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9bdd7700-1c57-429a-97ed-4a7ba99318f0 - samples

ABSTRACT: Fastq files from RNAseq of breast cancer bone metastases PDX of tumor HBC-124 treated by IACS-010759 (4 samples) or not (4 samples).

PROVIDER: EGAD00001009857 | EGA |

REPOSITORIES: EGA

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76c1500b-471f-4d6b-a9fd-5e7416861048 - samples

Project description:Fastq files from RNAseq of breast cancer bone metastases PDX after treatment with IACS-010759. Five PDX are resistants to treatment and 6 are responders.

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Expression data from Patient-derived tumor models (PDX) establish from bone metastases and match human breast primary tumor.

Project description:A significant proportion of patients with oestrogen receptor (ER) positive breast cancers (BC) develop resistance to endocrine treatments (ET) and relapse with metastatic disease. Bone is the most common metastatic site in ER+ patients, however bone metastases are technically challenging to biopsy and analyse. Difficulties concern both tumour tissue acquisition and techniques for analysis and RNA extractions. Patient-derived xenografts (PDX) of BC bone metastases have not been reported yet. For the first time we established PDX models from bone metastatic biopsies of patients progressing on ET and treated by vertebroplasty. PDX models were analysed at transcriptomic level and compared to patient’s early primary tumours to identify new therapeutic targets associated with endocrine resistance in the metastatic setting. Identification of activated signalling pathways in bone metastasis by comparative transcriptomic analyses of the bone metastasis derived PDX compared to the patients' primary breast tumor.

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Project description:Resistance to endocrine treatments and CDK4/6 inhibitors is considered a near-inevitability in most patients with estrogen receptor positive breast cancers (ER + BC). By genomic and metabolomics analyses of patients' tumours, metastasis-derived patient-derived xenografts (PDX) and isogenic cell lines we demonstrate that a fraction of metastatic ER + BC is highly reliant on oxidative phosphorylation (OXPHOS). Treatment by the OXPHOS inhibitor IACS-010759 strongly inhibits tumour growth in multiple endocrine and palbociclib resistant PDX. Mutations in the PIK3CA/AKT1 genes are significantly associated with response to IACS-010759. At the metabolic level, in vivo response to IACS-010759 is associated with decreased levels of metabolites of the glutathione, glycogen and pentose phosphate pathways in treated tumours. In vitro, endocrine and palbociclib resistant cells show increased OXPHOS dependency and increased ROS levels upon IACS-010759 treatment. Finally, in ER + BC patients, high expression of OXPHOS associated genes predict poor prognosis. In conclusion, these results identify OXPHOS as a promising target for treatment resistant ER + BC patients.

2023-06-27 | MTBLS3342 | MetaboLights

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Project description:Targeted sequencing analyses was made on samples of PDX engrafted with breast cancer bone metastases, 2 PDX acquired resistance to palbociclib.

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d8a9f2c4-e5da-40db-acea-ecdbf78c5a1d - samples

Project description:RNAseq sequencing of 10 breast cancer bone metastasis PDX. Samples were obtained from 5 PDX that acquired palbociclib resistance (palboR) and 5 from the parentale PDX (palboS).

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