Lenvatinib Exhibits Potent Anti-tumor Activity and Favorable Safety Profile in a Colorectal Cancer Xenograft Model.
1/5 보강
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
추출되지 않음
I · Intervention 중재 / 시술
lenvatinib at 0, 10, or 20 mg/kg for 20 days
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
[CONCLUSION] Lenvatinib exhibits potent anti-CRC activity with minimal systemic toxicity. Its therapeutic effects are mediated through ERK pathway inactivation, suppression of anti-apoptotic proteins, and induction of caspase-dependent apoptosis.
[BACKGROUND/AIM] Lenvatinib, a multikinase inhibitor, has shown potential anti-tumor activity in various cancers.
APA
Kuo CY, Liao TL, et al. (2026). Lenvatinib Exhibits Potent Anti-tumor Activity and Favorable Safety Profile in a Colorectal Cancer Xenograft Model.. Anticancer research, 46(2), 797-810. https://doi.org/10.21873/anticanres.17988
MLA
Kuo CY, et al.. "Lenvatinib Exhibits Potent Anti-tumor Activity and Favorable Safety Profile in a Colorectal Cancer Xenograft Model.." Anticancer research, vol. 46, no. 2, 2026, pp. 797-810.
PMID
41617418 ↗
Abstract 한글 요약
[BACKGROUND/AIM] Lenvatinib, a multikinase inhibitor, has shown potential anti-tumor activity in various cancers. This study evaluated its efficacy, safety, and apoptotic mechanisms in colorectal cancer (CRC) using HT-29 xenograft-bearing mice.
[MATERIALS AND METHODS] Mice were treated with lenvatinib at 0, 10, or 20 mg/kg for 20 days. Tumor growth, serum biochemistry, and histopathology were assessed. Protein expression related to ERK signaling and apoptosis was analyzed using immunohistochemistry.
[RESULTS] Lenvatinib significantly suppressed CRC tumor growth, delaying progression up to 14-fold compared with controls. No body-weight loss or hepatic/renal toxicity was observed, indicating good tolerability. Mechanistically, lenvatinib reduced phosphorylated ERK and anti-apoptotic proteins (BCL-2, c-FLIP, XIAP) by 30-50%, while enhancing cleaved caspase-3, -8, -9, BAX, and BAK expression by 1.2-1.5-fold, promoting apoptosis.
[CONCLUSION] Lenvatinib exhibits potent anti-CRC activity with minimal systemic toxicity. Its therapeutic effects are mediated through ERK pathway inactivation, suppression of anti-apoptotic proteins, and induction of caspase-dependent apoptosis.
[MATERIALS AND METHODS] Mice were treated with lenvatinib at 0, 10, or 20 mg/kg for 20 days. Tumor growth, serum biochemistry, and histopathology were assessed. Protein expression related to ERK signaling and apoptosis was analyzed using immunohistochemistry.
[RESULTS] Lenvatinib significantly suppressed CRC tumor growth, delaying progression up to 14-fold compared with controls. No body-weight loss or hepatic/renal toxicity was observed, indicating good tolerability. Mechanistically, lenvatinib reduced phosphorylated ERK and anti-apoptotic proteins (BCL-2, c-FLIP, XIAP) by 30-50%, while enhancing cleaved caspase-3, -8, -9, BAX, and BAK expression by 1.2-1.5-fold, promoting apoptosis.
[CONCLUSION] Lenvatinib exhibits potent anti-CRC activity with minimal systemic toxicity. Its therapeutic effects are mediated through ERK pathway inactivation, suppression of anti-apoptotic proteins, and induction of caspase-dependent apoptosis.
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