J. Gertz

3D genomic analysis reveals novel enhancer-hijacking caused by complex structural alterations that drive oncogene overexpression

The paper introduces HAPI, a 3D genomics method, to identify enhancer hijacking in cancer cell lines, revealing novel oncogene activation mechanisms.

ASPSCR1-TFE3 reprograms transcription by organizing enhancer loops around hexameric VCP/p97

This study identifies VCP/p97 as an obligate co-factor of ASPSCR1-TFE3, showing it organizes enhancer loops to drive oncogenic transcription in ASPS and RCC.

Estrogen receptor alpha mutations regulate gene expression and cell growth in breast cancer through microRNAs

Characterization of a novel estrogen- and progesterone-responsive endometrial cancer cell line: HCI-EC-23

This paper introduces a new endometrial cancer cell line, HCI-EC-23, which responds to estrogen and progesterone, and shows it has similar estrogen-responsive gene regulation to Ishikawa cells.

TXNIP loss expands Myc-dependent transcriptional programs by increasing Myc genomic binding

This study shows that TXNIP loss increases Myc genomic binding, expanding Myc-dependent transcriptional programs without increasing Myc levels or activity.

Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial cancer

This study investigates ER mutations in endometrial cancer, showing they alter gene expression and promote cancer phenotypes, and identifies potential therapeutic targets.

A breast cancer patient-derived xenograft and organoid platform for drug discovery and precision oncology

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.

Hotspot ESR1 mutations are multimodal and contextual drivers of breast cancer metastasis

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

ESR1 mutant breast cancers show elevated basal cytokeratins and immune activation

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

Estrogen receptor alpha mutations in breast cancer cells cause gene expression changes through constant activity and through secondary effects

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

Reciprocal regulation of pancreatic ductal adenocarcinoma growth and molecular subtype by HNF4α and SIX1/4

This study shows HNF4α suppresses PDAC growth and promotes the Classical subtype by repressing SIX1/4, which are critical for Basal-like subtype proliferation.

Estrogen-independent molecular actions of mutant estrogen receptor alpha in endometrial cancer

This study investigates estrogen-independent actions of the D538G ESR1 mutation in endometrial cancer, showing altered genomic binding, gene expression, and chromatin accessibility compared to wildtype ESR1.

Clinical and genomic crosstalk between glucocorticoid receptor and estrogen receptor α in endometrial cancer

The paper investigates the interaction between glucocorticoid receptor (GR) and estrogen receptor α (ER) in endometrial cancer, finding that GR expression correlates with poor prognosis and that their combined activity alters gene expression and genomic binding.