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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)

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 study, open(masking not used), uncontrolled control, single assignment, treatment purpose

DISEASE(S): Colorectal Cancer

PROVIDER: 2613978 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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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

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 Non-randomized

| 2645249 | ecrin-mdr-crc

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

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

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

Expression profiling of lung cancer cell lines

Project description:Purpose: To determine the 8-week disease control rate (DCR) of sorafenib monotherapy in patients with advanced non-small-cell lung cancer (NSCLC) in the BATTLE trial. Methods: Patients with pre-treated NSCLC, ECOG performance status (PS) 0-2, consented to biopsies to test for biomarker assessment. Sorafenib was given at 400 mg orally twice daily until tumor progression or an unacceptable toxicity. Tumor evaluations were performed at baseline and every 8 weeks. Correlations of outcomes by biomarker groups were analyzed. Results: 105 patients were eligible and 98 patients were evaluable. Median age was 62 (range 34-81) years, 51% of patients were male, 75% were former/current smokers, and 89% had an ECOG PS of 0-1. Median prior chemotherapies for stage IV NSCLC were two. Median follow-up was 9.4 (range: 1.3-32.2) months. Eight-week DCRs by histology were 59.1%, 57.1%, and 55.6% for adenocarcinomas, squamous cell carcinomas and other histologies respectively. Patients with tumors harboring EGFR mutations had significantly lower 8-week DCR compared to patients with wild-type tumors (23.1% vs. 64.2%, P=0.0119), and patients with tumors harboring K-RAS mutations had the highest 8-week DCR (67%). Most commonly reported treatment-related adverse events include hand-foot syndrome (59.6%), fatigue (42.3%), rash (40.4%), diarrhea (38.5%), and weight loss (38.5%). Conclusion: 8-week DCR was better in patients treated with sorafenib who had EGFR wild-type tumors (including those with K-RAS mutations) when compared to those who had EGFR mutations. Additional analyses are warranted to further explore the biology of these tumors and related patient outcomes with sorafenib treatment. ClinicalTrials.gov number, NCT00411671.

2012-06-18 | GSE32036 | GEO

Final efficacy and biomarker analysis of the sorafenib arm of the BATTLE (Biomarker-Integrated Approaches of Targeted Therapy for Lung Cancer Elimination) trial

Project description:Purpose: To determine the 8-week disease control rate (DCR) of sorafenib monotherapy in patients with advanced non-small-cell lung cancer (NSCLC) in the BATTLE trial. Methods: Patients with pre-treated NSCLC consented to baseline biopsies for pre-specified biomarkers assessment and biomarker discovery. Sorafenib was given at 400 mg orally twice daily until tumor progression or unacceptable toxicity. Outcomes by pre-specified biomarkers were analyzed and a Sorafenib sensitivity signature developed using high-throughput gene expression profiles of NSCLC cell lines and baseline biopsies. Results: 105 patients were eligible and 98 patients were evaluable. Median age was 62 (range 34-81) years, 51% of patients were male, 75% were former/current smokers, and 89% had an ECOG performance status of 0-1. Median prior chemotherapies for stage IV NSCLC were two. Median follow-up was 9.4 (range: 1.3-32.2) months. Overall, 8-week DCR was 58.2%. Patients with EGFR mutations had significantly lower 8-week DCR compared to patients with wild-type tumors (23.1% vs. 64.2%, P=0.0119), and patients with K-RAS mutations had the highest 8-week DCR (67%). Most commonly reported treatment-related adverse events include hand-foot syndrome (59.6%), fatigue (42.3%), rash (40.4%), diarrhea (38.5%), and weight loss (38.5%). Sorafenib sensitivity signature developed in cell lines was associated with an improved outcome. Conclusion: Patients with wild-type EGFR, including those with K-RAS mutation, may benefit from sorafenib as opposed to patients with EGFR mutation. We identify a gene expression signature associated with an improved outcome in patients with wild-type EGFR treated with sorafenib. BATTLE-2 trial is ongoing to validate those results. ClinicalTrials.gov number, NCT00411671.

2014-06-01 | GSE31428 | GEO

Multicenter Phese II Study of SOX plus Bevacizumab Therapy with Oxaliplatin Stop-and-Go Strategy and Oral S-1 plus Bevacizumab Maintenance Therapy in Advanced Colorectal CancerC

Project description:Interventions: (1)Initial therapy : SOX+bevacizumab therapy Bev : 7.5 mg/kg (90 min) L-OHP : 130 mg/m2 (120 min) S-1 : 80 - 120 mg/day (Day1-15) (2)Maintenance therapy : S-1+bevacizumab therapy Bev : 7.5 mg/kg (90 min) S-1 : 80 - 120 mg/day (Day1-15) (3)Reintroduced therapy : SOX+bevacizumab therapy Primary outcome(s): DDC ; Duration of disease control) Study Design: Single arm Non-randomized

| 2627046 | ecrin-mdr-crc

Processing of Drosophila endo-siRNAs depends on a specific Loquacious isoform

Project description:Drosophila melanogaster expresses three classes of small RNAs, which are classified according to their mechanisms of biogenesis. MicroRNAs are ~22-23-nt, ubiquitously expressed small RNAs that are sequentially processed from hairpin-like precursors by Drosha/Pasha and Dcr-1/Loquacious complexes. MicroRNAs usually associate with AGO1 and regulate the expression of protein-coding genes. Piwi-interacting RNAs (piRNAs) of ~24-28-nt associate with Piwi-family proteins and can arise from single-stranded precursors. piRNAs function in transposon silencing and are mainly restricted to gonadal tissues. Endo-siRNAs are found in both germline and somatic tissues. These ~21-nt RNAs are produced by a distinct Dicer, Dcr-2, and do not depend on Drosha/Pasha complexes. They predominantly bind to AGO2 and target both mobile elements and protein-coding genes. Surprisingly, a subset of endo-siRNAs strongly depend for their production on the dsRNA-binding protein Loquacious (Loqs), thought generally to be a partner for Dcr-1 and a co-factor for miRNA biogenesis. Endo-siRNA production depends on a specific Loqs isoform, Loqs-PD, which is distinct from the one, Loqs-PB, required for the production of microRNAs. Paralleling their roles in the biogenesis of distinct small RNA classes, Loqs-PD and Loqs-PB bind to different Dicer proteins, with Dcr-1/Loqs-PB complexes and Dcr-2/Loqs-PD complexes driving microRNA and endo-siRNA biogenesis, respectively. Small RNA profiling by high throughput sequencing

2009-07-31 | GSE17171 | GEO

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