221
Views
18
CrossRef citations to date
0
Altmetric
Review

Ras as a therapeutic target in hematologic malignancies

&
Pages 271-284 | Published online: 29 Jun 2007

Bibliography

  • BOS JL: All in the family? New insights and questions regarding interconnectivity of Ras, Rap1 and Ral. EMBO J. (1998) 17(23):6776-6782.
  • CAMPBELL SL, KHOSRAVI-FAR R, ROSSMAN KL, CLARK GJ, DER CJ: Increasing complexity of Ras signaling. Oncogene (1998) 17(11 Reviews):1395-1413.
  • SANTOS E, NEBREDA AR: Structural and functional properties of ras proteins. FASEB J. (1989) 3(10):2151-2163.
  • CHOY E, CHIU VK, SILLETTI J et al.: Endomembrane trafficking of ras: the CAAX motif targets proteins to the ER and Golgi. Cell (1999) 98(1):69-80.
  • GOLDSTEIN JL, BROWN MS: Regulation of the mevalonate pathway. Nature (1990) 343(6257):425-430.
  • REUTHER GW, DER CJ: The Ras branch of small GTPases: Ras family members don't fall far from the tree. Curr. Opin. Cell Biol. (2000) 12(2):157-165.
  • CASEY PJ, THISSEN JA, MOOMAW JF: Enzymatic modification of proteins with a geranylgeranyl isoprenoid. Proc. Natl. Acad. Sci. USA (1991) 88(19):8631-8635.
  • YOKOYAMA K, GOODWIN GW, GHOMASHCHI F, GLOMSET JA, GELB MH: A protein geranylgeranyltransferase from bovine brain: implications for protein prenylation specificity. Proc. Natl. Acad. Sci. USA (1991) 88(12):5302-5306.
  • CLARKE S: Protein isoprenylation and methylation at carboxyl-terminal cysteine residues. Annu. Rev. Biochem. (1992) 61:355-386.
  • ZHANG FL, CASEY PJ: Protein prenylation: molecular mechanisms and functional consequences. Annu. Rev. Biochem. (1996) 65:241-269.
  • HANCOCK JF, CADWALLADER K, MARSHALL CJ: Methylation and proteolysis are essential for efficient membrane binding of prenylated p21K-ras(B). EMBO J. (1991) 10(3):641-646.
  • CLARKE S, VOGEL JP, DESCHENES RJ, STOCK J: Posttranslational modification of the Ha-ras oncogene protein: evidence for a third class of protein carboxyl methyltransferases. Proc. Natl. Acad. Sci. USA (1988) 85(13):4643-4647.
  • BUDAY L, DOWNWARD J: Epidermal growth factor regulates p21ras through the formation of a complex of receptor, Grb2 adapter protein, and Sos nucleotide exchange factor. Cell (1993) 73(3):611-620.
  • MARGOLIS B, SKOLNIK EY: Activation of Ras by receptor tyrosine kinases. J. Am. Soc. Nephrol. (1994) 5(6):1288-1299.
  • MARSHALL CJ: Ras effectors. Curr. Opin. Cell Biol. (1996) 8(2):197-204.
  • PAZ A, HAKLAI R, ELAD-SFADIA G, BALLAN E, KLOOG Y: Galectin-1 binds oncogenic H-Ras to mediate Ras membrane anchorage and cell transformation. Oncogene (2001) 20(51):7486-7493.
  • ELAD-SFADIA G, HAKLAI R, BALAN E, KLOOG Y: Galectin-3 augments K-Ras activation and triggers a Ras signal that attenuates ERK but not phosphoinositide 3-kinase activity. J. Biol. Chem. (2004) 279(33):34922-34930.
  • ELAD-SFADIA G, HAKLAI R, BALLAN E, GABIUS HJ, KLOOG Y: Galectin-1 augments Ras activation and diverts Ras signals to Raf-1 at the expense of phosphoinositide 3-kinase. J. Biol. Chem. (2002) 277(40):37169-37175.
  • SHIELDS JM, PRUITT K, MCFALL A, SHAUB A, DER CJ: Understanding Ras: ‘it ain't over ‘til it's over’. Trends Cell Biol. (2000) 10(4):147-154.
  • KOLCH W, HEIDECKER G, LLOYD P, RAPP UR: Raf-1 protein kinase is required for growth of induced NIH/3T3 cells. Nature (1991) 349(6308):426-428.
  • VAN AELST L, BARR M, MARCUS S, POLVERINO A, WIGLER M: Complex formation between RAS and RAF and other protein kinases. Proc. Natl. Acad. Sci. USA (1993) 90(13):6213-6217.
  • LOH ML, VATTIKUTI S, SCHUBBERT S et al.: Mutations in PTPN11 implicate the SHP-2 phosphatase in leukemogenesis. Blood (2004) 103(6):2325-2331.
  • LEEVERS SJ, PATERSON HF, MARSHALL CJ: Requirement for Ras in Raf activation is overcome by targeting Raf to the plasma membrane. Nature (1994) 369(6479):411-414.
  • MORRISON DK, CUTLER RE: The complexity of Raf-1 regulation. Curr. Opin. Cell Biol. (1997) 9(2):174-179.
  • LEWIS TS, SHAPIRO PS, AHN NG: Signal transduction through MAP kinase cascades. Adv. Cancer Res. (1998) 74:49-139.
  • JANKNECHT R, ERNST WH, PINGOUD V, NORDHEIM A: Activation of ternary complex factor Elk-1 by MAP kinases. EMBO J. (1993) 12(13):5097-5104.
  • ADJEI AA: Blocking oncogenic Ras signaling for cancer therapy. J. Natl. Cancer Inst. (2001) 93(14):1062-1074.
  • KERKHOFF E, RAPP UR: Cell cycle targets of Ras/Raf signalling. Oncogene (1998) 17(11 Reviews):1457-1462.
  • DONNELLAN R, CHETTY R: Cyclin D1 and human neoplasia. Mol. Pathol. (1998) 51(1):1-7.
  • RODRIGUEZ-VICIANA P, WARNE PH, VANHAESEBROECK B, WATERFIELD MD, DOWNWARD J: Activation of phosphoinositide 3-kinase by interaction with Ras and by point mutation. EMBO. J. (1996) 15(10):2442-2451.
  • DOWNWARD J: Targeting RAS signalling pathways in cancer therapy. Nat. Rev. Cancer (2003) 3(1):11-22.
  • ABRAHAM E: Neutrophils and acute lung injury. Crit. Care Med. (2003) 31(4 Suppl.):S195-S199.
  • DATTA SR, DUDEK H, TAO X et al.: Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery. Cell (1997) 91(2):231-241.
  • CARDONE MH, ROY N, STENNICKE HR et al.: Regulation of cell death protease caspase-9 by phosphorylation. Science (1998) 282(5392):1318-1321.
  • SO CW, CLEARY ML: MLL-AFX requires the transcriptional effector domains of AFX to transform myeloid progenitors and transdominantly interfere with forkhead protein function. Mol. Cell Biol. (2002) 22(18):6542-6552.
  • LIN L, PENG SL: Coordination of NF-kappaB and NFAT antagonism by the forkhead transcription factor Foxd1. J. Immunol. (2006) 176(8):4793-4803.
  • MCBRIDE HM, NEUSPIEL M, WASIAK S: Mitochondria: more than just a powerhouse. Curr. Biol. (2006) 16(14):551-560.
  • OZES ON, MAYO LD, GUSTIN JA, PFEFFER SR, PFEFFER LM, DONNER DB: NF-kappaB activation by tumour necrosis factor requires the Akt serine-threonine kinase. Nature (1999) 401(6748):82-85.
  • QIU RG, CHEN J, KIRN D, MCCORMICK F, SYMONS M: An essential role for Rac in Ras transformation. Nature (1995) 374(6521):457-459.
  • PANWALKAR A, VERSTOVSEK S, GILES FJ: Mammalian target of rapamycin inhibition as therapy for hematologic malignancies. Cancer (2004) 100(4):657-666.
  • WOLTHUIS RM, BOS JL: Ras caught in another affair: the exchange factors for Ral. Curr. Opin. Genet. Dev. (1999) 9(1):112-117.
  • COLICELLI J: Human RAS superfamily proteins and related GTPases. Sci. STKE (2004) 2004(250):RE13.
  • CHIEN Y, WHITE MA: RAL GTPases are linchpin modulators of human tumour-cell proliferation and survival. EMBO Rep. (2003) 4(8):800-806.
  • WENNERBERG K, DER CJ: Rho-family GTPases: it's not only Rac and Rho (and I like it). J. Cell Sci. (2004) 117(Pt 8):1301-1312.
  • BRYMORA A, VALOVA VA, LARSEN MR, ROUFOGALIS BD, ROBINSON PJ: The brain exocyst complex interacts with RalA in a GTP-dependent manner: identification of a novel mammalian Sec3 gene and a second Sec15 gene. J. Biol. Chem. (2001) 276(32):29792-29797.
  • FRANKEL P, ARONHEIM A, KAVANAGH E et al.: RalA interacts with ZONAB in a cell density-dependent manner and regulates its transcriptional activity. EMBO J. (2005) 24(1):54-62.
  • SIDHU RS, CLOUGH RR, BHULLAR RP: Regulation of phospholipase C-delta1 through direct interactions with the small GTPase Ral and calmodulin. J. Biol. Chem. (2005) 280(23):21933-21941.
  • VAN DAM EM, ROBINSON PJ: Ral: mediator of membrane trafficking. Int. J. Biochem. Cell Biol. (2006) 38(11):1841-1847.
  • JENKINS GM, FROHMAN MA: Phospholipase D: a lipid centric review. Cell Mol. Life Sci. (2005) 62(19-20):2305-2316.
  • BEAUPRE DM, KURZROCK R: RAS and leukemia: from basic mechanisms to gene-directed therapy. J. Clin. Oncol. (1999) 17(3):1071-1079.
  • BOS JL: Ras oncogenes in human cancer: a review. Cancer Res. (1989) 49(17):4682-4689.
  • ALMOGUERA C, SHIBATA D, FORRESTER K, MARTIN J, ARNHEIM N, PERUCHO M: Most human carcinomas of the exocrine pancreas contain mutant c-K-ras genes. Cell (1988) 53(4):549-554.
  • RODENHUIS S: Ras and human tumors. Semin. Cancer Biol. (1992) 3(4):241-247.
  • BOWEN DT, FREW ME, HILLS R et al.: RAS mutation in acute myeloid leukemia is associated with distinct cytogenetic subgroups but does not influence outcome in patients younger than 60 years. Blood (2005) 106(6):2113-2119.
  • BACHER U, HAFERLACH T, SCHOCH C, KERN W, SCHNITTGER S: Implications of NRAS mutations in AML: a study of 2502 patients. Blood (2006) 107(10):3847-3853.
  • RITTER M, KIM TD, LISSKE P, THIEDE C, SCHAICH M, NEUBAUER A: Prognostic significance of N-RAS and K-RAS mutations in 232 patients with acute myeloid leukemia. Haematologica (2004) 89(11):1397-1399.
  • CHEN CY, LIN LI, TANG JL et al.: Acquisition of JAK2, PTPN11, and RAS mutations during disease progression in primary myelodysplastic syndrome. Leukemia (2006) 20(6):1155-1158.
  • PADUA RA, GUINN BA, AL-SABAH AI et al.: RAS, FMS and p53 mutations and poor clinical outcome in myelodysplasias: a 10-year follow-up. Leukemia (1998) 12(6):887-892.
  • DE SOUZA FERNANDEZ T, MENEZES DE SOUZA J, MACEDO SILVA ML, TABAK D, ABDELHAY E: Correlation of N-ras point mutations with specific chromosomal abnormalities in primary myelodysplastic syndrome. Leuk. Res. (1998) 22(2):125-134.
  • YUNIS JJ, BOOT AJ, MAYER MG, BOS JL: Mechanisms of ras mutation in myelodysplastic syndrome. Oncogene (1989) 4(5):609-614.
  • ROWINSKY EK, WINDLE JJ, VON HOFF DD: Ras protein farnesyltransferase: A strategic target for anticancer therapeutic development. J. Clin. Oncol. (1999) 17(11):3631-3652.
  • JAMES GL, GOLDSTEIN JL, BROWN MS: Polylysine and CVIM sequences of K-RasB dictate specificity of prenylation and confer resistance to benzodiazepine peptidomimetic in vitro. J. Biol. Chem. (1995) 270(11):6221-6226.
  • RUSSO P, OTTOBONI C, CRIPPA A, RIOU JF, O'CONNOR PM: RPR-115135, a new non peptidomimetic farnesyltransferase inhibitor, induces G0/G1 arrest only in serum starved cells. Int. J. Oncol. (2001) 18(4):855-862.
  • YONEMOTO M, SATOH T, ARAKAWA H et al.: J-104,871, a novel farnesyltransferase inhibitor, blocks Ras farnesylation in vivo in a farnesyl pyrophosphate-competitive manner. Mol. Pharmacol. (1998) 54(1):1-7.
  • RUSSO P, MALACARNE D, FALUGI C, TROMBINO S, O'CONNOR PM: RPR-115135, a farnesyltransferase inhibitor, increases 5-FU-cytotoxicity in ten human colon cancer cell lines: role of p53. Int. J. Cancer (2002) 100(3):266-275.
  • FALUGI C, TROMBINO S, GRANONE P, MARGARITORA S, RUSSO P: Increasing complexity of farnesyltransferase inhibitors activity: role in chromosome instability. Curr. Cancer Drug Targets (2003) 3(2):109-118.
  • BRITTEN CD, ROWINSKY EK, SOIGNET S et al.: A phase I and pharmacological study of the farnesyl protein transferase inhibitor L-778,123 in patients with solid malignancies. Clin. Cancer Res. (2001) 7(12):3894-3903.
  • DOLL RJ, KIRSCHMEIER P, BISHOP WR: Farnesyltransferase inhibitors as anticancer agents: critical crossroads. Curr. Opin. Drug Discov. Devel. (2004) 7(4):478-486.
  • MANNE V, YAN N, CARBONI JM et al.: Bisubstrate inhibitors of farnesyltransferase: a novel class of specific inhibitors of ras transformed cells. Oncogene (1995) 10(9):1763-1779.
  • JABBOUR E, KANTARJIAN H, CORTES J: Clinical activity of farnesyl transferase inhibitors in hematologic malignancies: possible mechanisms of action. Leuk. Lymphoma (2004) 45(11):2187-2195.
  • LIU M, BRYANT MS, CHEN J et al.: Antitumor activity of SCH 66336, an orally bioavailable tricyclic inhibitor of farnesyl protein transferase, in human tumor xenograft models and wap-ras transgenic mice. Cancer Res. (1998) 58(21):4947-4956.
  • CORTES JE, KURZROCK R, KANTARJIAN HM: Farnesyltransferase inhibitors: novel compounds in development for the treatment of myeloid malignancies. Semin. Hematol. (2002) 39(3 Suppl. 2):26-30.
  • END DW, SMETS G, TODD AV et al.: Characterization of the antitumor effects of the selective farnesyl protein transferase inhibitor R115777 in vivo and in vitro. Cancer Res. (2001) 61(1):131-137.
  • KARP JE: Farnesyl protein transferase inhibitors as targeted therapies for hematologic malignancies. Semin. Hematol. (2001) 38(3 Suppl. 7):16-23.
  • KARP JE, LANCET JE, KAUFMANN SH et al.: Clinical and biologic activity of the farnesyltransferase inhibitor R115777 in adults with refractory and relapsed acute leukemias: a Phase 1 clinical-laboratory correlative trial. Blood (2001) 97(11):3361-3369.
  • LANCET JE, KARP JE: Farnesyl transferase inhibitors in myeloid malignancies. Blood Rev. (2003) 17(3):123-129.
  • CORTES J, ALBITAR M, THOMAS D et al.: Efficacy of the farnesyl transferase inhibitor R115777 in chronic myeloid leukemia and other hematologic malignancies. Blood (2003) 101(5):1692-1697.
  • KURZROCK R, KANTARJIAN HM, CORTES JE et al.: Farnesyltransferase inhibitor R115777 in myelodysplastic syndrome: clinical and biologic activities in the phase 1 setting. Blood (2003) 102(13):4527-4534.
  • KURZROCK R, ALBITAR M, CORTES JE et al.: Phase II study of R115777, a farnesyl transferase inhibitor, in myelodysplastic syndrome.in. Oncol. (2004) 22(7):1287-1292.
  • ZIMMERMAN TM, HARLIN H, ODENIKE OM et al.: Dose-ranging pharmacodynamic study of tipifarnib (R115777) in patients with relapsed and refractory hematologic malignancies. J. Clin. Oncol. (2004) 22(23):4816-4822.
  • KIRSCHBAUM M, SELWYN STEIN A, TUSCANO J et al.: A Phase I study of the farnesyltransferase inhibitor tipifarnib in a week-on week-off dose schedule in acute myelogenous leukemia. ASH Annual Meeting Abstracts (2006) 108(11):1948.
  • KORYCKA A, SMOLEWSKI P, ROBAK T: The influence of farnesyl protein transferase inhibitor R115777 (Zarnestra) alone and in combination with purine nucleoside analogs on acute myeloid leukemia progenitors in vitro. Eur. J. Haematol. (2004) 73(6):418-426.
  • MESA RA: Tipifarnib: farnesyl transferase inhibition at a crossroads. Expert. Rev. Anticancer Ther. (2006) 6(3):313-319.
  • ALVAREZ RH, KANTARJIAN H, GARCIA-MANERO G et al.: Farnesyl transferase inhibitor (tipifarnib,zarnestra; Z) in combination with standard chemotherapy with idarubicin (Ida) and cytarabine (ara-C) for patients (pts) with newly diagnosed acute myeloid leukemia (AML) or high-risk myelodysplastic syndrome (MDS). ASH Annual Meeting Abstracts (2006) 108(11):1999.
  • KARP JE, FELDMAN EJ, MORRIS L et al.: Active oral regimen for elderly adults with newly diagnosed acute myelogenous leukemia (AML): Phase I trial of oral tipifarnib (T) combined with oral etoposide (E) for adults ≥age 70 who are not candidates for traditional cytotoxic chemotherapy (TCC). ASH Annual Meeting Abstracts (2006) 108(11):426.
  • REICHERT A, HEISTERKAMP N, DALEY GQ, GROFFEN J: Treatment of Bcr/Abl-positive acute lymphoblastic leukemia in P190 transgenic mice with the farnesyl transferase inhibitor SCH66336. Blood (2001) 97(5):1399-1403.
  • PETERS DG, HOOVER RR, GERLACH MJ et al.: Activity of the farnesyl protein transferase inhibitor SCH66336 against BCR/ABL-induced murine leukemia and primary cells from patients with chronic myeloid leukemia. Blood (2001) 97(5):1404-1412.
  • TAVERAS AG, KIRSCHMEIER P, BAUM CM: Sch-66336 (sarasar) and other benzocycloheptapyridyl farnesyl protein transferase inhibitors: discovery, biology and clinical observations. Curr. Top. Med. Chem. (2003) 3(10):1103-1114.
  • NAKAJIMA A, TAUCHI T, SUMI M, BISHOP WR, OHYASHIKI K: Efficacy of SCH66336, a farnesyl transferase inhibitor, in conjunction with imatinib against BCR-ABL-positive cells. Mol. Cancer Ther. (2003) 2(3):219-224.
  • BRODSKY AL: Apoptotic synergism between STI571 and the farnesyl transferase inhibitor SCH66336 on an imatinib-sensitive cell line. Blood (2003) 101(5):2070.
  • JORGENSEN HG, ALLAN EK, GRAHAM SM et al.: Lonafarnib reduces the resistance of primitive quiescent CML cells to imatinib mesylate in vitro. Leukemia (2005) 19(7):1184-1191.
  • COPLAND M, HAMILTON A, ELRICK LJ et al.: Dasatinib (BMS-354825) targets an earlier progenitor population than imatinib in primary CML but does not eliminate the quiescent fraction. Blood (2006) 107(11):4532-4539.
  • BORTHAKUR G, KANTARJIAN H, DALEY G et al.: Pilot study of lonafarnib, a farnesyl transferase inhibitor, in patients with chronic myeloid leukemia in the chronic or accelerated phase that is resistant or refractory to imatinib therapy. Cancer (2006) 106(2):346-352.
  • ROSE WC, LEE FY, FAIRCHILD CR et al.: Preclinical antitumor activity of BMS-214662, a highly apoptotic and novel farnesyltransferase inhibitor. Cancer Res. (2001) 61(20):7507-7517.
  • CORTES J, FADERL S, ESTEY E et al.: Phase I study of BMS-214662, a farnesyl transferase inhibitor in patients with acute leukemias and high-risk myelodysplastic syndromes. J. Clin. Oncol. (2005) 23(12):2805-2812.
  • COPLAND M, HAMILTON A, ALLAN EK, BRUNTON V, HOLYOAKE TL: BMS-214662 targets quiescent chronic myeloid leukaemia stem cells and enhances the activity of both imatinib and dasatinib (BMS-354825). ASH Annual Meeting Abstracts (2005) 106(11):693-.
  • WHYTE DB, KIRSCHMEIER P, HOCKENBERRY TN et al.: K- and N-Ras are geranylgeranylated in cells treated with farnesyl protein transferase inhibitors. J. Biol. Chem. (1997) 272(22):14459-14464.
  • DU W, PRENDERGAST GC: Geranylgeranylated RhoB mediates suppression of human tumor cell growth by farnesyltransferase inhibitors. Cancer Res. (1999) 59(21):5492-5496.
  • PRENDERGAST GC, OLIFF A:Farnesyltransferase inhibitors: antineoplastic properties, mechanisms of action, and clinical prospects. Semin. Cancer Biol. (2000) 10(6):443-452.
  • ASHAR HR, JAMES L, GRAY K et al.: The farnesyl transferase inhibitor SCH-66336 induces a G(2) --> M or G(1) pause in sensitive human tumor cell lines. Exp. Cell Res. (2001) 262(1):17-27.
  • WEAVER BA, BONDAY ZQ, PUTKEY FR, KOPS GJ, SILK AD, CLEVELAND DW: Centromere-associated protein-E is essential for the mammalian mitotic checkpoint to prevent aneuploidy due to single chromosome loss. J. Cell Biol. (2003) 162(4):551-563.
  • LANCET JE, KARP JE: Farnesyltransferase inhibitors in hematologic malignancies: new horizons in therapy. Blood (2003) 102(12):3880-3889.
  • JIANG K, COPPOLA D, CRESPO NC et al.: The phosphoinositide 3-OH kinase/AKT2 pathway as a critical target for farnesyltransferase inhibitor-induced apoptosis. Mol. Cell Biol. (2000) 20(1):139-148.
  • WANG E, CASCIANO CN, CLEMENT RP, JOHNSON WW: The farnesyl protein transferase inhibitor SCH-66336 is a potent inhibitor of MDR1 product P-glycoprotein. Cancer Res. (2001) 61(20):7525-7529.
  • PRENDERGAST GC, RANE N: Farnesyltransferase inhibitors: mechanism and applications. Expert. Opin. Investig. Drugs (2001) 10(12):2105-2116.
  • APPELS NM, BEIJNEN JH, SCHELLENS JH: Development of farnesyl transferase inhibitors: a review. Oncologist (2005) 10(8):565-578.
  • MARCIANO D, BEN-BARUCH G, MAROM M, EGOZI Y, HAKLAI R, KLOOG Y: Farnesyl derivatives of rigid carboxylic acids-inhibitors of ras-dependent cell growth. J. Med. Chem. (1995) 38(8):1267-1272.
  • KLOOG Y, COX AD: RAS inhibitors: potential for cancer therapeutics. Mol. Med. Today (2000) 6(10):398-402.
  • MAROM M, HAKLAI R, BEN-BARUCH G, MARCIANO D,EGOZI Y, KLOOG Y: Selective inhibition of Ras-dependent cell growth by farnesylthiosalisylic acid. J. Biol. Chem. (1995) 270(38):22263-22270.
  • HAKLAI R, WEISZ MG, ELAD G et al.: Dislodgment and accelerated degradation of Ras. Biochemistry (1998) 37(5):1306-1314.
  • ELAD G, PAZ A, HAKLAI R, MARCIANO D, COX A, KLOOG Y: Targeting of K-Ras 4B by S-trans, trans-farnesyl thiosalicylic acid. Biochim. Biophys. Acta. (1999) 1452(3):228-242.
  • GEORGE J, AFEK A, KEREN P et al.: Functional inhibition of Ras by S-trans, trans-farnesyl thiosalicylic acid attenuates atherosclerosis in apolipoprotein E knockout mice. Circulation (2002) 105(20):2416-2422.
  • NIV H, GUTMAN O, HENIS YI, KLOOG Y: Membrane interactions of a constitutively active GFP-Ki-Ras 4B and their role in signaling. Evidence from lateral mobility studies. J. Biol. Chem. (1999) 274(3):1606-1613.
  • ROTBLAT B, NIV H, ANDRE S, KALTNER H, GABIUS HJ,KLOOG Y: Galectin-1(L11A) predicted from a computed galectin-1 farnesyl-binding pocket selectively inhibits Ras-GTP. Cancer Res. (2004) 64(9):3112-3118.
  • GANA-WEISZ M, HAKLAI R, MARCIANO D, EGOZI Y, BEN-BARUCH G, KLOOG Y: The Ras antagonist S-farnesylthiosalicylic acid induces inhibition of MAPK activation. Biochem. Biophys. Res. Commun. (1997) 239(3):900-904.
  • YAARI S, JACOB-HIRSCH J, AMARIGLIO N, HAKLAI R, RECHAVI G, KLOOG Y: Disruption of cooperation between Ras and MycN in human neuroblastoma cells promotes growth arrest. Clin. Cancer Res. (2005) 11(12):4321-4330.
  • BLUM R, JACOB-HIRSCH J, AMARIGLIO N, RECHAVI G,KLOOG Y: Ras inhibition in glioblastoma down-regulates hypoxia-inducible factor-1alpha, causing glycolysis shutdown and cell death. Cancer Res. (2005) 65(3):999-1006.
  • EGOZI Y, WEISZ B, GANA-WEISZ M, BEN-BARUCH G, KLOOG Y: Growth inhibition of ras-dependent tumors in nude mice by a potent ras-dislodging antagonist. Int. J. Cancer (1999) 80(6):911-918.
  • JANSEN B, SCHLAGBAUER-WADL H, KAHR H et al.: Novel Ras antagonist blocks human melanoma growth. Proc. Natl. Acad. Sci. USA (1999) 96(24):14019-14024.
  • WEISZ B, GIEHL K, GANA-WEISZ M et al.: A new functional Ras antagonist inhibits human pancreatic tumor growth in nude mice. Oncogene (1999) 18(16):2579-2588.
  • JANSEN B, HEERE-RESS E, SCHLAGBAUER-WADL H et al.: Farnesylthiosalicyclic acid inhibits the growth of human Merkel cell carcinoma in SCID mice. J. Mol. Med. (1999) 77(11):792-797.
  • HALASCHEK-WIENER J, WACHECK V, SCHLAGBAUER-WADL H, WOLFF K, KLOOG Y, JANSEN B: A novel Ras antagonist regulates both oncogenic Ras and the tumor suppressor p53 in colon cancer cells. Mol. Med. (2000) 6(8):693-704.
  • LIU X, SUN Y, EHRLICH M et al.: Disruption of TGF-beta growth inhibition by oncogenic ras is linked to p27Kip1 mislocalization. Oncogene (2000) 19(51):5926-5935.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.