Please tell us about your clinical experience. How many patients do you treat, what types of cancer exhibit the MAGE-A10, MAGE-A4, and AFP target genes respectively? What is currently the most efficient treatment for each of those?

What’s unique about Adaptimmune’s way of producing artificial T-cell receptors? Is the co-expression of CD8α homodimer  really able to broaden the immune response against solid tumors, as the company cites?

The MAGEA genes (incl. MAGEA 4) have been associated with hereditary disorders, such as dyskeratosis congenita. Could Adaptimmune’s T-cell therapy develop into a useful treatment for such disorders in the future? Is there a risk to exacerbate such hereditary diseases when trying to treat underlying cancer cases?

A confirmed decrease of 100% in target lesions in a patient with hepatocellular carcinoma was seen in the third cohort of the Phase 1 ADP-A2AFP trial. How much do you attribute this success to the T-cell treatment, considering 3 other patients showed decreases of 36-42% in target lesions?

MAGE-A10 protein was identified as an intranuclear protein expressed in normal spermatogonia and spermatocytes but in no other healthy tissue vs being expressed in >50% percentages of cancer cells. Could there be any serious male-reproductory side-effects when targeting this gene to treat malignancies?

How realistic is the 2022 milestone for market approval of ADP-A2M4 therapy in the synovial sarcoma indication, considering the company is still screening and enrolling patients with sarcoma in the Phase 2 SPEARHEAD-1 trial?