Abstract
Recently, split intein-based detection sensors for RNA have been developed that can target custom sequences in a modular fashion. If multi-region, multi-sample sequencing were to be applied to a patient's cancer, truncal (that is, earliest-occurring) mutations could be identified and could serve as targets for these sense-and-respond modules. The next step would be to utilize an effective vector for treatment. A hyper-virulent herpes simplex virus could possibly serve as this vector, with concurrent immunosuppression to allow for unhindered infection of the tumor regions. Given that, the oncogenic mutations could serve as molecular 'kindling', with exogenous small molecule-mediated enhancement of replication after initial seeding of tumors and metastases. Then, a toxin may be induced to destroy the cancer entirely, ideally with a bystander effect.
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