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Multicenter Phase 1b/2 Trial of Nintedanib with TAS-102 in Patients with Metastatic Colorectal Cancer (mCRC) who had the progression or intolerant to standard therapies.

ABSTRACT: Interventions: 1 cycle is 28days. Nintedanib (150mg or 200mg) is orally administered twice daily and TAS-102 (35mg/m2) is orally administered twice daily in 1-5days and 8-12 days Primary outcome(s): 16 weeks progression free survival rate ( 16W PFS rate) Study Design: Single arm Non-randomized

DISEASE(S): Advanced Colorectal Cancer

PROVIDER: 2632430 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Multicenter Phase 1b/2 Trial of TAS-102 with Bevacizumab in Patients with Metastatic Colorectal Cancer (mCRC) who had the progression or intolerant to standard therapies.

Project description:Interventions: 1 cycle is 28days. TAS-102(35mg/m2) is administered orally twice daily in 1-5days and 8-12 days and Bevacizumab(5mg/kg) is administered by injection in day 1 and day15. Primary outcome(s): 4 month progression free survival by central assessment( 4M PFS) Study Design: Single arm Non-randomized

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Phase 1 Trial of Lonsurf with Irinotecan and Bevacizumab in Patients with Unresectable Metastatic Colorectal Cancer(mCRC).

Project description:Interventions: 1 cycle is 28days. Lonsurf(25mg/m2)is administered orally twice daily in 1-5days and 8-12 days. Irinotecan(100mg/m2) and Bevacizumab(5mg/kg) is administered by injection in day 1 and day15. Primary outcome(s): Recommended dose:RD Study Design: Single arm Non-randomized

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Gene expression profiling using RNA-Seq data of MMTV-Wnt1 tumor tissue from mice treated with E7386

Project description:We conducted an RNA-Seq analysis using total RNA extracted from MMTV-Wnt1 tumor tissues resected from mice orally administered E7386 at 25 or 50 mg/kg twice daily, or vehicle, for 3 days (Day 4) or 7 days (Day 8) and examined the differentially expressed gene levels compared with vehicle at days 4 and 8.

2020-12-21 | GSE158713 | GEO

Nintedanib induces senolytic effect via STAT3 inhibition

Project description:Selective removal of senescent cells, or the concept of senolytic therapy, has been proposed to be a potent strategy for overcoming age-related diseases and even reversing aging. We found that nintedanib, a tyrosine kinase inhibitor, selectively induced cell death in primary human diploid fibroblasts undergoing replicative senescence. Similar to ABT263, a well-known senolytic agent, nintedanib triggered intrinsic apoptosis in senescent cells. Additionally, at the concentration producing the senolytic effect, nintedanib arrested the cell cycle of nonsenescent cells in the G1 phase without cytotoxicity. Interestingly, compared with ABT263, nintedanib showed a different mode of activating caspase-9 in the intrinsic apoptotic pathway, in that nintedanib did not suppress the levels of Bcl-2 family proteins in senescent cells. In more detail, nintedanib suppressed the activation of the JAK2/STAT3 pathway, which caused drug-induced cell death in senescent cells. STAT3 knockdown in senescent cells also induced caspase activation. Moreover, nintedanib reduced the number of senescent cells stained based on senescence-associated β-galactosidase activity and airway resistance in a mouse model of bleomycin-induced lung fibrosis. Overall, we identified that nintedanib could be used as a new senolytic agent and that inhibiting STAT3 could be a potential approach for inducing selective cell death in senescent cells. Our findings will pave the way for expanding senolytic toolkits in response to various aging statuses and age-related diseases.

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Project description:Nintedanib is a potent anti-fibrotic angio-kinase inhibitor, which has shown clinical efficacy in combination with chemotherapy in locally advanced muscle invasive BC patients. Nintedanib inhibits Fibroblast Growth Factor receptors (FGFRs), validated targets in patients with BC harboring FGFR3/2 genetic alterations. Here, we aimed at studying its mechanisms of action to understand therapy their combination (n=4). Reads were mapped separately against the human and mouse genomes to differentiate tumor vs. stromal expression changes

2023-04-13 | GSE182833 | GEO

Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib;Alpelisib treated bladder tumors

2023-04-13 | GSE218575 | GEO

Gene Expression Changes Associated with Nintedanib Treatment in Idiopathic Pulmonary Fibrosis Fibroblasts [miRNA-seq]

Project description:We found strong protein-protein interactions within these dysregulated genes in nintedanib treated IPF fibroblast, with most genes involved in the pathways of cell cycle, mitotic cell cycle, and cell division. In IPF fibroblasts, we found nintedanib treatment was associated with downregulation of has-miR-92a-1-5p, which might de-repress SLC25A23 expression, and upregulation of has-miR-486-5p, which might repress DDX11, E2F1, and PLXNA4 expressions.

2019-04-08 | GSE124787 | GEO

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