The abstract is read at the publisher; the summary is JClub's.
T17-M, a TROP2-targeting aptamer-drug conjugate, binds TROP2-dependent targets and suppresses tumor growth in PDAC xenografts, including patient-derived models.
- Why it matters: PDAC is hard to treat, and antibody-free, selective delivery of cytotoxic payloads to tumor cells remains insufficiently explored.
- What they did: Using protein-SELEX, the study identified T17 and conjugated it to monomethyl auristatin E via an MC-Val-Cit-PAB linker to form T17-M, then tested binding, internalization, lysosomal processing, and antitumor effects in cellular and animal models.
- The result: T17-M reduced tumor growth, liver metastasis, and promoted immunogenic cell death markers (calreticulin exposure, ATP release, HMGB1 secretion), with dendritic-cell activation and CD8+ T cell infiltration in immunocompetent models, and improved control when combined with PD-1 blockade.
The findingWhy it mattersWhat they didThe result
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