Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA168215 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Recent randomized clinical trial revealed the additional effect of bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor (VEGF)-A, to conventional chemotherapy on survival of patients with metastatic colorectal cancer. However, a number of preclinical reports indicate resistant mechanisms to anti-angiogenic therapy in several tumor models. We investigated the phenotypic alterations of colorectal cancer xenograft during antiangiogenic therapy. TK-4, a solid tumor strain derived from human colon cancer, was orthotopically implanted into cecal walls of nude mice and treated with anti-VEGF antibody or control IgG for 35 days. Gene expression was analyzed using microarrays (Human Gene 1.0ST Array, Affymetrix).
2013-05-25 | E-GEOD-47087 | biostudies-arrayexpress
Project description:RSPO is a WNT pathway activator and functions as a potent regulator of stem cell growth in colon. RSPO family members were produced by several human tumors representing multiple tumor types including ovarian, pancreatic, colon, breast and lung cancer. Specific monoclonal antibody antagonists of RSPO family members were developed. In human patient-derived tumor xenograft models, anti-RSPO treatment markedly inhibited tumor growth either as single agents or in combination with chemotherapy. Furthermore, blockade of RSPO signaling reduced the tumorigenicity of cancer cells based on serial transplantation studies. In order to assess the impact of RSPO3 inhibition and gain insight in the anti-RSPO3 treatment mechanism of action, the global gene expression profiles of 4 human colorectal cancer patient derived models (PDX) were performed using Affymetrix microarray for the xenografts treated by the anti-RSPO3 antibody.
2016-03-03 | GSE73906 | GEO
Project description:To investigate the underlying mechanisms of the inhibitory effects of human anti-human FGFR2IIIc antibody on growth and migration of colorectal cancer cells, we used DNA microarray analysis to examine the cell signaling pathway alterations following the administration of anti-FGFR2IIIc antibody. Cells were plated at a density of 2.5 M-CM-^W 105 cells in a 60-mm dish, and grown overnight. Then 100 M-NM-<g/mL of monoclonal anti-human FGFR2IIIc antibody was added in each dish. For control groups, an equal amount of anti-GFP antibody was added in another dish. After 48 hr, total RNA was isolated from cells. For use in DNA microarray analysis, 50 ng RNA from each group of cells was labeled using the Low Input Quick Amp Labeling kit. Labeled RNA was further purified using the Qiagen RNeasy Mini kit. Labeled cRNA was hybridized to the Agilent human 44k oligonucleotide microarray, and washed using Agilent Gene Expression washing buffer.
2012-06-07 | E-GEOD-38544 | biostudies-arrayexpress
Project description:Recent randomized clinical trial revealed the additional effect of bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor (VEGF)-A, to conventional chemotherapy on survival of patients with metastatic colorectal cancer. However, a number of preclinical reports indicate resistant mechanisms to anti-angiogenic therapy in several tumor models. We investigated the phenotypic alterations of colorectal cancer xenograft during antiangiogenic therapy.
2013-05-25 | GSE47087 | GEO
Project description:Immune surveillance escaping is essential for survival of original tumor. Considering PB-020’s good pharmacokinetic properties, combined effect of PB-020 and immunotherapy drugs is worth studying. As PB-020 can effectively suppress mouse colorectal cancer cell lines in cell culture, we tested the effect of combining PB-020 with the anti-PD-1 monoclonal antibody RMP1-14 on the growth of subcutaneously implanted MC38 cells to C57BL/6 mice as a syngeneic mouse model of colorectal cancer. To clarify the molecular mechanism underling this anti-cancer therapy, we executed RNA sequencing of tumor sample obtained from the experiment above.
2022-12-14 | GSE189469 | GEO
Project description:To investigate the underlying mechanisms of the inhibitory effects of human anti-human FGFR2IIIc antibody on growth and migration of colorectal cancer cells, we used DNA microarray analysis to examine the cell signaling pathway alterations following the administration of anti-FGFR2IIIc antibody.
2012-06-08 | GSE38544 | GEO
Project description:Identification of surface antigens that exhibited cancer-specific expression is a crucial step in the development of novel antibody-targeted therapies. We here aimed to investigate the anti-tumor activity of a novel monoclonal antibody (mAb) 11C9 and identify the antibody tractable target in the hepatocellular cancer stem cells (HCSCs). This research has studied differentially expressed genes (DEGs) between CD90+HSP90+ cells and 11C9-treated CD90+HSP90+ cells. We collected those two types cells for RNA extraction and hybridization on Affymetrix microarrays.
2023-02-17 | GSE215984 | GEO
Project description:Gene expression alterations in human colon cancer xenograft treated with anti-VEGF antibody
| PRJNA203538 | ENA
Project description:CD24 is a potential oncogene reported to be overexpressed in a large variety of human malignancies. We have shown that CD24 is overexpressed in 90% of colorectal tumors at a fairly early stage in the multistep process of carcinogenesis. Anti-CD24 monoclonal antibodies (mAb) induce a significant growth inhibition in colorectal and pancreatic cancer cell lines that express the protein. This study is designed to investigate further the effects of CD24 down-regulation using mAb or small interfering RNA in vitro and in vivo. Western blot analysis showed that anti-CD24 mAb induced CD24 protein down-regulation through lysosomal degradation. mAb augmented growth inhibition in combination with five classic chemotherapies. Xenograft models in vivo showed that tumor growth was significantly reduced in mAb-treated mice. Similarly, stable growth inhibition of cancer cell lines was achieved by down-regulation of CD24 expression using short hairpin RNA (shRNA). The produced clones proliferated more slowly, reached lower saturation densities, and showed impaired motility. Most importantly, down-regulation of CD24 retarded tumorigenicity of human cancer cell lines in nude mice. Microarray analysis revealed a similar pattern of gene expression alterations when cells were subjected to anti-CD24 mAb or shRNA. Genes in the Ras pathway, mitogenactivated protein kinase, or BCL-2 family and others of oncogenic association were frequently down-regulated. As a putative new oncogene that is overexpressed in gastrointestinal malignancies early in the carcinogenesis process, CD24 is a potential target for early intervention in the prevention and treatment of cancer. The study compared gene expression profiles between human CRC cells HT29 before and after expression of 1 and 2 shRNA vectors directed at the human CD24 gene, GFP control gene, HT29 cells and Colo357, human pancreatic cancer cells, before and after the inhibition of the CD24 molecule using 72h treatment with anti-CD24 monoclonal antibodies.
2009-03-07 | E-GEOD-15102 | biostudies-arrayexpress
Project description:This microarray experiment was designed to identify genes and pathways modulated in ovarian cancer xenografts treated with anti-human VEGF mAb (Bevacizumab). Tumors were established in NOD/SCID mice by s.c. injection of human ovarian cancer cells (IGROV-1 and SKOV3). Mice were treated with the anti-VEGF monoclonal antibody Bevacizumab or with PBS (control). Total RNA was extracted from tumor samples and hybridized on Affymetrix GeneChip™ PrimeView™ Human Gene Expression Arrays. Each sample was derived from a different mouse (n=5 mice/group). In order to evaluate the effects of the anti-human VEGF mAb in the two models, expression data of IGROV-1 and SKOV3 derived tumors were normalized and analyzed separately. Raw microarray data, preprocessed data matrix and results of differential expression analysis are available together with the applied protocols.
2019-12-16 | E-MTAB-7683 | biostudies-arrayexpress