CGP 57148, a tyrosine kinase inhibitor, inhibits the growth of cells expressing BCR-ABL, TEL-ABL, and TEL-PDGFR fusion proteins - PubMed (original) (raw)
. 1997 Dec 15;90(12):4947-52.
Affiliations
- PMID: 9389713
Free article
CGP 57148, a tyrosine kinase inhibitor, inhibits the growth of cells expressing BCR-ABL, TEL-ABL, and TEL-PDGFR fusion proteins
M Carroll et al. Blood. 1997.
Free article
Abstract
CGP 57148 is a compound of the 2-phenylaminopyrimidine class that selectively inhibits the tyrosine kinase activity of the ABL and the platelet-derived growth factor receptor (PDGFR) protein tyrosine kinases. We previously showed that CGP 57148 selectively kills p210BCR-ABL-expressing cells. To extend these observations, we evaluated the ability of CGP 57148 to inhibit other activated ABL tyrosine kinases, including p185BCR-ABL and TEL-ABL. In cell-based assays of ABL tyrosine phosphorylation, inhibition of ABL kinase activity was observed at concentrations similar to that reported for p210BCR-ABL. Consistent with the in vitro profile of this compound, the growth of cells expressing activated ABL protein tyrosine kinases was inhibited in the absence of exogenous growth factor. Growth inhibition was also observed with a p185BCR-ABL-positive acute lymphocytic leukemia (ALL) cell line generated from a Philadelphia chromosome-positive ALL patient. As CGP 57148 inhibits the PDGFR kinase, we also showed that cells expressing an activated PDGFR tyrosine kinase, TEL-PDGFR, are sensitive to this compound. Thus, this compound may be useful for the treatment of a variety of BCR-ABL-positive leukemias and for treatment of the subset of chronic myelomonocytic leukemia patients with a TEL-PDGFR fusion protein.
Similar articles
- ARG tyrosine kinase activity is inhibited by STI571.
Okuda K, Weisberg E, Gilliland DG, Griffin JD. Okuda K, et al. Blood. 2001 Apr 15;97(8):2440-8. doi: 10.1182/blood.v97.8.2440. Blood. 2001. PMID: 11290609 - The tyrosine kinase inhibitor CGP 57148 (ST1 571) induces apoptosis in BCR-ABL-positive cells by down-regulating BCL-X.
Oetzel C, Jonuleit T, Götz A, van der Kuip H, Michels H, Duyster J, Hallek M, Aulitzky WE. Oetzel C, et al. Clin Cancer Res. 2000 May;6(5):1958-68. Clin Cancer Res. 2000. PMID: 10815921 - Selective inhibition of cell proliferation and BCR-ABL phosphorylation in acute lymphoblastic leukemia cells expressing Mr 190,000 BCR-ABL protein by a tyrosine kinase inhibitor (CGP-57148).
Beran M, Cao X, Estrov Z, Jeha S, Jin G, O'Brien S, Talpaz M, Arlinghaus RB, Lydon NB, Kantarjian H. Beran M, et al. Clin Cancer Res. 1998 Jul;4(7):1661-72. Clin Cancer Res. 1998. PMID: 9676840 - Mutated tyrosine kinases as therapeutic targets in myeloid leukemias.
Sattler M, Scheijen B, Weisberg E, Griffin JD. Sattler M, et al. Adv Exp Med Biol. 2003;532:121-40. doi: 10.1007/978-1-4615-0081-0_11. Adv Exp Med Biol. 2003. PMID: 12908554 Review. - [Preclinical and clinical profile of imatinib mesilate, a potent protein-tyrosine kinase inhibitor for CML therapy].
Toga W, Kondo M, Tokoro A. Toga W, et al. Nihon Yakurigaku Zasshi. 2003 Feb;121(2):119-28. doi: 10.1254/fpj.121.119. Nihon Yakurigaku Zasshi. 2003. PMID: 12616857 Review. Japanese.
Cited by
- Imatinib therapy of chronic myeloid leukemia significantly reduces carnitine cell intake, resulting in adverse events.
Burda P, Hlavackova A, Polivkova V, Curik N, Laznicka A, Krizkova J, Suttnar J, Klener P, Polakova KM. Burda P, et al. Mol Metab. 2024 Oct;88:102016. doi: 10.1016/j.molmet.2024.102016. Epub 2024 Aug 23. Mol Metab. 2024. PMID: 39182842 Free PMC article. - Tyrosine kinase inhibitor response of ABL-class acute lymphoblastic leukemia: the role of kinase type and SH3 domain.
van Outersterp I, Tasian SK, Reichert CEJ, Boeree A, de Groot-Kruseman HA, Escherich G, Boer JM, den Boer ML. van Outersterp I, et al. Blood. 2024 May 23;143(21):2178-2189. doi: 10.1182/blood.2023023120. Blood. 2024. PMID: 38394665 Free PMC article. - Tyrosine kinase inhibitor resistance in de novo BCR::ABL1-positive BCP-ALL beyond kinase domain mutations.
van Outersterp I, Boer JM, van de Ven C, Reichert CEJ, Boeree A, Kruisinga B, de Groot-Kruseman HA, Escherich G, Sijs-Szabo A, Rijneveld AW, den Boer ML. van Outersterp I, et al. Blood Adv. 2024 Apr 23;8(8):1835-1845. doi: 10.1182/bloodadvances.2023012162. Blood Adv. 2024. PMID: 38386975 Free PMC article. - Novel FIP1L1::KIT fusion in a myeloid neoplasm with eosinophilia, T-lymphoblastic transformation, and dasatinib response.
Alsouqi A, Kleinberger J, Werner TS, Awan R, Chopra S, Rea B, Aggarwal N, Yatsenko SA, Farah R, Bailey NG. Alsouqi A, et al. Haematologica. 2023 Nov 1;108(11):3181-3185. doi: 10.3324/haematol.2022.282636. Haematologica. 2023. PMID: 37102594 Free PMC article. No abstract available. - Clinical outcomes of medical treatments for progressive desmoid tumors following active surveillance: a systematic review.
Tsukamoto S, Takahama T, Mavrogenis AF, Tanaka Y, Tanaka Y, Errani C. Tsukamoto S, et al. Musculoskelet Surg. 2023 Mar;107(1):7-18. doi: 10.1007/s12306-022-00738-x. Epub 2022 Feb 12. Musculoskelet Surg. 2023. PMID: 35150408 Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Research Materials
Miscellaneous