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Phase II study investigating efficacy and safety of TFTD plus bevacizumab by RAS mutation status in patients with unresectable advanced or recurrent colorectal cancer refractory or intolerant to standard chemotherapy

ABSTRACT: Interventions: TFTD: 35 mg/m. given orally twice daily on days 1-5 and 8-12 in a 28-day cycle Bevacizumab: 5 mg/kg, administered by intravenous infusion for 30 min every 2 weeks Primary outcome(s): Disease control rate (DCR) by RAS mutation status Study Design: Single arm Non-randomized

DISEASE(S): Colorectal Cancer

PROVIDER: 2645249 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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PhaseII study investigating efficacy and safety of TFTD plus bevacizumab by RAS mutation status in patients with unresectable advanced or recurrent colorectal cancer refractory or intolerant to standard chemotherapy (JFMC51-1702-C7)

Project description:Interventions: TFTD: 35 mg/m. given orally twice daily on days 1-5 and 8-12 in a 28-day cycle, Bevacizumab: 5 mg/kg, administered by intravenous infusion for 30 min every 2 weeks Primary outcome(s): Disease control rate (DCR) by RAS mutation status Study Design: single arm study, open(masking not used), uncontrolled control, single assignment, treatment purpose

| 2613978 | ecrin-mdr-crc

A Phase 2 study of concurrent combination therapy of TFTD (TAS-102) and bevacizumab in patients of more than 70 years of age with unresectable, advanced/recurrent colorectal cancer (KSCC 1602)

Project description:Interventions: TFTD 35 mg/m2, po, bid at day 1-5 and day 8-12 and bevacizumab 5mg/kg, iv, every 2 weeks are concurrently administered. The administration is continued until the meeting of discontinuation criteria as 1 course of 28 days. Primary outcome(s): Progression-Free Survival Study Design: Single arm Non-randomized

| 2640480 | ecrin-mdr-crc

A Phase 2 study of concurrent combination therapy of TFTD (TAS-102) and bevacizumab in patients of more than 70 years of age with unresectable, advanced/recurrent colorectal cancer (KSCC 1602)

| 2615810 | ecrin-mdr-crc

Sitravatinib in combination with nivolumab plus ipilimumab in patients with advanced clear cell renal cell carcinoma: a phase 1 trial

Project description:Sitravatinib is an immunomodulatory tyrosine kinase inhibitor that can improve responses when combined with immune checkpoint therapy (ICT). We conducted a phase I trial to determine the optimal dose of triplet therapy with sitravatinib plus nivolumab plus ipilimumab in 22 previously untreated patients with advanced clear cell renal cell carcinoma (ccRCC). The primary endpoint was safety. The addition of even a low sitravatinib dose of 35 mg daily to nivolumab 3 mg/kg and ipilimumab 1 mg/kg resulted in high frequency of immune-related adverse events (irAEs). Subsequent dose reduction of ipilimumab to 0.7 mg/kg in combination with nivolumab 3 mg/kg allowed safe escalation of sitravatinib up to 100 mg daily. Key secondary endpoints were objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS), and overall survival (OS). Overall, the triplet combination in the dose-finding setting achieved an ORR of 45.5%, DCR of 86.4%, and a median PFS of 14.5 months with 72.7% of patients alive after a median follow-up of 15.7 months. Single-cell RNA-seq performed in longitudinally collected tumor biopsies from 12 patients treated with the triplet therapy identified a tumor cell-specific epithelial-mesenchymal transition (EMT)-like program associated with treatment resistance and poor outcomes in patients of this trial and in patients of the TCGA ccRCC cohort. Within the tumor microenvironment (TME), the emergence of treatment resistance was characterized by a transition from cytotoxic to exhausted T cell state and enrichment for M2-like myeloid cells. The observed changes in gene expression dynamics and cellular states in tumor cell and TME may help inform future strategies to optimize ICT efficacy.

2024-11-26 | GSE264586 | GEO

Microflow LC-MS/MS based proteomics of Escherichia Coli and Fosfomycin Experiment 2

Project description:Thermal proteome profiling of E. coli lysate treated with fosfomycin 0.02 mg/ml. Untargeted proteomics with 35 min gradient.

2022-10-09 | MSV000090499 | MassIVE

A phase II study of TFTD plus Bevacizumab in patients with unresectable advanced colorectal cancer

Project description:Interventions: TFTD: fixed dose Bevacizumab: fixed dose Primary outcome(s): Time to treatment failure Study Design: Single arm Non-randomized

| 2650700 | ecrin-mdr-crc

Modulation of the FOLFIRI-based standard 1st-line therapy with cetuximab, controlled by monitoring the RAS mutation load by liquid biopsy in RAS-mutated mCRC patients

Project description:Interventions: Group 1: FOLFIRI or mFOLFIRI (q14d) + cetuximab (q7d): o Irinotecan 180 mg/m² iv, 30 - 90 min, day 1 o Folinic acid (racemic) 400 mg/m² iv, 120 min, day 1 o [5-FU 400 mg/m² bolus, day 1] o 5-FU 2400 mg/m² iv over 46 h, day 1-2 o Cetuximab initially 400 mg/m² as a 120 min infusion (= 5 mg/min); subsequently 250 mg/m² iv as a 60 min infusion (= 10 mg/min), day 1 + 8 One cycle consists of 14 days Group 2: FOLFIRI (q14d): o Irinotecan 180 mg/m² iv, 30 - 90 min, day 1 o Folinic acid (racemic) 400 mg/m² iv, 120 min, day 1 o Fluorouracil (5-FU) 400 mg/m² bolus, day 1 o 5-FU 2400 mg/m² iv over 46 h, day 1-2 OR modified FOLFIRI (mFOLFIRI) (q14d): o Irinotecan 180 mg/m² iv, 30 - 90 min, day 1 o Folinic acid (racemic) 400 mg/m² iv, 120 min, day 1 o 5-FU 2400 mg/m² iv over 46 h, day 1-2 Primary outcome(s): The primary objective is to evaluate efficacy in terms of progression free survival (PFS) from the date of randomization in the study according to Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 criteria in experimental and control arms. Study Design: Allocation: Randomized controlled study; Masking: Open (masking not used); Control: active; Assignment: parallel; Study design purpose: treatment

| 2437805 | ecrin-mdr-crc

Evaluation of outcome and reason of treatment termination of TFTD for colorectal cancer : A retrospective cohort study

Project description:Primary outcome(s): We compare the difference of the overall survival by each reason (RECIST PD, PD by imaging beyond RECIST PD, Clinical PD , adverse event, others) for termination of TFTD.

| 2642797 | ecrin-mdr-crc

Dicer-microRNA-Myc circuit promotes transcription of hundreds of long noncoding RNAs

Project description:Long noncoding RNAs (lncRNAs) are important regulators of cell fate, and their mis-expression has been implicated in many diseases. While distinct polymerases generate messenger vs. noncoding ribosomal or tRNAs3, little is known about distinct mechanisms controlling lncRNA expression. Here we show that transcription of lncRNAs is quantitatively different from that of messenger RNAs (mRNAs)--as revealed by deficiency of Dicer (Dcr), a key ribonuclease that generates microRNAs (miRNAs). Loss of Dcr in mouse embryonic stem cells (mESCs) led surprisingly to decreased level of the majority of lncRNAs. The canonical Dgcr8-Dcr-miRNA pathway is required for robust lncRNA expression, at the level of transcriptional initiation and elongation of lncRNA genes rather than at the level of their stability. cMyc, an oncogenic transcription factor, whose expression is indirectly regulated by Dcr-miRNA in mESCs, is partly responsible for lncRNA transcription. Loss of cMyc led to a more dramatic decrease of lncRNAs than mRNAs, and cMyc overexpression rescues lncRNA expression in Dcr KO cells. A quantitative metric of “mRNA-lncRNA decoupling” revealed that Dcr and cMyc differentially regulate lncRNAs vs. mRNAs in diverse cell types and in vivo, as evidenced by hundreds of microarray experiments. Thus, Dcr and cMyc may allow numerous lncRNAs to be activated or deactivated as a class, implicating lncRNAs to potential regulatory roles in development and disease states where Dcr and cMyc have been associated with.

2014-06-15 | GSE55338 | GEO

Mutation intolerant genes and targets of FMRP are enriched for nonsynonymous alleles in schizophrenia.

Project description:Risk of schizophrenia is conferred by alleles occurring across the full spectrum of frequencies from common SNPs of weak effect through to ultra rare alleles, some of which may be moderately to highly penetrant. Previous studies have suggested that some of the risk of schizophrenia is attributable to uncommon alleles represented on Illumina exome arrays. Here, we present the largest study of exomic variation in schizophrenia to date, using samples from the United Kingdom and Sweden (10,011 schizophrenia cases and 13,791 controls). Single variants, genes, and gene sets were analyzed for association with schizophrenia. No single variant or gene reached genome-wide significance. Among candidate gene sets, we found significant enrichment for rare alleles (minor allele frequency [MAF]?<?0.001) in genes intolerant of loss-of-function (LoF) variation and in genes whose messenger RNAs bind to fragile X mental retardation protein (FMRP). We further delineate the genetic architecture of schizophrenia by excluding a role for uncommon exomic variants (0.01???MAF???0.001) that confer a relatively large effect (odds ratio [OR]?>?4). We also show risk alleles within this frequency range exist, but confer smaller effects and should be identified by larger studies.

| S-EPMC5669020 | biostudies-literature

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