Hedgehog Signaling Regulates Treg to Th17 Conversion Through Metabolic Rewiring in Breast Cancer.

The tumor immune microenvironment dynamically evolves to support tumor growth and progression. Immunosuppressive regulatory T cells (Treg) promote tumor growth and metastatic seeding in patients with breast cancer. Deregulation of plasticity between Treg and Th17 cells creates an immune regulatory framework that enables tumor progression.

Hedgehog blockade remodels the gut microbiota and the intestinal effector CD8 T cells in a mouse model of mammary carcinoma.

Given the gut microbiome's rise as a potential frontier in cancer pathogenesis and therapy, leveraging microbial analyses in the study of breast tumor progression and treatment could unveil novel interactions between commensal bacteria and disease outcomes. In breast cancer, the Hedgehog (Hh) signaling pathway is a potential target for treatment due to its aberrant activation leading to poorer prognoses and drug resistance. There are limited studies that have investigated the influences of orally administered cancer therapeutics, such as Vismodegib (a pharmacological, clinically used Hh inhibitor) on the gut microbiota.

Informing the new developments and future of cancer immunotherapy : Future of cancer immunotherapy.

The application of cancer immunotherapy (CIT) in reinforcing anti-tumor immunity in response to carcinogenesis and metastasis has shown promising advances, along with new therapeutic challenges, in the landscape of cancer care. To promote tumor growth and metastasis, cancer cells aim to manipulate their microenvironment by mediating a crosstalk with various immune cells through the secretion of chemokines, cytokines, and other associated factors. Understanding this crosstalk is the key to discovering the best targets for improved immunotherapies and clinical strategies in cancer treatment.