Genomics

Dataset Information

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FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy [KMF parental, KMF clone KT13 (FAK-/-), KT13 + GFP-FAK, KT13 + GFP-FAK R454, and KT13 + deltaGSK beta-catenin]


ABSTRACT: FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy [KMF parental, KMF clone KT13 (FAK-/-), KT13 + GFP-FAK, KT13 + GFP-FAK R454, and KT13 + deltaGSK beta-catenin]

PROVIDER: PRJNA530132 | ENA |

REPOSITORIES: ENA

Dataset's files

Source:
Action DRS
SRR8822580_1.fastq.gz Fastqsanger.gz
SRR8822580_2.fastq.gz Fastqsanger.gz
SRR8822590_1.fastq.gz Fastqsanger.gz
SRR8822590_2.fastq.gz Fastqsanger.gz
SRR8822581_1.fastq.gz Fastqsanger.gz
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Publications


Gene copy number alterations, tumor cell stemness, and the development of platinum chemotherapy resistance contribute to high-grade serous ovarian cancer (HGSOC) recurrence. Stem phenotypes involving Wnt-β-catenin, aldehyde dehydrogenase activities, intrinsic platinum resistance, and tumorsphere formation are here associated with spontaneous gains in Kras, Myc and FAK (KMF) genes in a new aggressive murine model of ovarian cancer. Adhesion-independent FAK signaling sustained KMF and human tumors  ...[more]

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