FBXW7 (F-Box And WD Repeat Domain Containing 7)

Importantly, targeting GLUT1 pharmacologically partially reverses the proliferative advantage conferred by ETV6 overexpression, highlighting a promising therapeutic vulnerability. Our findings establish the FBXW7-ETV6-GLUT1 regulatory axis as a critical driver of metabolic adaptation and tumor progression, offering potential strategies for targeted therapy in FBXW7-mutant EC.

Mixed and mixed-feature carcinomas share origins with pure endometrial serous and endometrioid carcinoma subtypes but exhibit distinct molecular alterations. These findings highlight the importance of molecular subtyping for diagnosis and treatment planning. Future research could focus on larger cohorts and targeted sequencing to better understand the pathogenesis of mixed and mixed-feature carcinomas in order to refine therapeutic strategies.

P2, N=28, Completed, Canadian Cancer Trials Group | Active, not recruiting --> Completed

Definitive diagnosis relies on molecular testing (such as FISH or NGS), which is crucial for differential diagnosis and prognostic evaluation. This subtype of CCSK is commonly associated with advanced clinical stage and early metastasis/recurrence, highlighting the necessity for improving risk stratification and clinical management.

P1, N=464, Recruiting, Debiopharm International SA | Trial completion date: Dec 2026 --> Jun 2028 | Trial primary completion date: Jun 2026 --> Dec 2027

FBXW7 acts as a tumour suppressor that mitigates MDR in ovarian cancer by negatively regulating the HSF-1/P-gp pathway. The findings have offered mechanistic insights into chemoresistance and highlight the therapeutic potential of targeting FBXW7-HSF-1 signaling in EOC management.

She received adjuvant letrozole and remains disease-free at 3 years post-surgery...When confined to the ovary, prognosis is excellent following surgical resection. Endocrine therapy may be considered on an individualized basis in hormone-responsive tumors, although its role in early-stage disease remains unproven.

Clinically, high expression levels of circIMP3 correlate with poorer event-free survival in prostate cancer patients, suggesting its potential as a prognostic biomarker. Additionally, the detection of circIMP3 in peripheral blood positions it as a promising target for liquid biopsy applications in PC diagnosis and monitoring.

Pairing genetic ASPM-i1 inhibition with standard chemotherapeutic agents used in the treatment of UBC, including cisplatin and gemcitabine, circumvents the treatment resistance of tumorigenic and stem-like UBC cells. In human UBC tissues, ASPM-i1 shows substantial cell-to-cell heterogeneity and is upregulated in a subset (46.4%) of tumors, correlating with poor clinical prognosis. This study reveals a crucial co-regulatory module of Notch and Wnt signaling that mediates stemness and chemotherapy resistance in tumorigenic UBC cells; its inhibition provides a novel approach to enhance chemosensitivity and improve therapeutic outcome in human UBC.

These findings uncover that KMT2D alteration drives chromatin reprogramming that facilitates adeno-to-squamous transition and identifies AURKA as a lineage-specific vulnerability, providing a precision strategy to overcome TKI resistance.Statement of significanceOur study identifies KMT2D loss as a key event of lineage switch that promotes adeno-to-squamous transition and TKI resistance in NSCLC. This epigenetic shift renders tumors dependent on AURKA, revealing a novel therapeutic target to counteract drug resistance and improve treatment outcomes.

We further identified F-box and WD repeat domain-containing 7 (FBXW7) as an upstream regulator that promotes ubiquitin-mediated degradation of AKAP13. Together, our findings reveal a novel FBXW7/AKAP13/YAP/chemokine signaling axis that promotes glioma pathogenesis through both tumor-autonomous invasion and TAM recruitment, highlighting a promising therapeutic target for this lethal malignancy.

P2, N=22, Recruiting, Zulfa Omer | Not yet recruiting --> Recruiting