicity of lung cancer cells
-
S.Chai, X.Xu, Y.Wang, et al. Ca2+/calmodulin-dependent protein kinase IIgamma enhances stem-like traits and tumorigenicity of lung cancer cells. Oncotarget. 2015;6:16069–16083.
-
(2015)
Oncotarget
, vol.6
, pp. 16069-16083
-
-
Chai, S.1
Xu, X.2
Wang, Y.3
-
80
-
-
84876296757
-
A broad view of scaffolding suggests that scaffolding proteins can actively control regulation and signaling of multienzyme complexes through allostery
-
R.Nussinov, B.Ma, C.-J.Tsai. A broad view of scaffolding suggests that scaffolding proteins can actively control regulation and signaling of multienzyme complexes through allostery. Biochim Biophys Acta. 2013;1834:820–829.
-
(2013)
Biochim Biophys Acta
, vol.1834
, pp. 820-829
-
-
Nussinov, R.1
Ma, B.2
Tsai, C.-J.3
-
81
-
-
84906938439
-
Oncogenic KRAS signalling in pancreatic cancer
-
S.Eser, A.Schnieke, G.Schneider, et al. Oncogenic KRAS signalling in pancreatic cancer. Br J Cancer. 2014;111:817–822.
-
(2014)
Br J Cancer
, vol.111
, pp. 817-822
-
-
Eser, S.1
Schnieke, A.2
Schneider, G.3
-
85
-
-
84922683604
-
‘Latent drivers’ expand the cancer mutational landscape
-
R.Nussinov, C.-J.Tsai. ‘Latent drivers’ expand the cancer mutational landscape. Curr Opin Struct Biol. 2015;32:25–32.
-
(2015)
Curr Opin Struct Biol
, vol.32
, pp. 25-32
-
-
Nussinov, R.1
Tsai, C.-J.2
-
87
-
-
81555232930
-
Molecular pathogenesis of pancreatic cancer and clinical perspectives
-
D.Matthaios, P.Zarogoulidis, I.Balgouranidou, et al. Molecular pathogenesis of pancreatic cancer and clinical perspectives. Oncology. 2011;81:259–272.
-
(2011)
Oncology
, vol.81
, pp. 259-272
-
-
Matthaios, D.1
Zarogoulidis, P.2
Balgouranidou, I.3
-
88
-
-
84859393143
-
Frequent detection of pancreatic lesions in asymptomatic high-risk individuals
-
quiz e14-
-
M.I.Canto, R.H.Hruban, E.K.Fishman, et al. Frequent detection of pancreatic lesions in asymptomatic high-risk individuals. Gastroenterology. 2012;142:796–804. quiz e14-5
-
(2012)
Gastroenterology
, vol.142
, pp. 796-804
-
-
Canto, M.I.1
Hruban, R.H.2
Fishman, E.K.3
-
90
-
-
52149123619
-
Core signaling pathways in human pancreatic cancers revealed by global genomic analyses
-
S.Jones, X.Zhang, D.W.Parsons, et al Core signaling pathways in human pancreatic cancers revealed by global genomic analyses. Science. 2008;321:1801–1806.
-
(2008)
Science
, vol.321
, pp. 1801-1806
-
-
Jones, S.1
Zhang, X.2
Parsons, D.W.3
-
91
-
-
84869091997
-
Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes
-
A.V.Biankin, N.Waddell, K.S.Kassahn, et al. Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes. Nature. 2012;491:399–405.
-
(2012)
Nature
, vol.491
, pp. 399-405
-
-
Biankin, A.V.1
Waddell, N.2
Kassahn, K.S.3
-
92
-
-
23044485887
-
Concordant loss of MTAP and p16/CDKN2A expression in pancreatic intraepithelial neoplasia: evidence of homozygous deletion in a noninvasive precursor lesion
-
S.R.Hustinx, L.M.Leoni, C.J.Yeo, et al. Concordant loss of MTAP and p16/CDKN2A expression in pancreatic intraepithelial neoplasia: evidence of homozygous deletion in a noninvasive precursor lesion. Modern Pathol: Official J United States Canadian Acad Pathology, Inc. 2005;18:959–963.
-
(2005)
Modern Pathol: Official J United States Canadian Acad Pathology, Inc
, vol.18
, pp. 959-963
-
-
Hustinx, S.R.1
Leoni, L.M.2
Yeo, C.J.3
-
93
-
-
84860321700
-
Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism
-
H.Ying, A.C.Kimmelman, C.A.Lyssiotis, et al. Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism. Cell. 2012;149:656–670.
-
(2012)
Cell
, vol.149
, pp. 656-670
-
-
Ying, H.1
Kimmelman, A.C.2
Lyssiotis, C.A.3
-
94
-
-
84863012865
-
Oncogenic Kras is required for both the initiation and maintenance of pancreatic cancer in mice. The
-
M.A.Collins, F.Bednar, Y.Zhang, et al. Oncogenic Kras is required for both the initiation and maintenance of pancreatic cancer in mice. The. J Clin Investigation. 2012;122:639–653.
-
(2012)
J Clin Investigation
, vol.122
, pp. 639-653
-
-
Collins, M.A.1
Bednar, F.2
Zhang, Y.3
-
95
-
-
84870709449
-
Metastatic pancreatic cancer is dependent on oncogenic Kras in mice
-
M.A.Collins, J.C.Brisset, Y.Zhang, et al. Metastatic pancreatic cancer is dependent on oncogenic Kras in mice. PLoS One. 2012;7:e49707.
-
(2012)
PLoS One
, vol.7
-
-
Collins, M.A.1
Brisset, J.C.2
Zhang, Y.3
-
96
-
-
65649108558
-
A gene expression signature associated with “K-Ras addiction” reveals regulators of EMT and tumor cell survival
-
A.Singh, P.Greninger, D.Rhodes, et al. A gene expression signature associated with “K-Ras addiction” reveals regulators of EMT and tumor cell survival. Cancer Cell. 2009;15:489–500.
-
(2009)
Cancer Cell
, vol.15
, pp. 489-500
-
-
Singh, A.1
Greninger, P.2
Rhodes, D.3
-
97
-
-
80054866000
-
Targeting protein prenylation for cancer therapy
-
N.Berndt, A.D.Hamilton, S.M.Sebti. Targeting protein prenylation for cancer therapy. Nat Rev Cancer. 2011;11:775–791.
-
(2011)
Nat Rev Cancer
, vol.11
, pp. 775-791
-
-
Berndt, N.1
Hamilton, A.D.2
Sebti, S.M.3
-
98
-
-
84900809617
-
Brief overview of selected approaches in targeting pancreatic adenocarcinoma
-
• The authors provide a brief and focused description of current strategies to target pancreatic adenocarcinom
-
W.R.Samore, C.S.Gondi. Brief overview of selected approaches in targeting pancreatic adenocarcinoma. Expert Opin Investig Drugs. 2014;23:793–807.• The authors provide a brief and focused description of current strategies to target pancreatic adenocarcinoma.
-
(2014)
Expert Opin Investig Drugs
, vol.23
, pp. 793-807
-
-
Samore, W.R.1
Gondi, C.S.2
-
100
-
-
84876948298
-
Adjuvant pharmacotherapy in the management of elderly patients with pancreatic cancer
-
R.Maréchal, A.Demols, J.-L.Van Laethem. Adjuvant pharmacotherapy in the management of elderly patients with pancreatic cancer. Drugs Aging. 2013;30:155–165.
-
(2013)
Drugs Aging
, vol.30
, pp. 155-165
-
-
Maréchal, R.1
Demols, A.2
Van Laethem, J.-L.3
-
101
-
-
84938070781
-
Pancreatic cancer: targeting KRAS and the vitamin D receptor via microtubules
-
A.Basseville, S.Bates, T.Fojo. Pancreatic cancer: targeting KRAS and the vitamin D receptor via microtubules. Nat Rev Clin Oncol. 2015;12:442–444.
-
(2015)
Nat Rev Clin Oncol
, vol.12
, pp. 442-444
-
-
Basseville, A.1
Bates, S.2
Fojo, T.3
-
102
-
-
0030727170
-
Prenylation-dependent association of Ki-Ras with microtubules. Evidence for a role in subcellular trafficking
-
J.A.Thissen, J.M.Gross, K.Subramanian, et al. Prenylation-dependent association of Ki-Ras with microtubules. Evidence for a role in subcellular trafficking. J Biol Chem. 1997;272:30362–30370.
-
(1997)
J Biol Chem
, vol.272
, pp. 30362-30370
-
-
Thissen, J.A.1
Gross, J.M.2
Subramanian, K.3
-
103
-
-
0034062812
-
H-ras but not K-ras traffics to the plasma membrane through the exocytic pathway
-
A.Apolloni, I.A.Prior, M.Lindsay, et al. H-ras but not K-ras traffics to the plasma membrane through the exocytic pathway. Mol Cell Biol. 2000;20:2475–2487.
-
(2000)
Mol Cell Biol
, vol.20
, pp. 2475-2487
-
-
Apolloni, A.1
Prior, I.A.2
Lindsay, M.3
-
104
-
-
79953756460
-
Subtypes of pancreatic ductal adenocarcinoma and their differing responses to therapy
-
E.A.Collisson, A.Sadanandam, P.Olson, et al. Subtypes of pancreatic ductal adenocarcinoma and their differing responses to therapy. Nat Med. 2011;17:500–503.
-
(2011)
Nat Med
, vol.17
, pp. 500-503
-
-
Collisson, E.A.1
Sadanandam, A.2
Olson, P.3
-
105
-
-
83355169753
-
Gemcitabine plus nab-paclitaxel is an active regimen in patients with advanced pancreatic cancer: a phase I/II trial
-
D.D.Von Hoff, R.K.Ramanathan, M.J.Borad, et al. Gemcitabine plus nab-paclitaxel is an active regimen in patients with advanced pancreatic cancer: a phase I/II trial. J Clin Oncol. 2011;29:4548–4554.
-
(2011)
J Clin Oncol
, vol.29
, pp. 4548-4554
-
-
Von Hoff, D.D.1
Ramanathan, R.K.2
Borad, M.J.3
-
106
-
-
84922236597
-
Microtubule-targeting agents augment the toxicity of DNA-damaging agents by disrupting intracellular trafficking of DNA repair proteins
-
M.S.Poruchynsky, E.Komlodi-Pasztor, S.Trostel, et al. Microtubule-targeting agents augment the toxicity of DNA-damaging agents by disrupting intracellular trafficking of DNA repair proteins. Proc Natl Acad Sci U S A. 2015;112:1571–1576.
-
(2015)
Proc Natl Acad Sci U S A
, vol.112
, pp. 1571-1576
-
-
Poruchynsky, M.S.1
Komlodi-Pasztor, E.2
Trostel, S.3
-
107
-
-
84920566345
-
A synthetic lethal screen identifies the Vitamin D receptor as a novel gemcitabine sensitizer in pancreatic cancer cells
-
V.Bhattacharjee, Y.Zhou, T.J.Yen. A synthetic lethal screen identifies the Vitamin D receptor as a novel gemcitabine sensitizer in pancreatic cancer cells. Cell Cycle. 2014;13:3839–3856.
-
(2014)
Cell Cycle
, vol.13
, pp. 3839-3856
-
-
Bhattacharjee, V.1
Zhou, Y.2
Yen, T.J.3
-
108
-
-
84938794719
-
Co-occurring genomic alterations define major subsets of KRAS - mutant lung adenocarcinoma with distinct biology, immune profiles, and therapeutic vulnerabilities
-
F.Skoulidis, L.A.Byers, L.Diao, et al. Co-occurring genomic alterations define major subsets of KRAS - mutant lung adenocarcinoma with distinct biology, immune profiles, and therapeutic vulnerabilities. Cancer Discov. 2015;5:860–877.
-
(2015)
Cancer Discov
, vol.5
, pp. 860-877
-
-
Skoulidis, F.1
Byers, L.A.2
Diao, L.3
-
109
-
-
78650236850
-
Chemotherapy, chemoresistance and the changing treatment landscape for NSCLC
-
A.Chang. Chemotherapy, chemoresistance and the changing treatment landscape for NSCLC. Lung Cancer. 2011;71:3–10.
-
(2011)
Lung Cancer
, vol.71
, pp. 3-10
-
-
Chang, A.1
-
110
-
-
0027551192
-
Glutathione S-transferase pi levels in a panel of lung cancer cell lines and its relation to chemo-radiosensitivity
-
T.Hida, Y.Ariyoshi, M.Kuwabara, et al. Glutathione S-transferase pi levels in a panel of lung cancer cell lines and its relation to chemo-radiosensitivity. Jpn J Clin Oncol. 1993;23:14–19.
-
(1993)
Jpn J Clin Oncol
, vol.23
, pp. 14-19
-
-
Hida, T.1
Ariyoshi, Y.2
Kuwabara, M.3
-
111
-
-
24944459001
-
Platinum-based versus non-platinum-based chemotherapy in advanced non-small-cell lung cancer: does cisplatin versus carboplatin make a difference?
-
author reply 7-
-
M.Tiseo, L.Boni, A.Ardizzoni, Platinum-based versus non-platinum-based chemotherapy in advanced non-small-cell lung cancer: does cisplatin versus carboplatin make a difference?. J Clin Oncol. 2005;23:6276–6278. author reply 7-8
-
(2005)
J Clin Oncol
, vol.23
, pp. 6276-6278
-
-
Tiseo, M.1
Boni, L.2
Ardizzoni, A.3
-
112
-
-
0024358188
-
DNA topoisomerase I–targeted chemotherapy of human colon cancer in xenografts
-
B.C.Giovanella, J.S.Stehlin, M.E.Wall, et al. DNA topoisomerase I–targeted chemotherapy of human colon cancer in xenografts. Science. 1989;246:1046–1048.
-
(1989)
Science
, vol.246
, pp. 1046-1048
-
-
Giovanella, B.C.1
Stehlin, J.S.2
Wall, M.E.3
-
113
-
-
0025084410
-
Establishment of a camptothecin analogue (CPT-11)-resistant cell line of human non-small cell lung cancer: characterization and mechanism of resistance
-
F.Kanzawa, Y.Sugimoto, K.Minato, et al. Establishment of a camptothecin analogue (CPT-11)-resistant cell line of human non-small cell lung cancer: characterization and mechanism of resistance. Cancer Res. 1990;50:5919–5924.
-
(1990)
Cancer Res
, vol.50
, pp. 5919-5924
-
-
Kanzawa, F.1
Sugimoto, Y.2
Minato, K.3
-
115
-
-
84937217164
-
A review on anticancer potential of bioactive heterocycle quinoline
-
O.Afzal, S.Kumar, M.R.Haider, et al A review on anticancer potential of bioactive heterocycle quinoline. Eur J Med Chem. 2015;97:871–910.
-
(2015)
Eur J Med Chem
, vol.97
, pp. 871-910
-
-
Afzal, O.1
Kumar, S.2
Haider, M.R.3
-
116
-
-
84881478108
-
PQ1, a quinoline derivative, induces apoptosis in T47D breast cancer cells through activation of caspase-8 and caspase-9
-
Y.Ding, T.A.Nguyen. PQ1, a quinoline derivative, induces apoptosis in T47D breast cancer cells through activation of caspase-8 and caspase-9. Apoptosis. 2013;18:1071–1082.
-
(2013)
Apoptosis
, vol.18
, pp. 1071-1082
-
-
Ding, Y.1
Nguyen, T.A.2
-
117
-
-
51049109896
-
Differential antiproliferative mechanisms of novel derivative of benzimidazo[1,2-alpha]quinoline in colon cancer cells depending on their p53 status
-
M.Sedic, M.Poznic, P.Gehrig, et al. Differential antiproliferative mechanisms of novel derivative of benzimidazo[1,2-alpha]quinoline in colon cancer cells depending on their p53 status. Mol Cancer Ther. 2008;7:2121–2132.
-
(2008)
Mol Cancer Ther
, vol.7
, pp. 2121-2132
-
-
Sedic, M.1
Poznic, M.2
Gehrig, P.3
-
118
-
-
71049121968
-
A combination of indol-3-carbinol and genistein synergistically induces apoptosis in human colon cancer HT-29 cells by inhibiting Akt phosphorylation and progression of autophagy
-
Y.Nakamura, S.Yogosawa, Y.Izutani, et al. A combination of indol-3-carbinol and genistein synergistically induces apoptosis in human colon cancer HT-29 cells by inhibiting Akt phosphorylation and progression of autophagy. Mol Cancer. 2009;8:100.
-
(2009)
Mol Cancer
, vol.8
, pp. 100
-
-
Nakamura, Y.1
Yogosawa, S.2
Izutani, Y.3
-
119
-
-
84942549290
-
An indolylquinoline derivative promotes apoptosis in human lung cancer cells by impairing mitochondrial functions
-
C.Y.Liu, P.T.Wu, J.P.Wang, et al An indolylquinoline derivative promotes apoptosis in human lung cancer cells by impairing mitochondrial functions. Apoptosis. 2015;20:1471–1482.
-
(2015)
Apoptosis
, vol.20
, pp. 1471-1482
-
-
Liu, C.Y.1
Wu, P.T.2
Wang, J.P.3
-
120
-
-
84941013285
-
RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK-positive lung cancer
-
G.Hrustanovic, V.Olivas, E.Pazarentzos, et al. RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK-positive lung cancer. Nat Med. 2015;21:1038–1047.
-
(2015)
Nat Med
, vol.21
, pp. 1038-1047
-
-
Hrustanovic, G.1
Olivas, V.2
Pazarentzos, E.3
-
121
-
-
84960496176
-
Management of advanced non-small cell lung cancers with known mutations or rearrangements: latest evidence and treatment approaches
-
M.Shea, D.B.Costa, D.Rangachari. Management of advanced non-small cell lung cancers with known mutations or rearrangements: latest evidence and treatment approaches. Ther Adv Respir Dis. 2015. doi:10.1177/1753465815617871.
-
(2015)
Ther Adv Respir Dis
-
-
Shea, M.1
Costa, D.B.2
Rangachari, D.3
-
122
-
-
84945491014
-
Targeting Chromatin-Mediated Transcriptional Control of Gene Expression in Non-Small Cell Lung Cancer Therapy: Preclinical Rationale and Clinical Results
-
A.Pasini, A.Delmonte, A.Tesei, et al. Targeting Chromatin-Mediated Transcriptional Control of Gene Expression in Non-Small Cell Lung Cancer Therapy: Preclinical Rationale and Clinical Results. Drugs. 2015;75:1757–1771.
-
(2015)
Drugs
, vol.75
, pp. 1757-1771
-
-
Pasini, A.1
Delmonte, A.2
Tesei, A.3
-
123
-
-
84945492841
-
Exploiting a novel miR-519c-HuR-ABCG2 regulatory pathway to overcome chemoresistance in colorectal cancer
-
K.K.To, W.W.Leung, S.S.Ng. Exploiting a novel miR-519c-HuR-ABCG2 regulatory pathway to overcome chemoresistance in colorectal cancer. Exp Cell Res. 2015;338:222–231.
-
(2015)
Exp Cell Res
, vol.338
, pp. 222-231
-
-
To, K.K.1
Leung, W.W.2
Ng, S.S.3
-
124
-
-
84927641895
-
Direct Attack on RAS: Intramolecular Communication and Mutation-Specific Effects
-
K.Marcus, C.Mattos. Direct Attack on RAS: Intramolecular Communication and Mutation-Specific Effects. Clin Cancer Res. 2015;21:1810–1818.
-
(2015)
Clin Cancer Res
, vol.21
, pp. 1810-1818
-
-
Marcus, K.1
Mattos, C.2
-
125
-
-
84927632705
-
Metabolic dependencies in RAS-driven cancers
-
A.C.Kimmelman. Metabolic dependencies in RAS-driven cancers. Clin Cancer Res. 2015;21:1828–1834.
-
(2015)
Clin Cancer Res
, vol.21
, pp. 1828-1834
-
-
Kimmelman, A.C.1
-
126
-
-
84964523699
-
Inhibitors of Ras-SOS Interactions
-
S.Lu, H.Jang, J.Zhang, et al. Inhibitors of Ras-SOS Interactions. ChemMedChem. 2015. DOI:10.1002/cmdc.201500481.
-
(2015)
ChemMedChem
-
-
Lu, S.1
Jang, H.2
Zhang, J.3
-
128
-
-
84937957816
-
Ras-GTP dimers activate the Mitogen-Activated Protein Kinase (MAPK) pathway
-
X.Nan, T.M.Tamguney, E.A.Collisson, et al. Ras-GTP dimers activate the Mitogen-Activated Protein Kinase (MAPK) pathway. Proc Natl Acad Sci U S A. 2015;112:7996–8001.
-
(2015)
Proc Natl Acad Sci U S A
, vol.112
, pp. 7996-8001
-
-
Nan, X.1
Tamguney, T.M.2
Collisson, E.A.3
-
129
-
-
84927144988
-
Mechanisms of Membrane Binding of Small GTPase K-Ras4B Farnesylated Hypervariable Region
-
H.Jang, S.J.Abraham, T.S.Chavan, et al. Mechanisms of Membrane Binding of Small GTPase K-Ras4B Farnesylated Hypervariable Region. J Biol Chem. 2015;290:9465–9477.
-
(2015)
J Biol Chem
, vol.290
, pp. 9465-9477
-
-
Jang, H.1
Abraham, S.J.2
Chavan, T.S.3
-
130
-
-
84948464277
-
High-affinity interaction of the K-Ras4B hypervariable region with the Ras active site
-
T.S.Chavan, H.Jang, L.Khavrutskii, et al. High-affinity interaction of the K-Ras4B hypervariable region with the Ras active site. Biophys J. 2015;109:2602–2613.
-
(2015)
Biophys J
, vol.109
, pp. 2602-2613
-
-
Chavan, T.S.1
Jang, H.2
Khavrutskii, L.3
-
131
-
-
84929077789
-
Regulation of RAF protein kinases in ERK signalling
-
H.Lavoie, M.Therrien. Regulation of RAF protein kinases in ERK signalling. Nat Rev Mol Cell Biol. 2015;16:281–298.
-
(2015)
Nat Rev Mol Cell Biol
, vol.16
, pp. 281-298
-
-
Lavoie, H.1
Therrien, M.2
-
132
-
-
84948469412
-
GTP Binding and Oncogenic Mutations May Attenuate Hypervariable Region (HVR)-Catalytic Domain Interactions in Small GTPase K-Ras4B, Exposing the Effector Binding Site
-
S.Lu, A.Banerjee, H.Jang, et al. GTP Binding and Oncogenic Mutations May Attenuate Hypervariable Region (HVR)-Catalytic Domain Interactions in Small GTPase K-Ras4B, Exposing the Effector Binding Site. J Biol Chem. 2015;290:28887–28900.
-
(2015)
J Biol Chem
, vol.290
, pp. 28887-28900
-
-
Lu, S.1
Banerjee, A.2
Jang, H.3
-
133
-
-
84969545626
-
DARC: mapping surface topography by ray-casting for effective virtual screening at protein interaction sites
-
R.Gowthaman, S.A.Miller, S.A.Rogers, et al. DARC: mapping surface topography by ray-casting for effective virtual screening at protein interaction sites. J Med Chem. 2015. DOI:10.1021/acs.jmedchem.5b00150.
-
(2015)
J Med Chem
-
-
Gowthaman, R.1
Miller, S.A.2
Rogers, S.A.3
-
134
-
-
84940891771
-
Stabilization of Protein-Protein Interactions in chemical biology and drug discovery
-
D.Bier, P.Thiel, J.Briels, et al. Stabilization of Protein-Protein Interactions in chemical biology and drug discovery. Prog Biophys Mol Biol. 2015;119:10–19.
-
(2015)
Prog Biophys Mol Biol
, vol.119
, pp. 10-19
-
-
Bier, D.1
Thiel, P.2
Briels, J.3
-
135
-
-
84940893619
-
Helix mimetics: recent developments
-
A.J.Wilson. Helix mimetics: recent developments. Prog Biophys Mol Biol. 2015;119:33–40.
-
(2015)
Prog Biophys Mol Biol
, vol.119
, pp. 33-40
-
-
Wilson, A.J.1
-
136
-
-
84921731523
-
Small-molecule inhibitors that target protein-protein interactions in the RAD51 family of recombinases
-
D.E.Scott, A.G.Coyne, A.Venkitaraman, et al Small-molecule inhibitors that target protein-protein interactions in the RAD51 family of recombinases. ChemMedChem. 2015;10:296–303.
-
(2015)
ChemMedChem
, vol.10
, pp. 296-303
-
-
Scott, D.E.1
Coyne, A.G.2
Venkitaraman, A.3
-
137
-
-
84873433440
-
Using a fragment-based approach to target protein-protein interactions
-
D.E.Scott, M.T.Ehebauer, T.Pukala, et al. Using a fragment-based approach to target protein-protein interactions. Chembiochem. 2013;14:332–342.
-
(2013)
Chembiochem
, vol.14
, pp. 332-342
-
-
Scott, D.E.1
Ehebauer, M.T.2
Pukala, T.3
-
138
-
-
84860538154
-
Structural biology and drug discovery for protein-protein interactions
-
H.Jubb, A.P.Higueruelo, A.Winter, et al. Structural biology and drug discovery for protein-protein interactions. Trends Pharmacol Sci. 2012;33:241–248.
-
(2012)
Trends Pharmacol Sci
, vol.33
, pp. 241-248
-
-
Jubb, H.1
Higueruelo, A.P.2
Winter, A.3
-
139
-
-
84922161680
-
YAP regulates S-phase entry in endothelial cells
-
•• In this work the authors observe that YAP is required for proliferation in endothelial cells but not HeLa cells. YAP is required for S-phase entry and its absence causes cells to accumulate in G1. These observations point to cell-cell contacts regulating cell-cycle via the Hippo/YAP1 and provide a key mechanism in promoting cell proliferation and surviva
-
Z.Shen, B.Z.Stanger, D.M.Koepp. YAP regulates S-phase entry in endothelial cells. PLoS One. 2015;10:e0117522.•• In this work the authors observe that YAP is required for proliferation in endothelial cells but not HeLa cells. YAP is required for S-phase entry and its absence causes cells to accumulate in G1. These observations point to cell-cell contacts regulating cell-cycle via the Hippo/YAP1 and provide a key mechanism in promoting cell proliferation and survival.
-
(2015)
PLoS One
, vol.10
-
-
Shen, Z.1
Stanger, B.Z.2
Koepp, D.M.3
|