A: Lanreotide treatment upregulated genes involved in T cell receptor (TCR) signaling, Ras signaling, and PI3K-Akt signaling pathways in both responders and non-responders. However, the effects were more pronounced in responders, suggesting that lanreotide may enhance T cell activation and differentiation in these patients.

A: Genes such as TXNIP (thioredoxin-interacting protein), POU2F2 (Oct-2), and IGF1R were found to be differentially expressed in responders versus non-responders. TXNIP was lower in responders across all T cell subsets, while POU2F2 was lower in Th cells and IGF1R was higher in Treg cells of non-responders.

A: Lanreotide treatment significantly affected the expression of genes involved in cytokine signaling, ubiquitination, and proteasome degradation in T cells from responders compared to non-responders. These changes correlated with clinical response to lanreotide therapy.

A: Lanreotide did not significantly affect cytokine production (IL-2 and IFNg), apoptosis, or the activation of transcription factors (NFAT, NF-kB, and ERK1/2) in healthy donor T cells in vitro, even at clinically relevant concentrations.

A: Lanreotide primarily acts by inhibiting tumor cell proliferation and hormone secretion through binding to SSTR2 and SSTR5. It also modulates immune function in NET patients, which correlates with clinical response.