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Study Using IMC-A12 (Cixutumumab) With or Without Cetuximab in Participants With Metastatic Colorectal Cancer Who Have Failed a Treatment Regimen That Consisted of a Prior Anti-EGFR Therapy

ABSTRACT: Participants with metastatic Colorectal Cancer (mCRC) who have progressed on a prior Anti-epidermal growth factor receptor (EGFR) regimen randomized to receive IMC-A12 monotherapy or combination therapy with cetuximab to assess response, survival, durations of response, safety and tolerability as well as pharmacodynamics of IMC-A12 and cetuximab

DISEASE(S): Colorectal Cancer,Colorectal Neoplasms,Disease Progression

PROVIDER: 2042264 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Intermitochondrial cement (IMC) harbors piRNA biogenesis machinery and exonuclease domain-containing proteins EXD1 and EXD2 in mouse spermatocytes

Project description:Germ granules are large cytoplasmic ribonucleoprotein complexes that emerge in the germline to participate in RNA regulation. The two most prominent germ granules are the intermitochondrial cement (IMC) in meiotic spermatocytes and the chromatoid body (CB) in haploid round spermatids, both functionally linked to the PIWI-interacting RNA (piRNA) pathway. In this study, we clarified the IMC function by identifying proteins that form complexes with a well-known IMC protein PIWIL2/MILI in the mouse testis. The PIWIL2 interactome included several proteins with known functions in piRNA biogenesis. We further characterized the expression and localization of two of the identified proteins, Exonuclease 3′–5′ domain-containing proteins EXD1 and EXD2, and confirmed their localization to the IMC. We showed that EXD2 interacts with PIWIL2, and that the mutation of Exd2 exonuclease domain in mice induces misregulation of piRNA levels originating from specific pachytene piRNA clusters, but does not disrupt male fertility. Altogether, this study highlights the central role of the IMC as a platform for piRNA biogenesis, and suggests that EXD1 and EXD2 function in the IMC-mediated RNA regulation in postnatal male germ cells.

2023-12-21 | GSE194043 | GEO

Expression data from distinct populations of iMC from the small intestine of Ackr4(+/gfp) mice

Project description:Mesenchymal cells play key roles in modulating tissue homeostasis in various organs, including the intestine. Here we show that the murine intestinal mesenchymal cells are heterogenous, comprising at least three distinct populations. In this dataset, we include the expression data obtained from sorted subsets of CD45-Ter119-EPCAM-GP38+CD31- murine intestinal mesenchymal cell (iMC) populations. The iMC populations were separated into: CD146+ cells, which expressed CD9 and CD29, but not Ackr4, SCA1, ICAM1 or PDGFRa; GFP+ fibroblasts, which expressed Ackr4, SCA1, ICAM1 and PDGFRa; and GFP- fibroblasts, which also expressed SCA1, ICAM1 and PDGFRa, but were negative for Ackr4 expression.

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A Study of Irinotecan and Cetuximab With or Without IMC-A12 for Treatment of Participants With Colon or Rectum Cancer Who Got Worse After Their First Treatment With Oxaliplatin and Bevacizumab

Project description:The purpose of this study is to determine the value of adding IMC-A12 to irinotecan and cetuximab in participants with metastatic colorectal cancer (CRC).

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TGF-beta-activated cancer-associated fibroblasts limit cetuximab efficacy in preclinical models of head and neck cancer

Project description:Most head and neck cancer (HNC) patients are resistant to cetuximab, an antibody against the epithelial growth factor receptor. Such therapy resistance is known to be mediated, in part, by stromal cells surrounding the tumor cells; however, the mechanisms underlying such a resistance phenotype remain unclear. To identify the mechanisms underlying cetuximab resistance in an unbiased manner, RNA-sequencing (RNA-seq) of HNC patient-derived xenografts (PDXs) was performed. Comparing the gene expression of HNC-PDXs before and after treatment with cetuximab indicated that the TGF-beta signaling pathway was upregulated in the stromal cells of PDXs that progressed to cetuximab (CetuximabProg-PDX). However, in PDXs that were extremely sensitive to cetuximab, and when tumors shrunk following cetuximab treatment (CetuximabSen-PDX), the TGF-beta pathway was downregulated in the stromal compartment. Histopathological analysis of PDXs showed that in CetuximabProg-PDX, TGF-beta-activation was detected in cancer-associated fibroblasts (CAFs). These TGF-beta-activated CAFs were sufficient to limit cetuximab efficacy in vitro and in vivo. Moreover, blocking the TGF-beta pathway using the SMAD3 inhibitor, SIS3, enhanced cetuximab efficacy and prevented the progression of CetuximabProg-PDX. Altogether, our findings indicate, for the first time, that TGF-beta-activated CAFs play a role in limiting cetuximab efficacy in HNC.

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2010-08-03 | E-GEOD-9600 | biostudies-arrayexpress

Global gene expression analysis between cetuximab-sensitive and cetuximab-resistant colorectal cancer cells

2016-07-17 | GSE71210 | GEO

A Study of IMC-1121B (Ramucirumab) in Colorectal Cancer

Project description:The purpose of this study is to test how long participants with colorectal cancer live without progressive disease when being treated with IMC-1121B (ramucirumab) and the modified FOLFOX-6 chemotherapy.

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Insulin-like growth factor-1 receptor inhibitor, AMG-479, in cetuximab-refractory head and neck squamous cell carcinoma

2010-08-03 | GSE9600 | GEO

Global gene expression analysis between cetuximab-sensitive and cetuximab-resistant colorectal cancer cells

Project description:Cetuximab is an epidermal growth factor receptor (EGFR)-blocking antibody approved for treatment of metastatic colorectal cancer. We examined differences in global gene expression between the syngeneic DiFi colorectal cancer cells, and a subline of DiFi cells with acquired resistance to cetuximab (DiFi5). We used Affymetrix HG-U133A array to compare the expression pattern of genes that are up-regulated or down-regulated between the parental DiFi colorectal cancer cells and the cetuximab-resistant DiFi5 cells. We generated a cetuximab-resistant DiFi subline, termed DiFi5, by chronic exposure of parental DiFi cells to serially increased doses of cetuximab (from 0.5 nM to 5 nM) for over 1 year. The resulting DiFi5 subline exhibits significant resistance to cetuximab-induced apoptosis. After we confirmed that the phenotype was stable over a period of time of more than 6 months, the RNA from DiFi and DiFi5 cells were extracted and hybridized to an Affymetrix HG-U133A array according to the manufacturerâs instructions. Following the hybridization, the array was scanned using a laser confocal scanner, and microarray image data were analyzed using DNA-Chip Analyzer (dChip), version 1.3, by the Sequencing and Microarray Facility at MD Anderson Cancer Center.

2016-07-17 | E-GEOD-71210 | biostudies-arrayexpress

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