Anticancer research · 2015
Inhibition of placental growth factor in renal cell carcinoma.
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Bessho Hideharu, Wong Bernice, Huang Dan, Siew Ee Yan, Huang Dachuan, Tan Jing, Ong Choon Kiat, Tan Soo Yong, Matsumoto Kazumasa, Iwamura Masatsugu, Teh Bin Tean
Аннотация
BACKGROUND/AIM: Placental growth factor (PlGF) is up-regulated in major malignant diseases or following antiangiogenic therapy, although it is present in low levels under normal physiological conditions. TB403, a monoclonal antibody against PlGF, was investigated in clear cell renal cell carcinoma (ccRCC) xenografts since it has been proposed as a potential target in oncology.
MATERIALS AND METHODS: Human ccRCCs were implanted in athymic nude mice to evaluate the efficacy of TB403 and to excise xenograft tumors for molecular experiments.
RESULTS: TB403 did not significantly inhibit tumor growth in treatment-naïve or sunitinib-resistant ccRCC xenografts. Gene expression profiling resulted in over-expression of the C1orf38 gene, which induced immunoreactivity in macrophages. Angiogenesis PCR arrays showed that VEGFR-1 was not expressed in ccRCC xenografts.
CONCLUSION: PlGF blockade did not have a broad antiangiogenic efficacy; however, it might be effective on-target in VEGFR1-expressing tumors. The inhibition of VEGF pathway may induce the activity of tumor-associated-macrophages for angiogenesis escape.
MATERIALS AND METHODS: Human ccRCCs were implanted in athymic nude mice to evaluate the efficacy of TB403 and to excise xenograft tumors for molecular experiments.
RESULTS: TB403 did not significantly inhibit tumor growth in treatment-naïve or sunitinib-resistant ccRCC xenografts. Gene expression profiling resulted in over-expression of the C1orf38 gene, which induced immunoreactivity in macrophages. Angiogenesis PCR arrays showed that VEGFR-1 was not expressed in ccRCC xenografts.
CONCLUSION: PlGF blockade did not have a broad antiangiogenic efficacy; however, it might be effective on-target in VEGFR1-expressing tumors. The inhibition of VEGF pathway may induce the activity of tumor-associated-macrophages for angiogenesis escape.
Предметные рубрики MeSH
AnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCarcinoma, Renal CellCell Line, TumorDrug Resistance, NeoplasmFemaleHumansIndolesKidney NeoplasmsMice, NudeNeovascularization, PathologicPlacenta Growth FactorPregnancy ProteinsPyrrolesSunitinibTranscriptomeTumor BurdenXenograft Model Antitumor Assays