NIN (Ninein)

SP-2-067 is a novel, selective AKA degrader that modulates IC expression by upregulating PD-L1 and downregulating LAG3, indicating its potential for immunomodulation through AUNIP- and NINEIN-mediated mechanisms. Additionally, AKA, AUNIP, and NINEIN are linked to a distinct immune cell profile, presenting an opportunity to reshape the tumor immune microenvironment and support combinatorial strategies with IC inhibitors in prostate cancer.

Functional experiments demonstrated that depletion of exon 18-included NIN isoform suppressed proliferation, migration, and invasion in breast cancer cells, induced S-phase arrest using dysregulation of the CDK2/Cyclin A axis, and significantly inhibited tumor growth in vivo. These findings revealed that the QKI/exon 18-included NIN isoform axis is a critical driver of breast cancer progression, highlighting its potential as a therapeutic target for BRCA treatment.

Duodenal adenomas associated with FAP usually occur in younger patients and are frequently multifocal. Histologi-cally, they show a significantly higher number of Paneth cells and an increased chromogranin expression was found in our series. Occasionally, neuroendocrine hyperplasia within the adenomas can be observed.