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Effects of intestinal microflora transplantation on the efficacy of PD-1 monoclonal antibody combined with TKI in the treatment of patients with secondary drug resistance to advanced liver cancer

ABSTRACT: Interventions: Experimental group:Tirelizumab combined with TKI therapy, after disease control, patients with further progression were treated with intestinal flora transplantation based on the original regimen Primary outcome(s): Disease control rate Study Design: Single arm

DISEASE(S): Hepatocellular Carcinoma

PROVIDER: 38658 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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TKI

Project description:TKI

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TFF3 drives Hippo dependent EGFR-TKI resistance in lung adenocarcinoma

Project description:Intrinsic and acquired resistance represent major obstacles to optimize outcomes in epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) targeted therapy in lung adenocarcinoma (LUAD). Hence, a deeper understanding of EGFR-TKI resistance mechanisms in LUAD will potentially assist in formulating strategies to delay or overcome such resistance. Herein, it was observed that trefoil factor 3 (TFF3) is a crucial mediator of the LUAD EGFR-TKI response. TFF3 conferred intrinsic resistance to EGFR inhibition in LUAD by promotion of EGFR activation. TFF3 expression was also increased in acquired EGFR-TKI resistant LUAD, accompanied by reduced EGFR activation. YAP, a key mediator of the Hippo signaling, was positively regulated by TFF3 by post-transcriptional mechanisms and was responsible for acquired EGFR-TKI resistance mediated by TFF3. Inhibition of TFF3 by a small molecule inhibitor not only enhanced EGFR-TKI sensitivity in LUAD cells but also restored the sensitivity of acquired EGFR-TKI resistant LUAD cells to EGFR-TKIs in vitro and in vivo. These findings demonstrate a pivotal function of TFF3 in mediating EGFR-TKI resistance in LUAD and may offer a potential therapeutic mechanism for delaying or overcoming resistance to EGFR-TKIs.

2025-10-31 | GSE276990 | GEO

BCAT1 contributes to the developmentproliferation and leukemogenesis of TKI-resistant CML

Project description:In this report, we revealed that branched chain amino acid transaminase 1 (BCAT1) is highly enriched in both mouse and human TKI-resistant CML cells. Leukemia was almost completely abrogated upon BCAT1 knockdown during transplantation in a BCR-ABLT315I-induced murine TKI-resistant CML model . Moreover, knockdown of BCAT1 led to a dramatic decrease in the proliferation of TKI-resistant human leukemia cell lines. BCAA/BCAT1 signaling enhanced the phosphorylation of CREB, which is required for maintenance of TKI-resistant CML cells. Importantly, blockade of BCAA/BCAT1 signaling efficiently inhibited leukemogenesis both in vivo and in vitro.

2024-05-30 | GSE262421 | GEO

Microarray expression profile of long noncoding RNAs in EGFR-TKI resistance of lung adenocarcinoma

Project description:Lung adenocarcinoma cells harboring epidermal growth factor receptor (EGFR) mutations are sensitive to EGFR tyrosine kinase inhibitors (TKIs). Prolonged cancer treatment will induce the development of acquired resistance to EGFR TKI. To gain insight into the molecular mechanisms of EGFR-TKIs resistance, we generate EGFR-TKI-resistant HCC827-8-1 cells to be analyzed by microarray with their parental HCC827cells. gefitinib resistant HCC827-8-1 cells with three replications; gefitinib-sensitive HCC827 cells with three replications

2016-08-23 | E-GEOD-74575 | biostudies-arrayexpress

Whole exome sequencing of EGFR-TKI naive and EGFR-TKI resistant lung adenocarcinoma samples

Project description:Whole exome sequencing was performed on set of 48 DNA samples obtained from 16 EGFR mutated NSCLC patients whose tumors progressed following EGFR-TKI treatment. The DNA samples included baseline biopsy, rebiopsy and blood from the same patient. By comparing the variants in rebiopsy tumors and baseline tumors we aim to understand the genomic alterations responsible for the development of EGFR-TKI resistance in NSCLC patients.

2022-02-11 | E-MTAB-11404 | biostudies-arrayexpress

Transcriptome profiling to determine molecular mechanisms of acquired EGFR TKI resistance

Project description:The goal of this study was to compare the transcriptome (RNA-seq) of EGFR TKI sensitive NSCLC cells with that of cells with acquired resistance to erlotinib. HCC827 and HCC4006 cells were continuously cultured in erlotinib until erlotinib resistant (ER) variants emerged. All ER variants were negative for T790M. RNA from parental and ER cells was isolated for transcriptomic profiling. RNA-seq analysis reveals that EGFR TKI resistance is associated with a mesenchymal gene expression signature.

2020-09-03 | GSE121634 | GEO

Differential mRNA expression analysis of EGFR-TKI-sensitive cells vs. EGFR-TKI-resistant cells

Project description:Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistance remains unknown. We determined gene expression profiling in EGFR-TKI-resistant cells using RNA-seq analysis

2021-04-18 | GSE172002 | GEO

Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 3]

Project description:To unravel the intricate interplay among Oxr1, ROS-induced genetic changes, and dynamics influencing TKI resistance and CML progression

2025-11-12 | GSE281955 | GEO

Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 2]

Project description:To unravel the intricate interplay among Oxr1, ROS-induced genetic changes, and dynamics influencing TKI resistance and CML progression

2025-11-12 | GSE281954 | GEO

Oxidation Resistance 1 (Oxr1) Dysregulation Promotes TKI Resistance and Blast Crisis in Chronic Myeloid Leukemia [dataset 1]

Project description:To unravel the intricate interplay among Oxr1, ROS-induced genetic changes, and dynamics influencing TKI resistance and CML progression

2025-11-12 | GSE281856 | GEO

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