Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA387596 | ENA |
REPOSITORIES: ENA
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Project description:The taxanes, namely Paclitaxel and Docetaxel, are important and widely used cancer chemotherapy drugs in the treatment of invasive and metastatic human breast cancer. Although treatment with the taxanes is beneficial to many patients, drug-responsive tumors in patients with metastatic breast cancer often display resistance to these drugs, either initially or over time following the continued administration of chemotherapy drugs. To investigate the patterns of cross-resistance with the taxane drugs and to identify potential mechanisms of resistance, we generated a series of MDA-MB-231 taxane resistant cell lines. We then used microarrays to determine gene expression differences between sensitive, Docetaxel and Paclitaxel resistant MDA-MB-231 cells. RNA isolated from three independent passages of sensitive, Docetaxel and Paclitaxel resistant cell lines and purified using the Qiagen RNeasy Mini Kit. Total RNA was processed and hybridized to Affymetrix Genechip HU133A arrays.
2011-04-22 | E-GEOD-28784 | biostudies-arrayexpress
Project description:The taxanes, namely Paclitaxel and Docetaxel, are important and widely used cancer chemotherapy drugs in the treatment of invasive and metastatic human breast cancer. Although treatment with the taxanes is beneficial to many patients, drug-responsive tumors in patients with metastatic breast cancer often display resistance to these drugs, either initially or over time following the continued administration of chemotherapy drugs. To investigate the patterns of cross-resistance with the taxane drugs and to identify potential mechanisms of resistance, we generated a series of MDA-MB-231 taxane resistant cell lines. We then used microarrays to determine gene expression differences between sensitive, Docetaxel and Paclitaxel resistant MDA-MB-231 cells.
2011-04-22 | GSE28784 | GEO
Project description:The present project aims to evaluate the gene expression profile of breast cancer tissue resistant to treatment with taxanes. Biopsies from tumor tissues were obtained from breast cancer patients without prior treatment. Histopathological analysis and ex vivo exposure to antineoplastic chemotherapeutics were carried out. Alamar Blue and lactate dehydrogenase release assays were performed for quantitative analysis of tumor viability after treatment and to asses the sensibility or resistant behaviour. Sensitive and resistant tumor tissues samples without prior exposure to therapeutic drugs were analyzed by gene expression microarrays.
2017-05-24 | GSE99225 | GEO
Project description:Taxane resistant breast cancer cells
| PRJEB13235 | ENA
Project description:Purpose: Breast cancer is a genetically heterogenous disease with subtypes differing in prognosis and chemosensitivity. The basal-like breast cancer (BLBC) molecular subtype is associated with poorer outcomes, but is more responsive to taxane-based chemotherapy. We evaluated the role of kinesins, motor proteins interacting with microtubules, in influencing taxane resistance. Experimental Design: Kinesin (KIF) expression was studied in one local dataset comprising all taxane resistant breast cancers in relation to taxane resistance. Data in the NCI-60 cell line dataset (GSE5846) nd the MDACC dataset (GSE20194) is separately detailed. Results: In the local dataset, the kinesin KIF26B is overexpressed in taxane-resistant residual breast cancers post-chemotherapy. Conclusions: We show that kinesin overexpression correlates with taxane resistance in BLBC cell lines and tissue. Our results suggest a potential approach to overcoming taxane resistance through concurrent or sequential use of kinesin inhibitors, highlighting the ATP-binding domain as a drug development target. Kinesin (KIF) expression was studied in one local dataset comprising all taxane resistant breast cancers in relation to taxane resistance. Data in the NCI-60 cell line dataset (GSE5846) and the MDACC dataset (GSE20194) is separately detailed.
2012-12-01 | E-GEOD-22796 | biostudies-arrayexpress
Project description:Purpose: Breast cancer is a genetically heterogenous disease with subtypes differing in prognosis and chemosensitivity. The basal-like breast cancer (BLBC) molecular subtype is associated with poorer outcomes, but is more responsive to taxane-based chemotherapy. We evaluated the role of kinesins, motor proteins interacting with microtubules, in influencing taxane resistance. Experimental Design: Kinesin (KIF) expression was studied in one local dataset comprising all taxane resistant breast cancers in relation to taxane resistance. Data in the NCI-60 cell line dataset (GSE5846) nd the MDACC dataset (GSE20194) is separately detailed. Results: In the local dataset, the kinesin KIF26B is overexpressed in taxane-resistant residual breast cancers post-chemotherapy. Conclusions: We show that kinesin overexpression correlates with taxane resistance in BLBC cell lines and tissue. Our results suggest a potential approach to overcoming taxane resistance through concurrent or sequential use of kinesin inhibitors, highlighting the ATP-binding domain as a drug development target.
2012-12-01 | GSE22796 | GEO
Project description:DNA hypermethylation in breast cancer: breast cancer tissues vs. normal breast tissues
| PRJNA154299 | ENA
Project description:Gene expression profiles in breast cancer: breast cancer tissues vs. normal breast tissues
| PRJNA154301 | ENA
Project description:Long noncoding RNA expression profile of chemotherapy-sensitive and resistant breast cancer tissues
| PRJNA912687 | ENA
Project description:The intention was to detect genes that are determining trastuzumab efficiency in HER2-positive breast cancer cell lines with different resistance phenotypes. While BT474 should be sensitive to the drug treatment, HCC1954 is expected to be resistant due to a PI3K mutation. The cell line BTR50 has been derived from BT474 and was cultured to be resistant as well. Based on RNA-Seq data, we performed differential expression analyses on these breast cancer cell lines with and without trastuzumab treatment. In detail, five separate tests were performed, namely resistant cells vs. wild type, i.e. HCC1954 and BTR50 vs. BT474, respectively, and untreated vs. drug treated cells. The significant genes of the first two tests should contribute to resistance. The significant genes of the test BT474 vs. its drug treated version should contribute to the trastuzumab effect. To exclude false positives from the combined gene set (#64), we removed ten genes that were also significant in the test BTR50 vs. its drug treated version. This way we ended up with 54 genes that are very likely to determine trastuzumab efficiency in HER2-positive breast cancer cell lines.
2015-04-21 | GSE55005 | GEO