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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 line...
2023-06-27 | MTBLS3342 | MetaboLights
An antipsychotic drug, Thioridazine has been shown to inhibit a broad spectrum of cancer cells. However, its molecular mechanism is still not well understood. In the present study, we have shown that thioridazine induces cytostatic effects in both parental and tamoxifen-resistant cancer cells throug...
2025-02-20 | MTBLS11870 | MetaboLights
Cancer cells are known to reprogram their metabolism to adapt to adverse conditions dictated by tumor growth and microenvironment. A subtype of cancer cells with stem-like properties, known as cancer stem cells (CSC), is thought to be responsible for tumor recurrence. In this study, we demonstrated ...
2019-08-19 | MTBLS678 | MetaboLights

Activating PIK3CA mutations, present in up to 40% of hormone receptor-positive (HR+), human epidermal growth factor receptor 2-negative (Her2-) breast cancer (BC) patients, can be effectively targeted with the alpha isoform-specific PI3K inhibitor Alpelisib. This treatment significantly improves ...

2026-08-21 | MTBLS11671 | MetaboLights

Tumor relapse from treatment-resistant cells (minimal residual disease, MRD) underlies most breast cancer related deaths. Yet, the molecular characteristics defining their malignancy have largely remained elusive. Here we integrated multi-omics data from a tractable organoid system with a metabol...

2021-09-14 | MTBLS1507 | MetaboLights
The development of breast cancer resistance to endocrine therapy results from an increase in cellular plasticity leading to the development of a steroid independent tumour. The p160 steroid coactivator protein SRC-1, through interactions with developmental proteins and other non-steroidal transcrip...
ORGANISM(S): Homo sapiens 
The estrogen receptor alpha (ERa) drives the growth of two-thirds of all breast cancers. Endocrine therapy impinges on estrogen-induced ERa activation to block tumor growth. However, half of ERa-positive breast cancers are tolerant or acquire endocrine therapy resistance. Here we demonstrate that br...
ORGANISM(S): Homo sapiens 
Analysis of the response to PBX1 deprivation either using an siRNA approach or using a chemicalcompound indirectly targeting it. Deprivation of PBX1 is hypothesized to be essential for the growth of endocrine therapy resistant breast cancer cells (LTED) Total RNA was obtained from cells treated with...
ORGANISM(S): Homo sapiens 
Tumor characteristics are decisive in the determination of treatment strategy for breast cancer patients. Patients with estrogen receptor a(ERa)-positive breast cancer can benefit from long-term hormonal treatment. Nonetheless, the majority of patients will develop resistance to these therapies. Her...
ORGANISM(S): Homo sapiens 
*** This submission includes RNA data, with DNA files available under a different accession number*** Purpose: Endocrine therapy resistance remains the greatest challenge for treating hormone receptor positive breast cancer patients. We aim to identify molecular mechanisms underlying endocrine ther...
ORGANISM(S): Homo sapiens 
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