F. Aberger

Hedgehog-Hippo pathway interactions promote T cell exclusion from the tumor microenvironment in basal cell carcinoma

This study shows that HH/GLI and Hippo/YAP pathway interactions suppress T cell chemotaxis and promote immunosuppression in BCC by downregulating chemokine signaling.

JUN mediates senescence and immune cell recruitment to prevent prostate cancer progression

This study shows JUN suppresses prostate cancer progression by inducing senescence and immune cell recruitment, with JUN depletion accelerating tumor growth.

STAT3 restricts prostate cancer metastasis and antiandrogen resistance by controlling LKB1/CREB signaling pathway

This study identifies STAT3's role in restricting prostate cancer metastasis and antiandrogen resistance by regulating the LKB1/CREB signaling pathway in mouse models and human patients.

The NLRP3/eIF2 axis drives cell cycle progression in acute myeloid leukemia

This study shows that inhibiting the NLRP3 inflammasome reduces AML cell proliferation by promoting eIF2 phosphorylation and cell cycle arrest.

Casein kinase 1D encodes a novel drug target in Hedgehog-GLI driven cancers and tumor-initiating cells resistant to SMO inhibition

This study identifies CSNK1D as a novel therapeutic target in Hedgehog-GLI driven cancers, showing its inhibition reduces tumor-initiating cell growth in both SMO-sensitive and -resistant settings.

Oncogenic GLI1 and STAT1/3 activation drives immunosuppressive tryptophan/kynurenine metabolism via synergistic induction of IDO1 in skin cancer cells

This study identifies IDO1-kynurenine pathway activation as a novel mechanism by which HH-IL6 and GLI-STAT signaling promote immunosuppression in skin cancer, suggesting combination therapy targeting these pathways.

Epidermal activation of Hedgehog signaling establishes an immunosuppressive microenvironment in basal cell carcinoma by modulating skin immunity

This study investigates how Hedgehog signaling in skin cancer modulates immune cells and resistance to immunotherapy, identifying potential targets for combination treatments.

Opioids trigger breast cancer metastasis through E-Cadherin downregulation and STAT3 activation promoting epithelial mesenchymal transition

This study shows opioids promote breast cancer metastasis by reducing E-Cadherin and activating STAT3, leading to epithelial-mesenchymal transition.

STAT3 promotes melanoma metastasis by CEBP-induced repression of the MITF pigmentation pathway

This study shows that STAT3 promotes melanoma metastasis by repressing the MITF pigmentation pathway through CEBP induction.