Camrelizumab Combined With Apatinib 、XELOX 、RFA in the Treatment of Liver Metastases of Colorectal Cancer
Ontology highlight
ABSTRACT:
DISEASE(S): Hepatic Metastasis Of Colorectal Cancer,Neoplasm Metastasis,Colorectal Neoplasms
PROVIDER: 2324991 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
Similar Datasets
Project description:Interventions: single arm:camrelizumab combined with apatinib mesylate
Primary outcome(s): PFS
Study Design: Single arm
| 2690370 | ecrin-mdr-crc
Project description:Purpose: Primary retroperitoneal liposarcomas (RLPSs) are rare heterogeneous tumors for which there are few effective therapies. Certain anti-angiogenic tyrosine kinase inhibitors have demonstrated efficacy against various solid tumors. The aims of this study were to investigate the effect of Apatinib against retroperitoneal liposarcoma cells and its underlying mechanism and to explore the anti-tumor efficacy of a combination of Apatinib and Epirubicin. Methods: SW872 cells were treated with Apatinib(18μM) for 24 h. The RNAs of the control group and experimental group were stored in TRIzol reagent at -80 ℃. Then mRNA extraction and RNA sequencing were performed by Beijing Mygenostics Co. Ltd., Beijing, China. A Bioanalyzer 2100 System (Agilent Technologies, Santa Clara, CA, USA) was used to assay RNA integrity. An AMPureXP system (BeckmanCoulter, Brea, CA, USA) was used to perform PCR on the products. Quality-tested library preparations were sequenced on the Illumina Novaseq platform (Illumina, San Diego, CA, USA). There were three biological replicates per condition. Differential expression analysis of both groups was performed using DESeq2R v. 1.20.0. The Benjamini-Hochberg multiple hypothesis test correction was performed to obtain the false discovery rate (FDR). The criteria used to select the DEGs were |log2(FoldChange)| > 0.5 and FDR < 0.05. When log2(FoldChange) > 0, the gene was considered upregulated. When log2(FoldChange) < 0, the gene was considered downregulated. profiler package in R (R Core Team, Vienna, Austria) was used for GO function and KEGG pathway enrichment analyses of the DEGs. Histograms and bubble graphs were plotted with the ggplot2 package in R v. 3.4.3. Results:To elucidate the mechanisms by which Apatinib inhibited liposarcoma cells, we used RNA-seq to evaluate relative genetic changes in the SW872 cells after being treated with Apatinib for 24 hs, and found 2,038 DEGs, including 1,059 significantly downregulated genes and 979 significantly upregulated genes. The output of the KEGG pathway enrichment analysis suggests that Apatinib might inhibit SW872 cell proliferation through p53, DNA replication, and other important signaling pathways. GO enrichment analysis was performed on the genes that were significantly altered after Apatinib application.High-throughput RNA sequencing showed that Apatinib downregulated the expression of TYMS and RRM2. Conclusions: Apatinib showed strong efficacy against liposarcoma both in vitro and in vivo. Apatinib might inhibit liposarcoma cell proliferation through the RRM2/PI3K/AKT/mTOR signaling pathway and downregulate PD-L1 via the TYMS/STAT3 signaling pathway.
2021-11-03 | GSE185783 | GEO
Project description:Interventions: experimental group:Apatinib combined with oxaliplatin and capecitabine (XELOX) g
Primary outcome(s): Disease free survival
Study Design: Single arm
| 2759132 | ecrin-mdr-crc
Project description:This study makes an observation over the objective response rate of Apatinib and XELOX combination regimen in the first-line treatment of metastatic colorectal cancer. All the participants will receive the treatment of Apatinib and XELOX combination regimen.
| 2219525 | ecrin-mdr-crc
Project description:Targeted therapy for patients with EGFR mutations by tyrosine kinase inhibitors (TKIs) has provided a significant benefit to patients. However, gradually developed resistance to the therapy becomes a major challenge in clinical practice. Herein, we report that Apatinib, an anti-angiogenic drug, strongly and specifically inhibits Gefitinib-resistant cancer cells but not their parental sensitive cells. Gefitinib-resistant lung cancer cell line (PC9GR) was established from its parental sensitive line (PC9) with a traditional EGFR mutation after long time exposure to Gefitinib. The established PC9GR cells had over 250 fold increased resistance to Gefitinib than its sensitive parental PC9 cells. Apatinib demonstrated much stronger (~5 fold) growth inhibition on PC9GR cells than on PC9 and other lung cancer cell lines. This inhibition was mostly achieved through cell cycle rest in G1 phase as demonstrated by transcriptome and protein expression data. Oral intake of Apatinib in mouse model significantly inhibited establishment and growth of PC9GR implanted tumors. VEGFR2 phosphorylation in PC9GR tumors after Apatinib treatment was significantly reduced along with less micro-vessel formation. Apatinib may provide a benefit to patients with acquired resistance to TKI treatment.
2019-05-15 | GSE129221 | GEO
Project description:Interventions: Case series:Mesylate Apatinib
Primary outcome(s): R0 resection rate;AE
Study Design: Case series
| 2676351 | ecrin-mdr-crc
Project description:Interventions: Experimental group:Apatinib 250mg po, qd, continuous taken; XELOX: Oxaliplatin 135 mg/m2 Ivgtt d1, Capecitabine 1000mg/m2 d1-14, q3w;Control group:Bevacizumab 7.5mg/kg, q3w; XELOX: Oxaliplatin 135 mg/m2 Ivgtt d1, Capecitabine 1000mg/m2 d1-14, q3w
Primary outcome(s): Progress-free survival (PFS)
Study Design: Non randomized control
| 2687981 | ecrin-mdr-crc
Project description:Methods83 patients with hepatocellular carcinoma (HCC) admitted to the interventional oncology department were randomly divided into two groups. Apatinib and camrelizumab were administered to 42 patients in group A, whereas sorafenib was administered to 41 patients in group B for three months. The clinical efficacy was evaluated in terms of objective response rate (ORR), and disease control rate (DCR). Certain tumor markers like alpha-fetoprotein (AFP), carbohydrate antigen 199 (CA199), carcinoembryonic antigen (CEA), hypoxia-inducible factor (HIF-1), immune function T lymphocyte subsets (CD3+, CD4+, CD8+, CD4+/CD8+) were determined before and after treatment. The serum levels of vascular endothelial growth factor (VEGF), osteopontin (OPN), aspartate aminotransferase (AST), and epidermal growth factor 7 (EGF7)] were observed. The survival time between the two groups was compared, such as progression-free survival (PFS) and median survival (MS). Finally, the toxicity and side effects data were also obtained.ResultsThe ORR and DCR of group A were 69.05% and 88.10%, respectively, which were significantly higher (P<0.05) than group B (ORR=53.66% and DCR=70.73%). After treatment, the AFP, CA199, CEA, and HIF-1 levels of both groups decreased significantly (P<0.05), and the respective biomarker levels of group A were lower than those of group B (P<0.05). Following treatment, CD3+, CD4+, CD4+/CD8+ index in group A significantly increased (P<0.05) while CD8+ level was significantly decreased (P<0.05). Compared to group B, a significant increase was observed in group A's CD3+, CD4+, and CD4+/CD8+ index. There were no significant changes in CD3+, CD4+, CD8+, CD4+/CD8+ indexes before and after treatment in group B (P>0.05). The serum level of VEGF, OPN, EGF-7 and AST indexes of group A&B were decreased significantly (P<0.05). Compared with group B, the VEGF, OPN, EGF7 and AST indexes of group A were significantly reduced (P<0.05). PFS and MS in group A were significantly higher than in group B (P<0.05). There was no significant difference between groups A and B in terms of toxicity and adverse effects (P>0.05).ConclusionIn treating HCC, combining apatinib and camrelizumab can reduce tumor markers, enhance the immune system and curative effect, and prolong patient survival. The underline mechanism is related to the down-regulation of VEGF, OPN and HIF-1 indexes.
| S-EPMC10090460 | biostudies-literature
Project description:IntroductionCurrent clinical guidelines recommend systematic antitumour therapy as the primary treatment option for patients with stage IIIb hepatocellular carcinoma (HCC) based on the China liver cancer (CNLC) staging criteria. Several different targeted therapeutics have been applied in combination with immunotherapeutic regimens to date in patients with advanced HCC. The present study was developed to evaluate the relative safety and efficacy of hepatectomy of HCC in combination with targeted apatinib treatment and immunotherapeutic camrelizumab treatment CNLC-IIIb stage HCC patients with the goal of providing evidence regarding the potential value of this therapeutic regimen in individuals diagnosed with advanced HCC.Methods and analysisThis is a multicentre phase II trial with single-arm in which patients undergo hepatectomy in combination with targeted treatment (apatinib) and immunotherapy (camrelizumab). Patients will undergo follow-up every 2-3 months following treatment initiation to record any evidence of disease progression and adverse event incidence for a minimum of 24 months following the discontinuation of treatment until reaching study endpoint events or trial termination. The primary endpoint for this study is patient mortality.Ethics and disseminationThis study protocol was approved by the Ethics Committee of the Guangxi Medical University Cancer Hospital (KS2022[124]). The results of this study will be submitted for publication in a peer-reviewed journal.Trial registration numberNCT05062837.
| S-EPMC10546157 | biostudies-literature
Project description:Gallbladder carcinoma (GBC) with proficient mismatch repair (pMMR)/microsatellite stable (MSS) is associated with limited response to programmed death-1 (PD-1) inhibitor monotherapy. Limited data of PD-1 blockade combined with anti-angiogenic therapy in GBC are reported. One recurrent GBC patient with pMMR/MSS was treated with camrelizumab plus apatinib. After 4 cycles of combination therapy, the patient achieved a durable complete response with manageable toxicity. The next-generation sequencing and immunohistochemistry analysis showed that tumor mutation burden (TMB) was 7.26 mutants/Mb and PD-L1 expression was 10% (tumor proportion score) and 20% (immune proportion score). This case suggests that camrelizumab in combination with apatinib may be an effective treatment option for GBC patients with pMMR/MSS status, who have moderate expression of TMB and PD-L1. Additionally, TMB and PD-L1 expression may serve as potential biomarkers for predicting PD-1 inhibitor response of GBC. Furthermore, this needs to be verified in future studies.
| S-EPMC8792461 | biostudies-literature