ER positive

Our findings establish MAP3K1 and MAP2K4 as key tumor suppressors in BRCA that operate via the JNK2-p53-FOSL1 axis. Their inactivation provides an alternative mechanism for p53 pathway disruption, adhering to the "minimal necessary alteration" principle in cancer signaling. This study highlights the dual regulatory mechanisms controlling FRA1 expression and offers insights into breast cancer heterogeneity, with potential implications for targeted therapy and patient stratification.

BRCA2 cancers tended to present with more advanced features, while BRCA1 cancers were more often detected at earlier stage. These findings underscore the value of BRCA testing not only for PARP inhibitor eligibility but also for subtype-specific risk assessment and individualized preventive strategies.

Higher CTC signature ITH was associated with increased Oncotype DX risk and higher overall grade. These findings highlight the value of our CTC signature in disease progression and the role of ITH on recurrence risk.

P3, N=701, Active, not recruiting, Celcuity Inc | Recruiting --> Active, not recruiting | Trial primary completion date: Jun 2025 --> Jun 2026

A manual IHC program for BC was established in a tertiary hospital in southern Ethiopia. The service reached facilities up to 500 km away. Facilities that reported the cold ischemia and formalin time have met standards of care. The median age of BC was 38 years, and two-third were hormone positive, consistent with other reports in the country. Future work will include more regional training on preanalytical variables and developing capacity to evaluate HER2neu 2+ equivocal cases.

The present findings are from a limited number of heterogenous studies and hence must be interpreted with caution. https://www.crd.york.ac.uk/prospero/, identifier CRD42025641361.

One team (favouring high glycolysis, stem-like, basal-like, mesenchymal/hybrid and tamoxifen-resistant phenotype) was found to be associated with aggressive progression and worse survival...Importantly, altering one axis of plasticity often drove coordinated responses along other axes and vice versa. Our findings establish phenotypic plasticity in cancer as a coordinated, multi-axis dynamical process, thus suggesting novel strategies to disrupt systems-level reprogramming enabling metastasis and therapeutic resistance.

Focusing on TCP1, a chaperonin subunit upregulated in high-risk tumors, we demonstrate that TCP1 knockdown in breast cancer cell lines substantially impairs cell migration (~50% reduction in wound closure) and invasion (P < 0.01). These findings reveal functionally distinct malignant cell states within breast cancer and identify TCP1 as a promising therapeutic target to disrupt aggressive, stem-like tumor cell programs, ultimately guiding more personalized treatment strategies.

P=N/A, N=21, Recruiting, Parul Barry | Trial completion date: Jul 2028 --> Mar 2028 | Trial primary completion date: Dec 2026 --> Apr 2026

The advent of CDK4/6 inhibitors, namely, palbociclib, ribociclib and abemaciclib, has changed the management of oestrogen receptor (ER)-positive/HER2-negative advanced breast tumours. Nonetheless, the acquired resistance to CDK4/6 inhibitors remains a major therapeutic challenge. Thus, the identification of molecular drivers involved in the resistance to these drugs is crucial for the design of novel therapeutic approaches and the selection of patient-centred strategies in various types of tumours.

To test this hypothesis, we treated MCF-7 and T47D ER-positive breast cancer cells with 17-β-estradiol (E2), either alone or in combination with selective ERα antagonist AZD9496, selective ERβ antagonist PHTPP, DNA methyltransferase (DNMT) inhibitor RG108, and selective ER degrader Fulvestrant (Ful). RG108 strengthened UV-C-induced pyroptosis, and Ful reversed the inhibitory effects of E2 on UV-C-induced pyroptosis of MCF-7 and T47D cells. Taken together, our study suggests that E2 down-regulated GSDME expression in ERα-positive breast cancer by promoting GSDME promoter methylation, and inhibited UV-C-induced pyroptosis.