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Adv."],"published-print":{"date-parts":[[2026,10,16]]},"abstract":"<jats:p>\n                    Oncogenic gene fusions are key drivers of cancer, yet most remain undruggable by current therapies. Here, we establish CRISPR-\n                    <jats:italic toggle=\"yes\">Psp<\/jats:italic>\n                    Cas13b as a personalizable platform for systematic silencing of various fusion transcripts. We reveal that recognition and cleavage of the breakpoint sequence by\n                    <jats:italic toggle=\"yes\">Psp<\/jats:italic>\n                    Cas13b disrupt the fusion transcript, resulting in efficient protein depletion.\n                    <jats:italic toggle=\"yes\">Psp<\/jats:italic>\n                    Cas13b cleavage produces aberrant, translation-incompetent target RNA species, a subset of which harbors internal deletions proximal to the cleavage site. We demonstrate that targeting the BCR::ABL1 breakpoint sequence efficiently degrades both wild-type and drug-resistant BCR::ABL1 mutants, which are the primary drivers of tyrosine kinase inhibitor resistance and relapse in chronic myeloid leukemia. Molecular profiling revealed that\n                    <jats:italic toggle=\"yes\">Psp<\/jats:italic>\n                    Cas13b impairs BCR::ABL1 tyrosine phosphokinase activity and triggers extensive transcriptomic and proteomic remodeling, leading to erythroid differentiation and apoptosis in drug-resistant cells. Beyond BCR::ABL1, personalized design of\n                    <jats:italic toggle=\"yes\">Psp<\/jats:italic>\n                    Cas13b effectively silences other undruggable oncogenic fusions. Collectively, this study establishes a molecular framework for precise targeting of undruggable or drug-resistant oncogenic transcripts.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.ady0296","type":"journal-article","created":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T17:58:53Z","timestamp":1792173533000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":0,"title":["Programmable and selective silencing of oncogenic fusion transcripts by CRISPR-Cas13b via breakpoint sequence recognition"],"prefix":"10.1126","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0330-5200","authenticated-orcid":true,"given":"Wenxin","family":"Hu (\u80e1\u6587\u6b23)","sequence":"first","affiliation":[{"name":"Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia."},{"name":"Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC 3052, Australia."},{"name":"Collaborative Centre for Genomic Cancer Medicine, University of Melbourne, Parkville, Victoria, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0008-7469-7716","authenticated-orcid":true,"given":"Honglin","family":"Chen (\u9648\u7ad1\u9716)","sequence":"additional","affiliation":[{"name":"Peter MacCallum Cancer Centre, Melbourne, VIC 3000, Australia."},{"name":"Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, VIC 3052, Australia."},{"name":"Collaborative Centre for Genomic Cancer Medicine, University of Melbourne, Parkville, Victoria, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3113-9588","authenticated-orcid":true,"given":"Steven","family":"He","sequence":"additional","affiliation":[{"name":"Children\u2019s Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, NSW Australia 2052."},{"name":"School of Women\u2019s and Children\u2019s Health, UNSW Sydney, Sydney, NSW, Australia."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4322-8561","authenticated-orcid":true,"given":"Joshua M. 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