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High throughput sequencing of small cell lung cancer chemosensitive H69 and corresponding chemoresistant H69AR

ABSTRACT: High throughput sequencing of small cell lung cancer chemosensitive H69 and corresponding chemoresistant H69AR

PROVIDER: PRJNA929197 | ENA |

REPOSITORIES: ENA

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High throughput sequencing of small cell lung cancer chemosensitive H69 and corresponding chemoresistant H69AR

Project description:Small cell lung cancer (SCLC) is the most aggressive subtype of lung cancer. Although most patients are initially sensitive to first-line chemotherapy with combined cisplatin and etoposide, chemotherapy drugs resistance easily develops and quickly leads to tumor progression. Therefore, understanding mechanisms of chemotherapy drugs resistance and how to reverse it is key to improving the prognosis of patients with SCLC. The parental SCLC cell lines H69 and corresponding doxorubicin-induced multidrug resistant variant (H69AR) were used to explore the mechanism of chemoresistance in SCLC.

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Gene expression patterns of chemoresistant and chemosensitive serous epithelial ovarian tumors with possible predictive value in response to initial chemotherapy

Project description:Chemotherapy (CT) resistance in ovarian cancer is broad and encompasses diverse, unrelated drugs, suggesting more than one mechanism of resistance. We aimed to analyze the gene expression patterns in primary serous epithelial ovarian cancer (EOC) samples displaying different responses to first-line CT in an attempt to identify specific molecular signatures associated with response to CT. Initially, the expression profiles of 15 chemoresistant serous EOC tumors [time to recurrence (TTR) ≤6 months] and 10 chemosensitive serous EOC tumors (TTR ≥30 months) were independently analyzed which allowed the identification of specific sets of differentially expressed genes that might be functionally implicated in the evolution of the chemoresistant or the chemosensitive phenotype. Our data suggest that the intrinsic chemoresistance in serous EOC cells may be attributed to the combined action of different molecular mechanisms and factors linked with drug influx and efflux and cell proliferation, as possible implications of other molecular events including altered metabolism, apoptosis and inflammation cannot be excluded. Next, gene expression comparison using hierarchical clustering clearly distinguished chemosensitive and chemo- resistant tumors from the 25 serous EOC samples (training set), and consecutive class prediction analysis was used to develop a 43-gene classifier that was further validated in an independent cohort of 15 serous EOC patients and 2 patients with other ovarian cancer histotypes (test set). The 43-gene predictor set properly classified serous EOC patients at high risk for early (≤22 months) versus late (>22 months) relapse after initial CT. Thus, gene expression array technology can effectively classify serous EOC tumors according to CT response. The proposed 43-gene model needs further validation. 2 condition experiment: chemoresistant clinical samples versus chemosensitive samples

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Transcriptomic comparison of chemosensitive and chemoresistant cells

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Staphylococcus hominis strain:H69

Project description:Staphylococcus hominis strain:H69 Genome sequencing and assembly

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MicroRNA profiling of human cholangiocyte H69 cells after culturing with lipopolysaccharide

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Gene expression from H69M versus H69 SCLC cell lines

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