-
1
-
-
0028331587
-
Farnesyltransferase inhibitors: Ras research yields a potential cancer therapeutic
-
Gibbs J., Oliff A., Kohl N.E. Farnesyltransferase inhibitors: Ras research yields a potential cancer therapeutic. Cell. 77:1994;175-178.
-
(1994)
Cell
, vol.77
, pp. 175-178
-
-
Gibbs, J.1
Oliff, A.2
Kohl, N.E.3
-
2
-
-
0033620684
-
Farnesyltransferase inhibitors: Targeting the molecular basis of cancer
-
This is a recent comprehensive review of the biological effects of FTIs.
-
Oliff A. Farnesyltransferase inhibitors: targeting the molecular basis of cancer. Biochim Biophys Acta. 1423:1999;C19-C30. This is a recent comprehensive review of the biological effects of FTIs.
-
(1999)
Biochim Biophys Acta
, vol.1423
-
-
Oliff, A.1
-
3
-
-
0029966304
-
Protein prenyltransferases
-
Casey P.J., Seabra M.C. Protein prenyltransferases. J Biol Chem. 271:1996;5289-5292.
-
(1996)
J Biol Chem
, vol.271
, pp. 5289-5292
-
-
Casey, P.J.1
Seabra, M.C.2
-
4
-
-
0029898894
-
Protein prenylation: Molecular mechanisms and functional consequences
-
Zhang F.L., Casey P.J. Protein prenylation: molecular mechanisms and functional consequences. Annu Rev Biochem. 65:1996;241-269.
-
(1996)
Annu Rev Biochem
, vol.65
, pp. 241-269
-
-
Zhang, F.L.1
Casey, P.J.2
-
5
-
-
0027323459
-
Benzodiazepine peptidomimetics: Potent inhibitors of Ras farnesylation in animal cells
-
James G.L., Goldstein J.L., Brown M.S., Rawson T.E., Somers T.C., McDowell R.S., Crowley C.W., Lucas B.K., Levinson A.D., Marsters J.C. Benzodiazepine peptidomimetics: potent inhibitors of Ras farnesylation in animal cells. Science. 260:1993;1937-1942.
-
(1993)
Science
, vol.260
, pp. 1937-1942
-
-
James, G.L.1
Goldstein, J.L.2
Brown, M.S.3
Rawson, T.E.4
Somers, T.C.5
McDowell, R.S.6
Crowley, C.W.7
Lucas, B.K.8
Levinson, A.D.9
Marsters, J.C.10
-
6
-
-
0027248872
-
Selective inhibition of ras-dependent transformation by a farnesyltransferase inhibitor
-
Kohl N.E., Mosser S.D., deSolms S.J., Giuliani E.A., Pompliano D.L., Graham S.L., Smith R.L., Scolnick E.M., Oliff A., Gibbs J.B. Selective inhibition of ras-dependent transformation by a farnesyltransferase inhibitor. Science. 260:1993;1934-1937.
-
(1993)
Science
, vol.260
, pp. 1934-1937
-
-
Kohl, N.E.1
Mosser, S.D.2
DeSolms, S.J.3
Giuliani, E.A.4
Pompliano, D.L.5
Graham, S.L.6
Smith, R.L.7
Scolnick, E.M.8
Oliff, A.9
Gibbs, J.B.10
-
7
-
-
0028318136
-
Farnesyltransferase inhibition causes morphological reversion of ras-transformed cells by a complex mechanism that involves regulation of the actin cytoskeleton
-
Prendergast G.C., Davide J.P., deSolms S.J., Giuliani E., Graham S., Gibbs J.B., Oliff A., Kohl N.E. Farnesyltransferase inhibition causes morphological reversion of ras-transformed cells by a complex mechanism that involves regulation of the actin cytoskeleton. Mol Cell Biol. 14:1994;4193-4202.
-
(1994)
Mol Cell Biol
, vol.14
, pp. 4193-4202
-
-
Prendergast, G.C.1
Davide, J.P.2
DeSolms, S.J.3
Giuliani, E.4
Graham, S.5
Gibbs, J.B.6
Oliff, A.7
Kohl, N.E.8
-
8
-
-
0028835253
-
A peptidomimetic inhibitor of farnesyl:protein transferase blocks the anchorage-dependent and -independent growth of human tumor cell lines
-
Sepp-Lorenzino L., Ma Z., Rands E., Kohl N.E., Gibbs J.B., Oliff A., Rosen N. A peptidomimetic inhibitor of farnesyl:protein transferase blocks the anchorage-dependent and -independent growth of human tumor cell lines. Cancer Res. 55:1995;5302-5309.
-
(1995)
Cancer Res
, vol.55
, pp. 5302-5309
-
-
Sepp-Lorenzino, L.1
Ma, Z.2
Rands, E.3
Kohl, N.E.4
Gibbs, J.B.5
Oliff, A.6
Rosen, N.7
-
9
-
-
0031983131
-
A farnesyltransferase inhibitor induces tumor regression in transgenic mice harboring multiple oncogenic mutations by mediating alterations in both cell cycle control and apoptosis
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•], this study established that tumor regression induced by FTI treatment in H-Ras transgenic models is based upon both cycle cell inhibition and p53-independent apoptosis.
-
•], this study established that tumor regression induced by FTI treatment in H-Ras transgenic models is based upon both cycle cell inhibition and p53-independent apoptosis.
-
(1998)
Mol Cell Biol
, vol.18
, pp. 85-92
-
-
Barrington, R.E.1
Subler, A.2
Rands, E.3
Omer, C.A.4
Miller, P.J.5
Hundley, J.E.6
Koester, S.J.7
Troyer, D.A.8
Bearss, D.J.9
Conner, M.W.10
-
10
-
-
0029150669
-
Inhibition of farnesyltransferase induces regression of mammary and salivary carcinomas in ras transgenic mice
-
Kohl N.E., Omer C.A., Conner M.W., Anthony N.J., Davide J.P., deSolms S.J., Giuliani E.A., Gomez R.J., Graham S.L., Hamilton K.et al. Inhibition of farnesyltransferase induces regression of mammary and salivary carcinomas in ras transgenic mice. Nat Med. 1:1995;792-797.
-
(1995)
Nat Med
, vol.1
, pp. 792-797
-
-
Kohl, N.E.1
Omer, C.A.2
Conner, M.W.3
Anthony, N.J.4
Davide, J.P.5
DeSolms, S.J.6
Giuliani, E.A.7
Gomez, R.J.8
Graham, S.L.9
Hamilton, K.10
-
11
-
-
0028603395
-
Protein farnesyltransferase inhibitors block the growth of ras-dependent tumors in nude mice
-
Kohl N.E., Redner F., Mosser S., Guiliani E.A., deSolms S.J., Conner M.W., Anthony N.J., Holtz W.J., Gomez R.P., Lee T.J.et al. Protein farnesyltransferase inhibitors block the growth of ras-dependent tumors in nude mice. Proc Natl Acad Sci USA. 91:1994;9141-9145.
-
(1994)
Proc Natl Acad Sci USA
, vol.91
, pp. 9141-9145
-
-
Kohl, N.E.1
Redner, F.2
Mosser, S.3
Guiliani, E.A.4
DeSolms, S.J.5
Conner, M.W.6
Anthony, N.J.7
Holtz, W.J.8
Gomez, R.P.9
Lee, T.J.10
-
12
-
-
14344254868
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Antitumor activity of SCH 6636, an orally bioavailable tricyclic inhibitor of farnesyl protein transferase, in human tumor xenograft models and Wap-Ras transgenic mice
-
•], this study indicated that the antineoplastic effects of FTIs in H-Ras transgenic models involves both cell cycle inhibition and p53-independent apoptosis.
-
•], this study indicated that the antineoplastic effects of FTIs in H-Ras transgenic models involves both cell cycle inhibition and p53-independent apoptosis.
-
(1998)
Cancer Res
, vol.58
, pp. 4947-4956
-
-
Liu, M.1
Bryant, M.S.2
Chen, J.3
Lee, S.4
Yaremko, B.5
Lipari, P.6
Malkowski, M.7
Ferrari, E.8
Nielsen, L.9
Prioli, N.10
-
13
-
-
0032521211
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Antitumor effect of a farnesyl protein transferase inhibitor in mammary and lymphoid tumors overexpressing N-ras in transgenic mice
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This study shows that FTIs can induce regression of N-Ras-dependent tumors without inhibiting N-Ras isoprenylation (presumably due to alternate geranylgeranylation of N-Ras by GGT-I [29]).
-
Mangues R., Corral T., Kohl N.E., Symmans W.F., Lu S., Malumbres M., Gibbs J.B., Oliff A., Pellicer A. Antitumor effect of a farnesyl protein transferase inhibitor in mammary and lymphoid tumors overexpressing N-ras in transgenic mice. Cancer Res. 58:1998;1253-1259. This study shows that FTIs can induce regression of N-Ras-dependent tumors without inhibiting N-Ras isoprenylation (presumably due to alternate geranylgeranylation of N-Ras by GGT-I [29]).
-
(1998)
Cancer Res
, vol.58
, pp. 1253-1259
-
-
Mangues, R.1
Corral, T.2
Kohl, N.E.3
Symmans, W.F.4
Lu, S.5
Malumbres, M.6
Gibbs, J.B.7
Oliff, A.8
Pellicer, A.9
-
14
-
-
0028869067
-
Inhibition of human tumor xenograft growth by treatment with the farnesyltransferase inhibitor B956
-
Nagasu T., Yoshimatsu K., Rowell C., Lewis M.D., Garcia A.M. Inhibition of human tumor xenograft growth by treatment with the farnesyltransferase inhibitor B956. Cancer Res. 55:1995;5310-5314.
-
(1995)
Cancer Res
, vol.55
, pp. 5310-5314
-
-
Nagasu, T.1
Yoshimatsu, K.2
Rowell, C.3
Lewis, M.D.4
Garcia, A.M.5
-
15
-
-
0032900619
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Treatment with farnesyl-protein transferase inhibitor induces regression of mammary tumors in transforming growth factor (TGF) alpha and TGF alpha/neu transgenic mice by inhibition of mitogenic activity and induction of apoptosis
-
Norgaard P., Law B., Joseph H., Page D.L., Shyr Y., Mays D., Peitenpol J.A., Kohl N.E., Oliff A., Coffey R.J.et al. Treatment with farnesyl-protein transferase inhibitor induces regression of mammary tumors in transforming growth factor (TGF) alpha and TGF alpha/neu transgenic mice by inhibition of mitogenic activity and induction of apoptosis. Clin Cancer Res. 5:1999;35-42.
-
(1999)
Clin Cancer Res
, vol.5
, pp. 35-42
-
-
Norgaard, P.1
Law, B.2
Joseph, H.3
Page, D.L.4
Shyr, Y.5
Mays, D.6
Peitenpol, J.A.7
Kohl, N.E.8
Oliff, A.9
Coffey, R.J.10
-
16
-
-
0031050738
-
Farnesyltransferase inhibitors induce apoptosis in Ras-transformed cells denied substratum attachment
-
Lebowitz P.F., Sakamuro D., Prendergast G.C. Farnesyltransferase inhibitors induce apoptosis in Ras-transformed cells denied substratum attachment. Cancer Res. 57:1997;708-713.
-
(1997)
Cancer Res
, vol.57
, pp. 708-713
-
-
Lebowitz, P.F.1
Sakamuro, D.2
Prendergast, G.C.3
-
17
-
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0032417689
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Farnesyltransferase inhibitors induce cytochrome c release and caspase 3 activation preferentially in transformed cells
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This study established that cytokines suppress the ability of FTIs to induce apoptosis of cells transformed by mutated K-Ras. With [16], the results offered a possible explanation for how FTIs can elicit tumor regression in Ras transgenic models (where there may be a deficiency in certain cytokine-mediated survival cues).
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Suzuki N., Urano J., Tamanoi F. Farnesyltransferase inhibitors induce cytochrome c release and caspase 3 activation preferentially in transformed cells. Proc Natl Acad Sci USA. 95:1998;15356-15361. This study established that cytokines suppress the ability of FTIs to induce apoptosis of cells transformed by mutated K-Ras. With [16], the results offered a possible explanation for how FTIs can elicit tumor regression in Ras transgenic models (where there may be a deficiency in certain cytokine-mediated survival cues).
-
(1998)
Proc Natl Acad Sci USA
, vol.95
, pp. 15356-15361
-
-
Suzuki, N.1
Urano, J.2
Tamanoi, F.3
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18
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0033198386
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Activation of the IGF-PI3′K pathway masks the proapoptotic effects of farnesyltransferase inhibitors
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This study provided evidence that the status of the PI3K-AKT pathway determines whether FTIs suppress proliferation or induce apoptosis. It also identified fundamental differences in survival signals needed in normal and Ras-transformed cells, the latter of which rely on either AKT activation or an FTI-targeted pathway. Furthermore, this study suggests that clinical efficacy may require a combination of FTIs and pharmacological inhibitors for PI3K or AKT.
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Du W., Liu A., Prendergast G.C. Activation of the IGF-PI3′K pathway masks the proapoptotic effects of farnesyltransferase inhibitors. Cancer Res. 59:1999;4208-4212. This study provided evidence that the status of the PI3K-AKT pathway determines whether FTIs suppress proliferation or induce apoptosis. It also identified fundamental differences in survival signals needed in normal and Ras-transformed cells, the latter of which rely on either AKT activation or an FTI-targeted pathway. Furthermore, this study suggests that clinical efficacy may require a combination of FTIs and pharmacological inhibitors for PI3K or AKT.
-
(1999)
Cancer Res
, vol.59
, pp. 4208-4212
-
-
Du, W.1
Liu, A.2
Prendergast, G.C.3
-
19
-
-
0030749458
-
Farnesyltransferase inhibitors and cancer treatment: Targeting simply Ras?
-
Cox A.D., Der C.J. Farnesyltransferase inhibitors and cancer treatment: targeting simply Ras? Biochim Biophys Acta. 1333:1997;F51-F71.
-
(1997)
Biochim Biophys Acta
, vol.1333
-
-
Cox, A.D.1
Der, C.J.2
-
20
-
-
0032541625
-
Non-Ras targets for farnesyltransferase inhibitors: Focus on Rho
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This is a recent review that surveys in more detail the questions concerning the FTI mechanism and the evidence that FTIs act by affecting Rho activity in transformed cells.
-
Lebowitz P.F., Prendergast G.C. Non-Ras targets for farnesyltransferase inhibitors: focus on Rho. Oncogene. 17:1998;1439-1447. This is a recent review that surveys in more detail the questions concerning the FTI mechanism and the evidence that FTIs act by affecting Rho activity in transformed cells.
-
(1998)
Oncogene
, vol.17
, pp. 1439-1447
-
-
Lebowitz, P.F.1
Prendergast, G.C.2
-
21
-
-
0021711754
-
Metabolic turnover of human c-RasH p21 protein of EJ bladder carcinoma and its normal cellular and viral homologs
-
Ulsh L.S., Shih T.Y. Metabolic turnover of human c-RasH p21 protein of EJ bladder carcinoma and its normal cellular and viral homologs. Mol Cell Biol. 4:1984;1647-1652.
-
(1984)
Mol Cell Biol
, vol.4
, pp. 1647-1652
-
-
Ulsh, L.S.1
Shih, T.Y.2
-
22
-
-
0032577481
-
Gene trapping identifies inhibitors of oncogenic transformation: The tissue inhibitor of metalloproteinases-3 (TIMP3) and collagen type I-alpha-2 (COL1A2) are epidermal growth factor-regulated growth repressors
-
Andreu T., Beckers T., Thoenes E., Hilgard P., von Melchner H. Gene trapping identifies inhibitors of oncogenic transformation: the tissue inhibitor of metalloproteinases-3 (TIMP3) and collagen type I-alpha-2 (COL1A2) are epidermal growth factor-regulated growth repressors. J Biol Chem. 273:1998;13848-13854.
-
(1998)
J Biol Chem
, vol.273
, pp. 13848-13854
-
-
Andreu, T.1
Beckers, T.2
Thoenes, E.3
Hilgard, P.4
Von Melchner, H.5
-
23
-
-
0029845481
-
Suppression of tumorigenicity in Ras-transformed fibroblasts by alpha 2(I) collagen
-
Travers H., French N.S., Norton J.D. Suppression of tumorigenicity in Ras-transformed fibroblasts by alpha 2(I) collagen. Cell Growth Diff. 7:1996;1353-1360.
-
(1996)
Cell Growth Diff
, vol.7
, pp. 1353-1360
-
-
Travers, H.1
French, N.S.2
Norton, J.D.3
-
24
-
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0033121278
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Elevation of α2(I) collagen, a suppressor of Ras transformation, is required for stable phenotypic reversion by farnesyltransferase inhibitors
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This study showed that FTIs must regulate gene expression to induce phenotypic reversion, a phenomenon which is correlated closely with loss of anchorage-independent growth capacity in fibroblast models.
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Du W., Lebowitz P.F., Prendergast G.C. Elevation of α2(I) collagen, a suppressor of Ras transformation, is required for stable phenotypic reversion by farnesyltransferase inhibitors. Cancer Res. 59:1999;2059-2063. This study showed that FTIs must regulate gene expression to induce phenotypic reversion, a phenomenon which is correlated closely with loss of anchorage-independent growth capacity in fibroblast models.
-
(1999)
Cancer Res
, vol.59
, pp. 2059-2063
-
-
Du, W.1
Lebowitz, P.F.2
Prendergast, G.C.3
-
25
-
-
0027998986
-
The CAAX peptidomimetic compound B581 specifically blocks farnesylated, but not geranylgeranylated or myristylated, oncogenic ras signaling and transformation
-
Cox A.D., Garcia A.M., Westwick J.K., Kowalczyk J.J., Lewis M.D., Brenner D.A., Der C.J. The CAAX peptidomimetic compound B581 specifically blocks farnesylated, but not geranylgeranylated or myristylated, oncogenic ras signaling and transformation. J Biol Chem. 269:1994;1-4.
-
(1994)
J Biol Chem
, vol.269
, pp. 1-4
-
-
Cox, A.D.1
Garcia, A.M.2
Westwick, J.K.3
Kowalczyk, J.J.4
Lewis, M.D.5
Brenner, D.A.6
Der, C.J.7
-
26
-
-
0028892646
-
Evidence that farnesyl transferase inhibitors suppress Ras transformation by interfering with Rho activity
-
Lebowitz P.F., Davide J.P., Prendergast G.C. Evidence that farnesyl transferase inhibitors suppress Ras transformation by interfering with Rho activity. Mol Cell Biol. 15:1995;6613-6622.
-
(1995)
Mol Cell Biol
, vol.15
, pp. 6613-6622
-
-
Lebowitz, P.F.1
Davide, J.P.2
Prendergast, G.C.3
-
27
-
-
0030952552
-
Inhibition of the prenylation of K-Ras, but not H- Or N-Ras, is highly resistant to CAAX peptidomimetics and requires both a farnesyltransferase and a geranylgeranyltransferase-I inhibitor in human tumor cell lines
-
Lerner E.C., Zhang T.T., Knowles D.B., Qian Y.M., Hamilton A.D., Sebti S.M. Inhibition of the prenylation of K-Ras, but not H- or N-Ras, is highly resistant to CAAX peptidomimetics and requires both a farnesyltransferase and a geranylgeranyltransferase-I inhibitor in human tumor cell lines. Oncogene. 15:1997;1283-1288.
-
(1997)
Oncogene
, vol.15
, pp. 1283-1288
-
-
Lerner, E.C.1
Zhang, T.T.2
Knowles, D.B.3
Qian, Y.M.4
Hamilton, A.D.5
Sebti, S.M.6
-
28
-
-
0031960133
-
Effects of the farnesyltransferase inhibitor UCF-1C/manumycin on growth and p21-Ras post-translational processing in NIH3T3 cells
-
Servais P., Gulbis B., Fokan D., Galand P. Effects of the farnesyltransferase inhibitor UCF-1C/manumycin on growth and p21-Ras post-translational processing in NIH3T3 cells. Int J Cancer. 76:1998;601-608.
-
(1998)
Int J Cancer
, vol.76
, pp. 601-608
-
-
Servais, P.1
Gulbis, B.2
Fokan, D.3
Galand, P.4
-
29
-
-
0030923192
-
K- And N-Ras is geranylgeranylated in cells treated with farnesyl protein transferase inhibitors
-
Whyte D.B., Kirschmeier P., Hockenberry T.N., Nunez-Olivia I., James L., Catino J.J., Bishop W.R., Pai J.K. K- and N-Ras is geranylgeranylated in cells treated with farnesyl protein transferase inhibitors. J Biol Chem. 272:1997;14459-14464.
-
(1997)
J Biol Chem
, vol.272
, pp. 14459-14464
-
-
Whyte, D.B.1
Kirschmeier, P.2
Hockenberry, T.N.3
Nunez-Olivia, I.4
James, L.5
Catino, J.J.6
Bishop, W.R.7
Pai, J.K.8
-
31
-
-
0032440248
-
Functional interaction between RhoB and the transcription factor DB1
-
Lebowitz P., Prendergast G.P. Functional interaction between RhoB and the transcription factor DB1. Cell Adhes Comm. 4:1998;1-11.
-
(1998)
Cell Adhes Comm
, vol.4
, pp. 1-11
-
-
Lebowitz, P.1
Prendergast, G.P.2
-
32
-
-
0028998476
-
Regulation of Ras-related RhoB protein expression during the cell cycle
-
Zalcman G., Closson V., Linares-Cruz G., Leregours F., Honore N., Tavitian A., Olofsson B. Regulation of Ras-related RhoB protein expression during the cell cycle. Oncogene. 10:1995;1935-1945.
-
(1995)
Oncogene
, vol.10
, pp. 1935-1945
-
-
Zalcman, G.1
Closson, V.2
Linares-Cruz, G.3
Leregours, F.4
Honore, N.5
Tavitian, A.6
Olofsson, B.7
-
33
-
-
0033539150
-
Regulation of epidermal growth factor receptor traffic by the small GTPase RhoB
-
This study defined a function for RhoB in trafficking of the epidermal growth factor receptor. Elucidation of this function suggests a broad and important role for RhoB in cell growth control, due to its ability to regulate cell surface expression of various cytokine and adhesion receptors.
-
Gample A.P., Parker P., Mellor H. Regulation of epidermal growth factor receptor traffic by the small GTPase RhoB. Curr Biol. 9:1999;955-958. This study defined a function for RhoB in trafficking of the epidermal growth factor receptor. Elucidation of this function suggests a broad and important role for RhoB in cell growth control, due to its ability to regulate cell surface expression of various cytokine and adhesion receptors.
-
(1999)
Curr Biol
, vol.9
, pp. 955-958
-
-
Gample, A.P.1
Parker, P.2
Mellor, H.3
-
34
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0032570560
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PRK1 is targeted to endosomes by the small GTPase, RhoB
-
This study established that RhoB recruits PRK/PKN to the endosome, analogous to the manner in which Ras recruits its effector kinase Raf to the plasma membrane.
-
Mellor J., Flynn P., Nobes C.D., Hall A., Parker P.J. PRK1 is targeted to endosomes by the small GTPase, RhoB. J Biol Chem. 273:1998;4811-4814. This study established that RhoB recruits PRK/PKN to the endosome, analogous to the manner in which Ras recruits its effector kinase Raf to the plasma membrane.
-
(1998)
J Biol Chem
, vol.273
, pp. 4811-4814
-
-
Mellor, J.1
Flynn, P.2
Nobes, C.D.3
Hall, A.4
Parker, P.J.5
-
35
-
-
0030916369
-
Farnesyltransferase inhibitors alter the prenylation and growth-stimulating function of RhoB
-
Lebowitz P., Casey P.J., Prendergast G.C., Thissen J. Farnesyltransferase inhibitors alter the prenylation and growth-stimulating function of RhoB. J Biol Chem. 272:1997;15591-15594.
-
(1997)
J Biol Chem
, vol.272
, pp. 15591-15594
-
-
Lebowitz, P.1
Casey, P.J.2
Prendergast, G.C.3
Thissen, J.4
-
36
-
-
0029057465
-
Critical role of Rho in cell transformation by oncogenic Ras
-
Prendergast G.C., Khosravi-Far R., Solski P., Kurzawa H., Lebowitz P., Der C.J. Critical role of Rho in cell transformation by oncogenic Ras. Oncogene. 10:1995;2289-2296.
-
(1995)
Oncogene
, vol.10
, pp. 2289-2296
-
-
Prendergast, G.C.1
Khosravi-Far, R.2
Solski, P.3
Kurzawa, H.4
Lebowitz, P.5
Der, C.J.6
-
37
-
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0033016719
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Cell growth inhibition by farnesyltransferase inhibitors is mediated by gain of geranylgeranylated RhoB
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This study showed that the elevation of RhoB-GG elicited by FTI treatment is sufficient to mediate both the cytoskeletal and antiproliferative activities of FTIs in transformed cells. Evidence that RhoB is necessary for FTIs to mediate these effects was shown in [16,26,35]. The finding that RhoB-GG can mimic aspects of FTI treatment established in principle the idea that gain-of-function effects have an important role in FTI biology.
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Du W., Lebowitz P., Prendergast G.C. Cell growth inhibition by farnesyltransferase inhibitors is mediated by gain of geranylgeranylated RhoB. Mol Cell Biol. 19:1999;1831-1840. This study showed that the elevation of RhoB-GG elicited by FTI treatment is sufficient to mediate both the cytoskeletal and antiproliferative activities of FTIs in transformed cells. Evidence that RhoB is necessary for FTIs to mediate these effects was shown in [16,26,35]. The finding that RhoB-GG can mimic aspects of FTI treatment established in principle the idea that gain-of-function effects have an important role in FTI biology.
-
(1999)
Mol Cell Biol
, vol.19
, pp. 1831-1840
-
-
Du, W.1
Lebowitz, P.2
Prendergast, G.C.3
-
38
-
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0033231190
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Geranylgeranylated RhoB mediates suppression of human tumor cell growth by farnesyltransferase inhibitors
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This study proved that RhoB-GG is sufficient to inhibit the proliferation of frank human carcinoma cells with diverse genetic alterations, in a manner which correlated with FTI susceptibility. There was no correlation between susceptibility to RhoB-GG and Ras or p53 status, similar to FTIs [8]. RhoB-GG elevation elicited by FTIs can explain how FTIs can block malignant growth of cells which lack Ras mutations or a requirement for Ras.
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Du W., Prendergast G.C. Geranylgeranylated RhoB mediates suppression of human tumor cell growth by farnesyltransferase inhibitors. Cancer Res. 57:1999;5492-5496. This study proved that RhoB-GG is sufficient to inhibit the proliferation of frank human carcinoma cells with diverse genetic alterations, in a manner which correlated with FTI susceptibility. There was no correlation between susceptibility to RhoB-GG and Ras or p53 status, similar to FTIs [8]. RhoB-GG elevation elicited by FTIs can explain how FTIs can block malignant growth of cells which lack Ras mutations or a requirement for Ras.
-
(1999)
Cancer Res
, vol.57
, pp. 5492-5496
-
-
Du, W.1
Prendergast, G.C.2
-
39
-
-
0032939619
-
Rho GTPases are overexpressed in human tumors
-
Fritz G., Just I., Kaina B. Rho GTPases are overexpressed in human tumors. Int J Cancer. 81:1999;682-687.
-
(1999)
Int J Cancer
, vol.81
, pp. 682-687
-
-
Fritz, G.1
Just, I.2
Kaina, B.3
-
40
-
-
0032935495
-
An essential part for Rho-associated kinase in the transcellular invasion of tumor cells
-
Itoh K., Yoshioka K., Akedo H., Uehata M., Ishizaki T., Narumiya S. An essential part for Rho-associated kinase in the transcellular invasion of tumor cells. Nat Med. 5:1999;221-225.
-
(1999)
Nat Med
, vol.5
, pp. 221-225
-
-
Itoh, K.1
Yoshioka, K.2
Akedo, H.3
Uehata, M.4
Ishizaki, T.5
Narumiya, S.6
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41
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-
0032410157
-
Orthotopic models are necessary to predict therapy of transplantable tumors in mice
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Killion J.J., Radinsky R., Fidler I.J. Orthotopic models are necessary to predict therapy of transplantable tumors in mice. Cancer Metast Rev. 17:1999;279-284.
-
(1999)
Cancer Metast Rev
, vol.17
, pp. 279-284
-
-
Killion, J.J.1
Radinsky, R.2
Fidler, I.J.3
-
42
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-
0031762299
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Inhibition of corneal inflammation by the topical use of Ras farnesyltransferase inhibitors: Selective inhibition of macrophage localization
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Sonoda K.H., Sakamoto T., Yoshikawa H., Ashizuka S., Ohshima Y., Kishihara K., Nomoto K., Ishibashi T., Inomata H. Inhibition of corneal inflammation by the topical use of Ras farnesyltransferase inhibitors: selective inhibition of macrophage localization. Invest Ophthalmol Vis Sci. 39:1999;2245-2251.
-
(1999)
Invest Ophthalmol Vis Sci
, vol.39
, pp. 2245-2251
-
-
Sonoda, K.H.1
Sakamoto, T.2
Yoshikawa, H.3
Ashizuka, S.4
Ohshima, Y.5
Kishihara, K.6
Nomoto, K.7
Ishibashi, T.8
Inomata, H.9
-
43
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-
0029952467
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Resistance of a variant ras-transformed cell line to phenotypic reversion by farnesyl transferase inhibitors
-
Prendergast G.C., Davide J.P., Lebowitz P.F., Wechsler-Reya R., Kohl N.E. Resistance of a variant ras-transformed cell line to phenotypic reversion by farnesyl transferase inhibitors. Cancer Res. 56:1996;2626-2632.
-
(1996)
Cancer Res
, vol.56
, pp. 2626-2632
-
-
Prendergast, G.C.1
Davide, J.P.2
Lebowitz, P.F.3
Wechsler-Reya, R.4
Kohl, N.E.5
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44
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0033578751
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A mutant form of human protein farnesyltransferase exhibits increased resistance to farnesyltransferase inhibitors
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This study provides a genetic tool that will allow conclusive proof that the antineoplastic and cytoskeletal effects of FTIs are indeed due to inhibition of FT rather than to off-target effects.
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Del Villar K., Urano J., Guo L., Tamanoi F. A mutant form of human protein farnesyltransferase exhibits increased resistance to farnesyltransferase inhibitors. J Biol Chem. 274:1999;27010-27017. This study provides a genetic tool that will allow conclusive proof that the antineoplastic and cytoskeletal effects of FTIs are indeed due to inhibition of FT rather than to off-target effects.
-
(1999)
J Biol Chem
, vol.274
, pp. 27010-27017
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-
Del Villar, K.1
Urano, J.2
Guo, L.3
Tamanoi, F.4
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45
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0033524358
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Effect of farnesyltransferase overxpression on cell growth and transformation
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This study provided evidence that FT itself can be oncogenic when overexpressed in NIH3T3 cells. Higher levels of FT activity were seen in cells overexpressing FT subunits, but it was not established conclusively whether increased enzyme activity was required for transformation.
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Nagase T., Kawata S., Nakajima H., Tamura S., Yamasaki E., Fukui K., Yamamoto K., Miyagawa J., Matsumura I., Matsuda Y., Matsuzawa Y. Effect of farnesyltransferase overxpression on cell growth and transformation. Int J Cancer. 80:1999;126-133. This study provided evidence that FT itself can be oncogenic when overexpressed in NIH3T3 cells. Higher levels of FT activity were seen in cells overexpressing FT subunits, but it was not established conclusively whether increased enzyme activity was required for transformation.
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(1999)
Int J Cancer
, vol.80
, pp. 126-133
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Nagase, T.1
Kawata, S.2
Nakajima, H.3
Tamura, S.4
Yamasaki, E.5
Fukui, K.6
Yamamoto, K.7
Miyagawa, J.8
Matsumura, I.9
Matsuda, Y.10
Matsuzawa, Y.11
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46
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0033582455
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Inhibition of DNA synthesis by a farnesyltransferase inhibitor involves inhibition of the p70(s6k) pathway
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Law B.K., Norgaard P., Gnudi L., Kahn B.B., Poulson H.S., Moses H.L. Inhibition of DNA synthesis by a farnesyltransferase inhibitor involves inhibition of the p70(s6k) pathway. J Biol Chem. 274:1999;4743-4748.
-
(1999)
J Biol Chem
, vol.274
, pp. 4743-4748
-
-
Law, B.K.1
Norgaard, P.2
Gnudi, L.3
Kahn, B.B.4
Poulson, H.S.5
Moses, H.L.6
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47
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0033594480
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PDK1 acquires PDK2 activity in the presence of a synthetic peptide derived from the carboxyl terminus of PRK2
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This study suggests crosstalk between Rho and AKT pathways which may be germane to the pro-apoptotic effects of FTIs in certain settings. PRK (also known as PKN) is a Rho effector kinase that can associate with PDK1, the kinase responsible for phosphorylating one of two sites in the AKT regulatory domain that control AKT activity. Upon PRK interaction, the substrate specificity of PDK1 shifts such that it can recognize and phosphorylate a second site in the AKT regulatory domain (the 'PDK2' site). Phosphorylation of both sites fully activates AKT. While one study has reported no effect of FTI treatment on phosphorylation of the second 'PDK2' site [46], this issue should be investigated carefully in various tumor cell types given the potential PRK-PDK1 linkage.
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Balendran A., Casamayor A., Deak M., Paterson M., Gaffney P., Currie R., Downes C.P., Alessi D.R. PDK1 acquires PDK2 activity in the presence of a synthetic peptide derived from the carboxyl terminus of PRK2. Curr Biol. 9:1999;393-404. This study suggests crosstalk between Rho and AKT pathways which may be germane to the pro-apoptotic effects of FTIs in certain settings. PRK (also known as PKN) is a Rho effector kinase that can associate with PDK1, the kinase responsible for phosphorylating one of two sites in the AKT regulatory domain that control AKT activity. Upon PRK interaction, the substrate specificity of PDK1 shifts such that it can recognize and phosphorylate a second site in the AKT regulatory domain (the 'PDK2' site). Phosphorylation of both sites fully activates AKT. While one study has reported no effect of FTI treatment on phosphorylation of the second 'PDK2' site [46], this issue should be investigated carefully in various tumor cell types given the potential PRK-PDK1 linkage.
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(1999)
Curr Biol
, vol.9
, pp. 393-404
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Balendran, A.1
Casamayor, A.2
Deak, M.3
Paterson, M.4
Gaffney, P.5
Currie, R.6
Downes, C.P.7
Alessi, D.R.8
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48
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0032539559
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Farnesyl transferase inhibitors cause enhanced mitotic sensitivity to taxol and epothilones
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Moasser M.M., Sepp-Lorenzino L., Kohl N.E., Oliff A., Balog A., Su D.S., Danishefsky S.J., Rosen N. Farnesyl transferase inhibitors cause enhanced mitotic sensitivity to taxol and epothilones. Proc Natl Acad Sci USA. 95:1998;1369-1374.
-
(1998)
Proc Natl Acad Sci USA
, vol.95
, pp. 1369-1374
-
-
Moasser, M.M.1
Sepp-Lorenzino, L.2
Kohl, N.E.3
Oliff, A.4
Balog, A.5
Su, D.S.6
Danishefsky, S.J.7
Rosen, N.8
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49
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0033214457
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Antitumor efficacy of a novel class of non-thiol-containing peptidomimetic inhibitors of farnesyltransferase and geranylgeranyltransferase I: Combination therapy with the cytotoxic agents cisplatin, taxol, and gemcitabine
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Sun J., Blaskovich M.A., Knowles D., Qian Y., Ohkanda J., Bailey R.D., Hamilton A.D., Sebti S.M. Antitumor efficacy of a novel class of non-thiol-containing peptidomimetic inhibitors of farnesyltransferase and geranylgeranyltransferase I: combination therapy with the cytotoxic agents cisplatin, taxol, and gemcitabine. Cancer Res. 59:1999;4919-4926.
-
(1999)
Cancer Res
, vol.59
, pp. 4919-4926
-
-
Sun, J.1
Blaskovich, M.A.2
Knowles, D.3
Qian, Y.4
Ohkanda, J.5
Bailey, R.D.6
Hamilton, A.D.7
Sebti, S.M.8
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50
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0029921232
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The farnesyltransferase inhibitor FTI-277 radiosensitizes H-ras-transformed rat embryo fibroblasts
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Bernhard E.J., Kao G., Cox A.D., Sebti S.M., Hamilton A.D., Muschel R.J., McKenna W.G. The farnesyltransferase inhibitor FTI-277 radiosensitizes H-ras-transformed rat embryo fibroblasts. Cancer Res. 56:1996;1727-1730.
-
(1996)
Cancer Res
, vol.56
, pp. 1727-1730
-
-
Bernhard, E.J.1
Kao, G.2
Cox, A.D.3
Sebti, S.M.4
Hamilton, A.D.5
Muschel, R.J.6
McKenna, W.G.7
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51
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0032522849
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Inhibiting Ras prenylation increases the radiosensitivity of human tumor cell lines with activating mutations of ras oncogenes
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This study provided strong evidence that FTIs are likely to have clinical utility as radiosensitizers.
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Bernhard E.J., McKenna W.G., Hamilton A.D., Sebti S.M., Qian Y., Wu J.M., Muschel R.J. Inhibiting Ras prenylation increases the radiosensitivity of human tumor cell lines with activating mutations of ras oncogenes. Cancer Res. 58:1998;1754-1761. This study provided strong evidence that FTIs are likely to have clinical utility as radiosensitizers.
-
(1998)
Cancer Res
, vol.58
, pp. 1754-1761
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Bernhard, E.J.1
McKenna, W.G.2
Hamilton, A.D.3
Sebti, S.M.4
Qian, Y.5
Wu, J.M.6
Muschel, R.J.7
-
52
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0030659043
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RhoB encoding a UV-inducible ras-related small GTP-binding protein is regulated by GTPases of the rho family and independent of JNK, ERK, and p38 MAP kinase
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Fritz G., Kaina B. rhoB encoding a UV-inducible ras-related small GTP-binding protein is regulated by GTPases of the rho family and independent of JNK, ERK, and p38 MAP kinase. J Biol Chem. 272:1997;30637-30644.
-
(1997)
J Biol Chem
, vol.272
, pp. 30637-30644
-
-
Fritz, G.1
Kaina, B.2
-
53
-
-
0028849261
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The ras-related small GTP-binding protein RhoB is immediate-early inducible by DNA damaging treatments
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Fritz G., Kaina B., Aktories K. The ras-related small GTP-binding protein RhoB is immediate-early inducible by DNA damaging treatments. J Biol Chem. 270:1995;25172-25177.
-
(1995)
J Biol Chem
, vol.270
, pp. 25172-25177
-
-
Fritz, G.1
Kaina, B.2
Aktories, K.3
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