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Temozolomide, Cisplatin, and Nivolumab in People With Colorectal Cancer

ABSTRACT: This study will test whether the combination of cisplatin, nivolumab, and temozolomide is an effective treatment for in people with advanced and/or metastatic colorectal cancer that is mismatch repair-proficient (MMR-proficient). The researchers will also look at how safe the study drug combination is in participants.

DISEASE(S): Adenocarcinoma,Colorectal Adenocarcinoma,Colorectal Neoplasms

PROVIDER: 2344524 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Determining the Effects of Temozolomide Followed by Nivolumab in Patients With Colorectal Cancer

Project description:The purpose of this study is to find out whether temozolomide followed by nivolumab is an effective treatment for MMR-proficient colorectal cancer, while causing few or mild side effects.

| 2300172 | ecrin-mdr-crc

Interrelationships between replication infidelity and genome composition

Project description:An enduring issue in evolutionary and cancer biology is how replication infidelity influences genome composition and vice versa. Here we examine this issue by sequencing the genomes of diploid budding yeast strains that are either mismatch repair (MMR) proficient or deficient and encode wild type or mutator variants of the three major nuclear DNA replicases. Analysis of over 43,000 mutations that accumulated in the absence of selective pressure demonstrates that the nuclear DNA replication machinery generates less than one mismatch per genome and in combination with MMR, achieves a genome-wide per base error rate of 1.7 x 10-10. Absent both MMR and purifying selection, replication error patterns strongly depend on replication origin proximity, replication fork direction, and the local DNA sequence. Preferred sequences were observed for base substitutions and deletions. Error rates also vary with replication time, in linker versus nucleosome-bound DNA, in 5'- and 3'-untranslated regions, in coding regions and in intergenic DNA. This genome-wide view shows that replication fidelity is amazingly high but heterogeneous, in patterns that suggest the underlying mechanisms by which replication modulates genome stability and composition and vice versa. Six to ten isolates were sequenced for each combination of DNA polymerase (WT, pol1-L868M, pol2-M644G, pol3-L612M) and mismatch repair (proficient, deficient) genotypes. A single WT isolate was sequenced following micrococcal nuclease digestion.

2014-08-25 | E-GEOD-56939 | biostudies-arrayexpress

Genomic profiling of colorectal cancer from patients with Lynch syndrome and Familial colorectal cancer type X with comparison to sporadic microsatelite stable and instable colorectal cancer

Project description:Lynch syndrome and Familial colorectal cancer type X (FCCTX) are clinically diagnosed using the same criteria, but genomic differences exist between these two groups and the genomic profiles share similarities with their sporadic counterparts, mismatch repair (MMR) deficient and proficient tumors, respectively. Array-based comparative genomic hybridization was performed on 91 tumors, comprising 23 Lynch syndrome (AH), 23 FCCTX (AA), 23 sporadic MMR deficient (AM) and 22 sporadic MMR proficient tumors, in order to identify differences between Lynch syndrome and FCCTX.

2012-06-01 | E-GEOD-38405 | biostudies-arrayexpress

Genome-wide analysis of miRNA levels in colon cancer

Project description:Analysis of miRNA levels found in tissue obtained from proficient mismatch repair (pMMR) TNM stage 2|3|4 colon tumor, deficient MMR (dMMR) colon tumor, and normal colon.

2010-03-18 | GSE18392 | GEO

Gene profile of glioblastoma cells treated with y15 and temozolomide

Project description:The gene expression profiles were identified in glioblastoma cells treated with FAK inhibitor Y15, temozolomide alone or with combination of Y15 and Temozolomide DBTRG and U87 were treated with FAK inhibitor Y15 at 10 microM for 24 h; U87 cells were treated with Temozolomide 100 microM for 24 h and Y15+temozolomide at the same dose as each agent alone

2013-01-12 | E-GEOD-43452 | biostudies-arrayexpress

NIVOLUMAB Plus IPILIMUMAB and TEMOZOLOMIDE in Microsatellite Stable, MGMT Silenced Metastatic Colorectal Cancer

Project description:This is a Phase II, multicenter, single-arm trial designed to evaluate the efficacy and safety of nivolumab (NIVO), ipilimumab (IPI) and temozolomide (TMZ) combination in 27 patients with MSS, MGMT-silenced mCRC with initial clinical benefit following lead-in treatment with single-agent TMZ. Immune checkpoint inhibitors have been shown to trigger durable antitumor effects in a subset of patients. A high number of tumor mutations (so called ‘tumor mutational burden’) has recently been found associated with increased immunogenicity (due to a high number of neoantigens) and improved treatment efficacy across several different solid tumors. In mCRCs, only a small fraction of tumors (<5%) display a high mutational load and are usually associated with inactivation of mismatch repair genes such as MLH1, MSH2 and MSH6. Checkpoint inhibitors may have increased activity in dMMR/microsatellite instability-high (MSI-H) tumors, a hypothesis which was tested in various Phase II trials with positive results. On the opposite, mismatch repair proficient colorectal cancer is unresponsive to immune checkpoint inhibitors. Previous reports indicate that acquired resistance to TMZ may emerge through the induction of a microsatellite-instability-positive phenotype and recent data showed that inactivation of MMR, driven by acquired resistance to the clinical agent temozolomide, increased mutational load, promoted continuous renewal of neoantigens in human colorectal cancers and triggered immune surveillance in mouse models. On all of the above grounds, the investigators hypothesize that treatment of microsatellite stable MGMT hypermethylated CRCs with alkylating agents could reshape the tumor genetic landscape by increasing the tumor mutational burden, leading to achieve potential sensitization to immunotherapy.

| 2296546 | ecrin-mdr-crc

Genomic profiling of colorectal cancer from patients with Lynch syndrome and Familial colorectal cancer type X with comparison to sporadic microsatelite stable and instable colorectal cancer

2012-06-02 | GSE38405 | GEO

Antibody DS-8273a Administered in Combination With Nivolumab in Subjects With Advanced Colorectal Cancer

Project description:This trial is being performed in two parts: Dose Escalation and Dose Expansion. The primary objective for the Dose Escalation part is to determine the safety and tolerability at different doses of DS-8273a administered in combination with nivolumab and to identify the dose combination for the Dose Expansion cohort in subjects with mismatch repair (MMR)-proficient advanced colorectal cancer. The primary objectives for the Dose Expansion part are: * To further evaluate the safety and tolerability of DS-8273a administered at the selected dose in combination with nivolumab in subjects with MMR-proficient advanced colorectal cancer * To evaluate preliminary anti-tumor activity of DS-8273a plus nivolumab administered at the selected dose in subjects with MMR-proficient advanced colorectal cancer

| 2231940 | ecrin-mdr-crc

Genome-wide analysis of miRNA levels in colon cancer

Project description:Analysis of miRNA levels found in tissue obtained from proficient mismatch repair (pMMR) TNM stage 2|3|4 colon tumor, deficient MMR (dMMR) colon tumor, and normal colon. miRNA levels obtained from macrodissected colon tumors with > 70% H&E staining were compared with normal colon tissue. Additional comparisons based on mismatch repair status identified by loss of hMLH1 protein and microsattelite instability assay and TNM stage were carried out. This submission provides access to the data discussed in our paper. The supplementary file 'GSE18392_non-normalized_data.txt' file contains non-normalized data for Samples GSM458618-GSM458762.

2010-03-18 | E-GEOD-18392 | biostudies-arrayexpress

Gene profile of glioblastoma cells treated with y15 and temozolomide

Project description:The gene expression profiles were identified in glioblastoma cells treated with FAK inhibitor Y15, temozolomide alone or with combination of Y15 and Temozolomide

2013-01-12 | GSE43452 | GEO

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