{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T03:10:20Z","timestamp":1792465820800,"version":"4.5.0"},"reference-count":29,"publisher":"American Society of Clinical Oncology (ASCO)","issue":"26","content-domain":{"domain":["ascopubs.org"],"crossmark-restriction":true},"short-container-title":["JCO"],"published-print":{"date-parts":[[2024,9,10]]},"abstract":"<jats:sec>\n                    <jats:title>PURPOSE<\/jats:title>\n                    <jats:p>BCR::ABL1 quantification is widely regarded as the standard for monitoring measurable residual disease (MRD) in Philadelphia chromosome\u2013positive (Ph+) ALL. However, recent evidence of BCR::ABL1 multilineage involvement questions the significance of BCR::ABL1 MRD. We aimed to define the prognostic role of MRD as assessed by BCR::ABL1 or lymphoid-specific immunoglobulin\/T-cell receptor ( IG\/TR) gene markers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>PATIENTS AND METHODS<\/jats:title>\n                    <jats:p>We conducted BCR::ABL1 and IG\/TR quantification after each treatment cycle in 264 patients treated in the GRAAPH-2014 trial, which used four cycles of reduced-intensity chemotherapy with nilotinib, followed by hematopoietic stem-cell transplantation (HSCT).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      Comparing BCR::ABL1 and IG\/TR MRD revealed residual BCR::ABL1-positive non-ALL cells in 98 (43%) of 228 patients, defining multilineage Ph+ ALL. Despite poorer BCR::ABL1 responses, patients with multilineage Ph+ ALL had similar disease-free survival (DFS; hazard ratio [HR], 0.83 [95% CI, 0.49 to 1.41]; P = .50). Although BCR::ABL1 response failed to predict outcomes, IG\/TR positivity (\u22650.01%) was strongly associated with lower DFS (after cycle 2, HR, 2.49 [95% CI, 1.40 to 4.40]; P = .002; after cycle 4, HR, 4.13 [95% CI, 1.82 to 9.38]; P = .001). In multivariable analysis, both IG\/TR positivity after cycle 2 and initial WBC count \u226530 \u00d7 10\n                      <jats:sup>9<\/jats:sup>\n                      \/L predicted poorer DFS, enabling to define a high-risk group having a 4-year DFS of 56.5% compared with 87.6% (HR, 3.72 [95% CI, 1.93 to 7.15]; P &lt; .001). Moreover, allogeneic HSCT significantly improved DFS in the high-risk group (HR, 0.33 [95% CI, 0.18 to 0.60]; P &lt; .001), whereas the standard-risk group had favorable outcomes regardless of allogeneic HSCT.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSION<\/jats:title>\n                    <jats:p>Our findings challenge the significance of BCR::ABL1 monitoring in adult Ph+ ALL and demonstrate the prognostic role of IG\/TR MRD. This study provides a framework for using MRD to guide treatment strategies in adults with Ph+ ALL.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1200\/jco.24.00108","type":"journal-article","created":{"date-parts":[[2024,7,19]],"date-time":"2024-07-19T16:01:12Z","timestamp":1721404872000},"page":"3140-3150","update-policy":"https:\/\/doi.org\/10.1200\/crossmark","source":"Crossref","is-referenced-by-count":48,"title":["Significance of Measurable Residual Disease in Adult Philadelphia Chromosome\u2013Positive ALL: A GRAAPH-2014 Study"],"prefix":"10.1200","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9987-7237","authenticated-orcid":false,"given":"Rathana","family":"Kim","sequence":"first","affiliation":[{"name":"Hematology Laboratory, H\u00f4pital Saint-Louis, Assistance Publique-H\u00f4pitaux de Paris (AP-HP), Universit\u00e9 Paris Cit\u00e9, Paris, France"},{"name":"INSERM U944, CNRS UMR 7212 GenCellDis, Institut de Recherche Saint-Louis (IRSL), Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9341-8104","authenticated-orcid":false,"given":"Yves","family":"Chalandon","sequence":"additional","affiliation":[{"name":"Division of Hematology, Department of Oncology, Geneva University Hospitals and Faculty of Medicine, University of Geneva, Geneva, Switzerland"},{"name":"Swiss Group for Clinical Cancer Research (SAKK)"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philippe","family":"Rousselot","sequence":"additional","affiliation":[{"name":"Hematology Department, Centre Hospitalier de Versailles, Unit\u00e9 mixte de recherche 1184 Commissariat \u00e0 l'Energie Atomique, University Paris-Saclay, Le Chesnay, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Michel","family":"Cayuela","sequence":"additional","affiliation":[{"name":"Hematology Laboratory, H\u00f4pital Saint-Louis, Assistance Publique-H\u00f4pitaux de Paris (AP-HP), Universit\u00e9 Paris Cit\u00e9, Paris, France"},{"name":"EA 3518, Institut de Recherche Saint-Louis (IRSL), Universit\u00e9 Paris Cit\u00e9, Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fran\u00e7oise","family":"Huguet","sequence":"additional","affiliation":[{"name":"Hematology Department, Institut Universitaire de Cancer Toulouse-Oncopole, CHU de Toulouse, Toulouse, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie","family":"Balsat","sequence":"additional","affiliation":[{"name":"Hematology Department, Hospices Civils de Lyon, H\u00f4pital Lyon Sud, Pierre Benite, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4620-8782","authenticated-orcid":false,"given":"Marie","family":"Passet","sequence":"additional","affiliation":[{"name":"Hematology Laboratory, H\u00f4pital Saint-Louis, Assistance Publique-H\u00f4pitaux de Paris (AP-HP), Universit\u00e9 Paris Cit\u00e9, Paris, 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