S. Oesterreich

The paper characterizes ILC and ILC-like cell lines through multi-omic analysis to identify molecular similarities with patient tumors and potential therapeutic targets.

This study shows ER fusion proteins in breast cancer cell lines drive ligand-independent pro-oncogenic pathways, with subtype- and fusion-specific effects.

The paper introduces a new invasive lobular carcinoma cell line, WCRC-25, and demonstrates its molecular features and therapeutic response to PI3K/AKT inhibition.

This study uses spatial molecular profiling to show that mixed invasive ductal-lobular breast cancers have distinct molecular subtypes, oncogenic signatures, and mutations in different tumor regions, leading to prognostic uncertainty and therapeutic challenges.

The paper establishes the EstroGene database, which compiles 246 experiments from 136 datasets to analyze estrogen receptor regulomes in breast cancer, revealing diverse temporal, context-dependent, and directional responses.

This study identifies WNT4's role in regulating cancer metabolism through mitochondrial intracellular signaling in breast and gynecologic cancers, linking genetic variants to metabolic remodeling.

This study shows that loss of E-cadherin in ILC leads to increased IGF1R activation and sensitivity to inhibitors, suggesting a therapeutic target and biomarker for ILC.

The paper develops patient-derived xenografts and organoids for breast cancer to enable drug screening and precision oncology, showing efficacy of an FDA-approved drug in a clinical case.

This study identifies ESR1 mutations as drivers of breast cancer metastasis by altering cell adhesion and migration through genomic and transcriptomic reprogramming.

This study shows ESR1 mutant breast cancers exhibit basal cytokeratin expression and immune activation, linked to chromatin reprogramming and paracrine signaling.

This study analyzes acquired mutations and transcriptional changes in long-term estrogen-deprived breast cancer recurrences, identifying common genetic and expression alterations associated with endocrine resistance.

This study identifies distinct B cell signatures and tertiary lymphoid structures in HPV+ and HPV- HNSCC, highlighting their role in antitumor immunity.

This study shows that ER mutations in breast cancer cells cause gene expression changes through constant activity and secondary effects, not just ligand independence.

This study identifies WNT4 as a mediator of estrogen-driven mTOR signaling and mitochondrial function in lobular carcinoma cells, with implications for anti-estrogen resistance.

The paper uses single-cell RNA sequencing to compare transcriptional heterogeneity between invasive ductal and lobular breast cancer cell lines, identifying CDH1 loss effects and potential mediators of ILC-specific features.

This study identifies 3′-UTR shortening as a mechanism driving subtype-specific cancer growth by disrupting ceRNA networks involving housekeeping genes in breast cancer.

The paper compares immune cell infiltration in primary and metastatic breast tumors, finding reduced immune cell abundance but increased M2-like macrophages in metastases.

This study shows that loss of E-cadherin increases IGF1R pathway activation and makes breast cancers more responsive to anti-IGF1R therapies.

This paper characterizes the 2D and 3D phenotypes of four human invasive lobular carcinoma cell lines, revealing unique features compared to invasive ductal carcinoma cell lines.

This study uses exome-capture RNA-sequencing on decade-old breast cancer specimens and matched bone metastases to identify clinically actionable gene expression changes in metastatic progression.