{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T23:34:44Z","timestamp":1790465684415,"version":"4.1.0"},"reference-count":49,"publisher":"American Society of Hematology","issue":"5","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2001,3,1]]},"abstract":"<jats:p>BCR\/ABL, the oncoprotein responsible for chronic myeloid leukemia (CML), transforms hematopoietic cells through both Ras-dependent and -independent mechanisms. Farnesyl protein transferase inhibitors (FTIs) were designed to block mutant Ras signaling, but they also inhibit the growth of transformed cells with wild-type Ras, implying that other farnesylated targets contribute to FTI action. In the current study, the clinical candidate FTI SCH66336 was characterized for its ability to inhibit BCR\/ABL transformation. When tested against BCR\/ABL-BaF3 cells, a murine cell line that is leukemogenic in mice, SCH66336 potently inhibited soft agar colony formation, slowed proliferation, and sensitized cells to apoptotic stimuli. Quantification of activated guanosine triphosphate (GTP)-bound Ras protein and electrophoretic mobility shift assays for AP-1 DNA binding showed that Ras effector pathways are inhibited by SCH66336. However, SCH66336 was more inhibitory than dominant-negative Ras in assays of soft agar colony formation and cell proliferation, suggesting activity against targets other than Ras. Cell cycle analysis of BCR\/ABL-BaF3 cells treated with SCH66336 revealed G2\/M blockade, consistent with recent reports that centromeric proteins that regulate the G2\/M checkpoint are critical farnesylated targets of FTI action. Mice injected intravenously with BCR\/ABL-BaF3 cells developed acute leukemia and died within 4 weeks with massive splenomegaly, elevated white blood cell counts, and anemia. In contrast, nearly all mice treated with SCH66336 survived and have remained disease-free for more than a year. Furthermore, SCH66336 selectively inhibited the hematopoietic colony formation of primary human CML cells. As an oral, nontoxic compound with a mechanism of action distinct from that of ABL tyrosine kinase inhibition, FTI SCH66336 shows promise for the treatment of BCR\/ABL-induced leukemia.<\/jats:p>","DOI":"10.1182\/blood.v97.5.1404","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T12:46:40Z","timestamp":1027774000000},"page":"1404-1412","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":140,"title":["Activity of the farnesyl protein transferase inhibitor SCH66336 against BCR\/ABL-induced murine leukemia and primary cells from patients with chronic myeloid leukemia"],"prefix":"10.1182","volume":"97","author":[{"given":"David G.","family":"Peters","sequence":"first","affiliation":[{"name":"From the Whitehead Institute, Cambridge, MA; Division of Hematology\/ Oncology, Massachusetts General Hospital, Boston, MA; and the Department of Tumor Biology, the Schering-Plough Research Institute, Kenilworth, NJ."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Russell R.","family":"Hoover","sequence":"additional","affiliation":[{"name":"From the Whitehead Institute, Cambridge, MA; Division of Hematology\/ Oncology, Massachusetts General Hospital, Boston, MA; and the Department of Tumor Biology, the Schering-Plough Research Institute, Kenilworth, NJ."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa J.","family":"Gerlach","sequence":"additional","affiliation":[{"name":"From the Whitehead Institute, Cambridge, MA; Division of Hematology\/ Oncology, Massachusetts General Hospital, Boston, MA; and the Department of Tumor Biology, the Schering-Plough Research Institute, Kenilworth, NJ."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eugene Y.","family":"Koh","sequence":"additional","affiliation":[{"name":"From the Whitehead Institute, Cambridge, MA; Division of Hematology\/ Oncology, Massachusetts General Hospital, Boston, MA; and the Department of Tumor Biology, the Schering-Plough Research Institute, Kenilworth, NJ."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haiyan","family":"Zhang","sequence":"additional","affiliation":[{"name":"From the Whitehead Institute, Cambridge, MA; Division of Hematology\/ Oncology, Massachusetts General Hospital, Boston, MA; and the Department of Tumor Biology, the Schering-Plough Research Institute, Kenilworth, NJ."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin","family":"Choe","sequence":"additional","affiliation":[{"name":"From the Whitehead Institute, Cambridge, MA; Division of Hematology\/ Oncology, Massachusetts General Hospital, Boston, MA; and the Department of Tumor Biology, the Schering-Plough Research Institute, Kenilworth, NJ."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Kirschmeier","sequence":"additional","affiliation":[{"name":"From the Whitehead Institute, Cambridge, MA; Division of Hematology\/ Oncology, Massachusetts General Hospital, Boston, MA; and the Department of Tumor Biology, the Schering-Plough Research Institute, Kenilworth, NJ."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W. 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