K. Lehti

Enhanced NK cell proficiency in solid tumors through antigen-specific memory via NKG2C/A-HLA-E/ABC recruited to tumors by CXCR2

This study shows that antigen-specific memory NK cells can be generated in ovarian cancer, enhancing their cytotoxicity and tumor reactivity through NKG2C/A-HLA-E/ABC interactions and CXCR2-mediated migration.

Efficacy and safety of glycosphingolipid SSEA-4 targeting CAR-T cells in an ovarian carcinoma model

This study evaluates anti-SSEA-4 CAR-T cells in ovarian cancer models, showing efficacy against SSEA-4 positive cells but highlighting dose-dependent toxicity.

YAP and collagen remodelling support cell proliferation and tumour aggressiveness in uterine leiomyosarcoma

This study shows that YAP and collagen remodelling enable LMS cell proliferation and aggressiveness by adapting to low collagen and soft environments.

Mechanical confinement and DDR1 signalling synergise to regulate collagen-induced apoptosis in rhabdomyosarcoma cells

This study shows that dense collagen-rich environments induce apoptosis in rhabdomyosarcoma cells via DDR1 and TRPV4 signaling, explaining their preference for low collagen microenvironments.

Regulatory FOXP3+ T cells in uterine sarcomas are associated with favorable prognosis, low extracellular matrix expression and reduced YAP activation

This study identifies immune signatures in uterine sarcomas, finding that FOXP3+ regulatory T cells and M1-like macrophages correlate with better prognosis.

PROX1 transcription factor is a master regulator of myogenic and oncogenic features of rhabdomyosarcoma

This study identifies PROX1 as a master regulator of myogenic and oncogenic features in rhabdomyosarcoma, showing its role in stemness, tumor growth, and therapeutic potential through HDAC interactions.

Multi-modal meta-analysis of cancer cell line omics profiles identifies ECHDC1 as a novel breast tumor suppressor

The paper integrates multi-modal omics data from cancer cell lines to identify ECHDC1 as a novel breast tumor suppressor and discover synthetic lethal interactions.

FGFR4 phosphorylates MST1 to confer breast cancer cells resistance to MST1/2-dependent apoptosis

This study identifies FGFR4 as a kinase that phosphorylates MST1, thereby inhibiting MST1/2-dependent apoptosis and promoting breast cancer cell survival.