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Imatinib mesylate inhibits tumorigenicity of malignant fibrous histiocytoma cells in vivo.
Anticancer Res. 2007 Jan-Feb; 27(1A):423-9.AR

Abstract

BACKGROUND

Malignant fibrous histiocytoma (MFH) is one of the most diffuse and aggressive tumors among soft tissue sarcomas in adults, but still poorly characterized from the molecular viewpoint. MFH cell proliferation is inhibited selectively by imatinib mesylate, a tyrosine kinase inhibitor. The expressions of platelet-derived growth factor receptors (PDGFRs) and c-Kit have been previously examined in MFH cell lines and the inhibitory effect of imatinib mesylate on the MFH cell proliferation was tested. MFH cell lines showed various patterns of PDGFRs and c-Kit expression. Imatinib mesylate inhibited the proliferation of MFH cells that expressed PDGFRs and/or c-Kit.

MATERIALS AND METHODS

Four MFH cell lines were used (Nara H, Nara F, GBS-1 and TNMY1). The mRNA expression of PDGFRs and c-Kit was analyzed using RT-PCR; cell proliferation was analyzed using the MTS assay. Immunohistochemistry was used to analyze the inhibitory effect of imatinib mesylate on phosphorylation of PDGFRs and c-Kit in vivo. The Nara H and TNMY1 cell lines were implanted into nude mice and tumor growth was evaluated daily by measuring the two-dimensional diameters of the tumor nodule.

RESULTS

PDGFRs and c-Kit were expressed in Nara F, GBS-1 and TNMY1, but not in Nara H cells. Imatinib mesylate inhibited PDGFRs and c-Kit phosphorylation in TNMY1 cells affecting the tumorigenicity, in the control group (139 mm3 SD +/- 1.03) and treatment group (126.2 mm3 SD +/- 1.63) but did not affect the tumorigenicity of Nara H cells.

CONCLUSION

Imatinib mesylate reduced in vivo tumor growth of MFH that express PDGFRs and c-Kit associated with phosphorylation suppression.

Authors+Show Affiliations

Department of Orthopedic Surgery, Kobe University Graduate School of Medicine, Hyogo, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17352263

Citation

Irsan, Istan, et al. "Imatinib Mesylate Inhibits Tumorigenicity of Malignant Fibrous Histiocytoma Cells in Vivo." Anticancer Research, vol. 27, no. 1A, 2007, pp. 423-9.
Irsan I, Akisue T, Hara H, et al. Imatinib mesylate inhibits tumorigenicity of malignant fibrous histiocytoma cells in vivo. Anticancer Res. 2007;27(1A):423-9.
Irsan, I., Akisue, T., Hara, H., Fujimoto, T., Imabori, M., Doita, M., Kuroda, R., Fujioka, H., Kawamoto, T., Yamamoto, T., & Kurosaka, M. (2007). Imatinib mesylate inhibits tumorigenicity of malignant fibrous histiocytoma cells in vivo. Anticancer Research, 27(1A), 423-9.
Irsan I, et al. Imatinib Mesylate Inhibits Tumorigenicity of Malignant Fibrous Histiocytoma Cells in Vivo. Anticancer Res. 2007 Jan-Feb;27(1A):423-9. PubMed PMID: 17352263.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Imatinib mesylate inhibits tumorigenicity of malignant fibrous histiocytoma cells in vivo. AU - Irsan,Istan, AU - Akisue,Toshihiro, AU - Hara,Hitomi, AU - Fujimoto,Takuya, AU - Imabori,Masaya, AU - Doita,Minoru, AU - Kuroda,Ryosuke, AU - Fujioka,Hiroyuki, AU - Kawamoto,Teruya, AU - Yamamoto,Tetsuji, AU - Kurosaka,Masahiro, PY - 2007/3/14/pubmed PY - 2007/3/30/medline PY - 2007/3/14/entrez SP - 423 EP - 9 JF - Anticancer research JO - Anticancer Res. VL - 27 IS - 1A N2 - BACKGROUND: Malignant fibrous histiocytoma (MFH) is one of the most diffuse and aggressive tumors among soft tissue sarcomas in adults, but still poorly characterized from the molecular viewpoint. MFH cell proliferation is inhibited selectively by imatinib mesylate, a tyrosine kinase inhibitor. The expressions of platelet-derived growth factor receptors (PDGFRs) and c-Kit have been previously examined in MFH cell lines and the inhibitory effect of imatinib mesylate on the MFH cell proliferation was tested. MFH cell lines showed various patterns of PDGFRs and c-Kit expression. Imatinib mesylate inhibited the proliferation of MFH cells that expressed PDGFRs and/or c-Kit. MATERIALS AND METHODS: Four MFH cell lines were used (Nara H, Nara F, GBS-1 and TNMY1). The mRNA expression of PDGFRs and c-Kit was analyzed using RT-PCR; cell proliferation was analyzed using the MTS assay. Immunohistochemistry was used to analyze the inhibitory effect of imatinib mesylate on phosphorylation of PDGFRs and c-Kit in vivo. The Nara H and TNMY1 cell lines were implanted into nude mice and tumor growth was evaluated daily by measuring the two-dimensional diameters of the tumor nodule. RESULTS: PDGFRs and c-Kit were expressed in Nara F, GBS-1 and TNMY1, but not in Nara H cells. Imatinib mesylate inhibited PDGFRs and c-Kit phosphorylation in TNMY1 cells affecting the tumorigenicity, in the control group (139 mm3 SD +/- 1.03) and treatment group (126.2 mm3 SD +/- 1.63) but did not affect the tumorigenicity of Nara H cells. CONCLUSION: Imatinib mesylate reduced in vivo tumor growth of MFH that express PDGFRs and c-Kit associated with phosphorylation suppression. SN - 0250-7005 UR - https://www.unboundmedicine.com/medline/citation/17352263/Imatinib_mesylate_inhibits_tumorigenicity_of_malignant_fibrous_histiocytoma_cells_in_vivo_ L2 - http://ar.iiarjournals.org/cgi/pmidlookup?view=long&pmid=17352263 DB - PRIME DP - Unbound Medicine ER -