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A phase II trial of lenvatinib in patients with metastatic colorectal cancer after standard chemotherapy

ABSTRACT: Intervention type:DRUG. Intervention1:Lenvatinib, Dose form:CAPSULE, Route of administration:ORAL, intended dose regimen:24mg of lenvatinib is orally taken once daily for 28 days each course. Primary outcome(s): Disease control rate. Timepoint:Every 4 weeks (4th week, 8th week) until 8 weeks from the starting date of treatment , and every 8 weeks (16th week, 24th week, and so on ) after 9 weeks from the starting date of treatment.

DISEASE(S): Metastatic Colorectal Cancer

PROVIDER: 2612407 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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A phase II trial of lenvatinib in patients with metastatic colorectal cancer after standard chemotherapy

Project description:Intervention type:DRUG Name of intervention:Lenvatinib Dose form / Japanese Medical Device Nomenclature:CAPSULE Route of administration / Site of application:ORAL Dose per administration:24mg 24mg 24mg Dosing frequency / Frequency of use:QD Planned duration of intervention:Treatment will continue until the discontinuation criteria are met. Intended dose regimen:24mg of lenvatinib is orally taken once daily for 28 days each course detailes of teratment arms:Treatment will continue with lenvatinib 24mg qd until the criteria of interruption, resuming, reduction and discontinuation of treatment are met. Dose of lenvatinib will be reduced to 20mg, 14mg, 10mg, 8mg, and 4mg qd according to the reduction criteria, and treatment will be discontinued if unable to tolerate at 4mg qd. Comparative intervention name: Dose form / Japanese Medical Device Nomenclature: Route of administration / Site of application: Dose per administration: Dosing frequency / Frequency of use: Planned duration of intervention: Intended dose regimen: Primary outcome(s): Disease control rate Study Design: Open-label, single-arm and single-center trial, no treatment control standard of care control, No, open(masking not used),

| 98667 | ecrin-mdr-crc

Treatment of hepatocellular carcinoma with autologous platelets encapsulating sorafenib or lenvatinib: a novel therapy exploiting tumor-platelet interactions

Project description:Hepatocellular carcinoma (HCC) activates platelets through the action of adjacent sinusoidal cells. Activated platelets bind to tumor-associated endothelial cells and release growth factors that promote tumor progression. We hypothesized that tumor inhibitors encapsulated in platelets would function as drug carriers for tumor therapy. We propose a therapeutic strategy for HCC using autologous platelets encapsulating multiple tyrosine kinase inhibitors in a rat chemically-induced HCC model. Sorafenib or lenvatinib was encapsulated in platelets isolated from tumor-bearing rats in vitro. The rats were divided into groups that received repeated intravenous injections (twice a week for 10 weeks) of the following materials: placebo, sorafenib (SOR), lenvatinib (LEN), autologous platelets, autologous platelets encapsulating sorafenib (SOR-PLT), and autologous platelets encapsulating lenvatinib (LEN-PLT). The therapeutic effect was then analyzed by ultrasonography (US) and histopathological analysis. Histopathological and US analysis demonstrated extensive tumor necrosis in the tumor tissue of SOR-PLT or LEN-PLT, but not in other experimental groups. By liquid chromatography-mass spectrometry, more abundant sorafenib was detected in tumor tissues after SOR-PLT administration than in surrounding normal tissues, but no such difference in sorafenib level was observed with SOR administration. Therefore, the use of autologous platelets encapsulating drugs might be a novel therapeutic strategy for HCC. We investigated the effect of the drug encapsulation process on the degradation of resident mRNA inherited from megakaryocytes in platelets.

2021-12-15 | GSE190863 | GEO

Lenvatinib recruits cytotoxic GZMK+CD8 T cells in hepatocellular carcinoma

Project description:Lenvatinib targets multiple oncogenic kinases including vascular endothelial growth factor receptors (VEGFRs) and showed longer median progression-free survival than sorafenib, the only approved treatment for >10 years. With the successful combination therapy of anti-PD-L1 pembrolizumab and anti-VEGF bevacizumab for advanced HCC as well as encouraging experimental findings, lenvatinib was also expected to enhance anti-tumor effects by combining anti-PD-1 pembrolizumab compared to lenvatinib alone; however, the phase III clinical trial failed to show their synergetic survival benefits, highlighting the need for elucidating its mode of action in human HCC specimens after lenvatinib treatment. We performed multi-layer transcriptome analyses of surgically resected human HCC samples after lenvatinib treatment as a neo-adjuvant therapy using RNA-sequencing. Molecular pathway analyses and immunohistochemistry revealed that VEGF-mediated aberrant vascularity and cytotoxic GZMK+CD8 T cells infiltration were significantly improved in lenvatinib-treated HCC; however, the majority of these cytotoxic T cells were trapped in the intratumor fibrotic stroma, suggesting that lenvatinib-treated HCC is in the so-called excluded condition. Excluded tumors are generally believed to be less responsive to immune checkpoint inhibitors, which might be the reason the combination therapy failed to show the additive benefits.

2023-08-08 | GSE223201 | GEO

Single cell RNA sequencing of immune cells from lenvatinib-resistant mouse HCC model after lenvatinib or combined lenvatinib and CDK4/6 inhibitor palbociclib treatment

Project description:We used single-cell RNA sequencing (scRNA seq) to elucidate the alterations of tumor microenvironment upon combined treatment of lenvatinib and palbociclib (combo).

2023-09-27 | GSE218010 | GEO

RNA Sequencing of HCC cells after lenvatinib, gefitinib, and combination treatment

Project description:Using a kinome-centred CRISPR/Cas9 genetic screen, we identify here that inhibition of the epidermal growth factor receptor (EGFR) is synthetic lethal with lenvatinib in liver cancer cells. We found that the combination of the EGFR inhibitor gefitinib and lenvatinib displays potent anti-proliferative effect in HCC cell lines that express EGFR in vitro and of xenografted HCC cell lines or patient-derived HCC tumours in mice. Herre, we analyzed the different transcriptome profiling of HCC cells treated with DMSO, lenvatinib, gefitinib, and lenvatinib plus gefitinib by RNA-sequencing.

2021-07-22 | GSE157905 | GEO

Co-administration of MDR1 and BCRP or EGFR/PI3K inhibitors overcomes lenvatinib resistance in hepatocellular carcinoma

Project description:To investigate the mechanism of lenvatinib resistance, we established the lenvatinib resistant Huh7 (Huh7 LR) cells by continuous exposuring to lenvatinib (1–20 μM) for approximately 10 months. We then performed gene expression profiling analysis using data obtained from RNA-seq of Huh7 parental (Huh7 P) cells and the lenvatinib resistant Huh7 (Huh7 LR) cells.

2022-08-26 | GSE211850 | GEO

The p-MYH9/USP22/HIF-1α axis promotes lenvatinib resistance and cancer stemness in hepatocellular carcinoma

Project description:To understand the role of HIF1a in lenvatinib resistance, we conducted label-free quantitative proteome analysis in both control and lenvatinib resistance cell lines. This analysis revealed changes in the proteome due to the lenvatinib resistance, providing a valuable reference for further investigations.

2024-08-20 | PXD054805 | Pride

RNA-seq data for parental and lenvatinib-resistant HCC cells

Project description:RNA-seq data for parental and lenvatinib-resistant HCC (Hep3B, Huh7) cells

2022-03-23 | GSE186191 | GEO

RNA-seq analysis of combination effect of H3B-6527 and Lenvatinib treatment in the Hep3B in vivo model

Project description:To investigate the underlying mechanism of the enhanced combination effect of H3B-6527 and Lenvatinib, we conducted RNA-seq analysis of Hep3B cell line xenograft tumors following treatment of tumor bearing mice with one dose of H3B-6527 or Lenvatinib as single agents or in combination. Principal component analysis and hierarchical clustering of differentially expressed genes (differentially expressed genes with adjusted p value < 0.05) showed two largely separated groups in which vehicle and Lenvatinib samples are close to each other whereas the H3B-6527 and the combination samples show similar pattern (Fig. 4A and 4B), suggesting Lenvatinib at 10mg/kg does not drastically alter transcriptional profiles of tumor cells. We then performed pathway enrichment analysis of differentially expressed genes, which showed bile acid metabolism as the top upregulated pathway in H3B-6527 single-agent group, a well-known selective effect to the FGFR4 signaling pathway (Fig. 4C). E2F targets and MYC targets scored as the top downregulated pathways; an effect that is common among many receptor tyrosine kinases including FGFR4. Combination of H3B-6527 and Lenvatinib showed significant upregulation of hypoxia and glycolysis pathways, consistent with anti-angiogenic effect resulting in lack of oxygen and nutrients in tumor microenvironment (Fig. 4C). Moreover, the combination groups showed stronger effects on E2F targets as compared with the single agent groups, and explains the increased antitumor activity observed in efficacy experiments (Fig. 4D). In summary, the RNAseq analysis provided direct mechanistic evidence for the combined anti-angiogenic and anti-tumorigenic effects resulting in enhanced efficacy.

2022-07-13 | GSE198845 | GEO

RNA‐seq of comprehensively examine variations in MHCC-97H cells treated with various doses of lenvatinib at the transcriptomic level.

Project description:To determine the drug target of lenvatinib, RNAseq was used to evaluate the transcriptome differences between lenvatinib-treated MHCC-97H cells and their parental counterparts.Results show that SERPINE1 may be direct target of lenvatinib, and AKR1C1 have potential prognostic significance in the prediction of LR(lenvatinib-resistant) in HCC. AKR1C1 could be a promising therapeutic target for patients with LR-type liver cancer.

2022-11-01 | GSE214324 | GEO

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