{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,6]],"date-time":"2026-11-06T19:19:26Z","timestamp":1793992766374,"version":"4.8.0"},"reference-count":49,"publisher":"American Association for Cancer Research (AACR)","issue":"12","content-domain":{"domain":["aacrjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2015,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The CD19 antigen, expressed on most B-cell acute lymphoblastic leukemias (B-ALL), can be targeted with chimeric antigen receptor\u2013armed T cells (CART-19), but relapses with epitope loss occur in 10% to 20% of pediatric responders. We detected hemizygous deletions spanning the CD19 locus and de novo frameshift and missense mutations in exon 2 of CD19 in some relapse samples. However, we also discovered alternatively spliced CD19 mRNA species, including one lacking exon 2. Pull-down\/siRNA experiments identified SRSF3 as a splicing factor involved in exon 2 retention, and its levels were lower in relapsed B-ALL. Using genome editing, we demonstrated that exon 2 skipping bypasses exon 2 mutations in B-ALL cells and allows expression of the N-terminally truncated CD19 variant, which fails to trigger killing by CART-19 but partly rescues defects associated with CD19 loss. Thus, this mechanism of resistance is based on a combination of deleterious mutations and ensuing selection for alternatively spliced RNA isoforms.<\/jats:p>\n                  <jats:p>Significance: CART-19 yield 70% response rates in patients with B-ALL, but also produce escape variants. We discovered that the underlying mechanism is the selection for preexisting alternatively spliced CD19 isoforms with the compromised CART-19 epitope. This mechanism suggests a possibility of targeting alternative CD19 ectodomains, which could improve survival of patients with B-cell neoplasms. Cancer Discov; 5(12); 1282\u201395. \u00a92015 AACR.<\/jats:p>\n                  <jats:p>See related commentary by Jackson and Brentjens, p. 1238.<\/jats:p>\n                  <jats:p>This article is highlighted in the In This Issue feature, p. 1225<\/jats:p>","DOI":"10.1158\/2159-8290.cd-15-1020","type":"journal-article","created":{"date-parts":[[2015,10,29]],"date-time":"2015-10-29T23:17:50Z","timestamp":1446160670000},"page":"1282-1295","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":1218,"title":["Convergence of Acquired Mutations and Alternative Splicing of\n                    <i>CD19<\/i>\n                    Enables Resistance to CART-19 Immunotherapy"],"prefix":"10.1158","volume":"5","author":[{"given":"Elena","family":"Sotillo","sequence":"first","affiliation":[{"name":"1Division of Cancer Pathobiology, The Children's Hospital of Philadelphia, Philadelphia, 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