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Gemcitabine and Docetaxel in Patients With Relapsed or Refractory Metastatic Colorectal Adenocarcinoma

ABSTRACT: The primary goal of the trail was to determine the efficacy of combining Gemcitabine and Docetaxel in treatment of metastatic colorectal cancer with CHFR and/or Microsatellite Instability (MSI) phenotype.

DISEASE(S): Metastatic Colorectal Adenocarcinoma,Adenocarcinoma,Colorectal Cancer Recurrent,Relapsed Or Refractory Metastatic Colorectal Adenocarcinoma With Methylation Of Chfr And/or Microsatellite Instability

PROVIDER: 2128461 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Expression profiling of human primary breast cancer tissue before treatment with gemcitabine, epirubicine and docetaxel

2006-01-21 | GSE4056 | GEO

Expression profiling of human primary breast cancer tissue before treatment with gemcitabine, epirubicine and docetaxel

Project description:Gene expression profiles of human breast cancer tissues from 100 different patients treated with primary systemic chemotherapy (Gemcitabine, Epirubicin and Docetaxel) Keywords: expression profiling Human breast cancer tissues from 100 patients have been used to perform expression profiling analysis.

2006-01-21 | E-GEOD-4056 | biostudies-arrayexpress

Low endothelial cell FAK expression reduces pancreatic ductal adenocarcinoma liver metastasis after gemcitabine treatment

Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive cancers with a high level of liver metastasis. Despite substantial advances, resistance to therapy, including gemcitabine, is still a major obstacle to improved progression free survival. Recent studies have indicated that endothelial cell (EC) focal adhesion kinase (FAK) regulates DNA-damaging therapy induced angiocrine factors and chemosensitivity in malignant cells. However, the effect of EC-FAK regulated angiocrine signalling in chemosensitivity of metastatic PDAC remains unexplored. Here, we show that inducible loss of EC-FAK in both orthotopic and spontaneous mouse models of PDAC reduces liver metastasis and improves survival rates in gemcitabine treated, but not untreated, mice, without affecting primary tumour growth, tumour vascularization, blood vessel leakage or early metastatic events. Phosphoproteomics analysis show a downregulation of the MAPK/ RAF/ PAK signalling pathways in gemcitabine treated FAK-depleted ECs compared to gemcitabine treated WT ECs. Moreover, low levels of EC-FAK correlate with increased survival and reduced relapse in gemcitabine treated human PDAC patients, supporting the clinical relevance of our findings. Altogether, we have identified a new role of EC-FAK regulating PDAC liver metastasis upon gemcitabine treatment that impacts on survival.

2023-03-10 | PXD021542 | Pride

Human pancreatic adenocarcinoma contains a side population resistant to gemcitabine

Project description:BACKGROUND: Therapy resistance remains one of the major challenges to improve the prognosis of patients with pancreatic cancer. Chemoresistant cells, which potentially also display cancer stem cell (CSC) characteristics, can be isolated using the side population (SP) technique. Our aim was to search for a SP in human pancreatic ductal adenocarcinoma (PDAC) and to examine its chemoresistance and CSC phenotype. RESULTS: A SP was identified in all PDAC samples, expanded and analyzed as first-generation xenografts. This SP was more resistant to gemcitabine than the other tumour cells as analyzed in vivo. Whole-genome expression profiling of the SP revealed upregulation of genes related to therapy resistance, apoptotic regulation and epithelial-mesenchymal transition. In addition, the SP displayed higher tumourigenic (CSC) activity than the other main tumour cell population (MP) as analyzed in vitro by sphere-forming capacity. CONCLUSION: We identified a SP in human PDAC and uncovered a chemoresistant and CSC-associated phenotype. This SP may represent a new therapeutic target in pancreatic cancer. Micro-array analysis was performed on SP and MP samples of 5 xenografts, grown from 5 different human PDAC samples.

2016-01-04 | E-GEOD-36563 | biostudies-arrayexpress

Human pancreatic adenocarcinoma contains a side population resistant to gemcitabine

2016-01-04 | GSE36563 | GEO

Gemcitabine, Docetaxel, and Filgrastim in Treating Patients With Recurrent or Persistent Leiomyosarcoma or Soft Tissue Sarcoma

Project description:RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. Colony-stimulating factors such as filgrastim may increase the number of immune cells found in bone marrow or peripheral blood and may help a person’s immune system recover from the side effects of chemotherapy. PURPOSE: Phase II trial to study the effectiveness of combining gemcitabine, docetaxel, and filgrastim in treating patients who have recurrent or persistent leiomyosarcoma or soft tissue sarcoma that cannot be removed by surgery.

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RNA-seq of combinatory treatment of gemcitabine+UVI5008 and gemcitabine+MS275 in human pancreatic adenocarcinoma human cell lines

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2022-07-01 | E-MTAB-11922 | biostudies-arrayexpress

Transcriptional effects of CTGF inhibition and gemcitabine in the KPC mouse model of pancreatic ductal adenocarcinoma

Project description:Pancreatic ductal adenocarcinoma (PDA) is characterized by abundant desmoplasia and poor tissue perfusion. These features are proposed to limit access of therapies to neoplastic cells and blunt treatment efficacy. Indeed, several agents that target the PDA microenvironment promote chemotherapy delivery and improve anti-neoplastic responses in murine models of PDA. Here, we employed the FG-3019 monoclonal antibody directed against the pleiotropic matricellular signaling molecule connective tissue growth factor (CTGF/CCN2). FG-3019 treatment increased PDA cell killing and led to a dramatic tumor response without altering gemcitabine delivery. Microarray expression profiling revealed the down-regulation by FG-3019 of several anti-apoptotic transcripts, including the master regulator Xiap, down-regulation of which has been shown to sensitize PDA to gemcitabine. Decreases in XIAP protein by FG-3019 in the presence and absence of gemcitabine were confirmed by immunoblot, while increases in XIAP protein were seen in PDA cell lines treated with recombinant CTGF. Therefore, alterations in survival cues following targeting of tumor microenvironmental factors may play an important role in treatment responses in animal models and, by extension, PDA patients. Total RNA was isolated from KPC mouse PDA tumors 9 days after initiation of treatment with IgG (n=7 biological replicates), FG-3019 (n=5), IgG + gemcitabine (n=6), or FG-3019 + gemcitabine (n=6) and hybridized to Affymetrix 430A 2.0 microarrays. CEL files were processed by GC-RMA and rescaled using median per-gene normalization in GeneSpring GX 7.3.1.

2013-06-24 | E-GEOD-46203 | biostudies-arrayexpress

Expression data from prostate cancer cell lines C4-2B (docetaxel sensitive) and TaxR (docetaxel resistant) cells

2013-08-01 | GSE47040 | GEO

Expression data from prostate cancer cell lines C4-2B (docetaxel sensitive) and TaxR (docetaxel resistant) cells

Project description:Prostate cancer C4-2B cells were cultured in docetaxel in a dose-escalation manner. After nine months selection, cells were able to divide freely in 5 nM docetaxel, with a specific sets of genes been deregulated. We performed global gene expression analysis by cDNA microarrays to identify genes responsible for docetaxel resistance in TaxR cells. Docetaxel resistant TaxR cells were selected from C4-2B cells during long time docetaxel treatment. Genes responsible for docetaxel resistance were identified using C4-2B vs. TaxR RNA extraction and hybridization on Affymetrix microarrays.

2013-08-01 | E-GEOD-47040 | biostudies-arrayexpress

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