Subclonal evolution of CLL driver mutations is associated with relapse in ibrutinib- and acalabrutinib-treated patients
2022; Elsevier BV; Volume: 140; Issue: 4 Linguagem: Inglês
10.1182/blood.2021015132
ISSN1528-0020
AutoresGage S. Black, Xiaomeng Huang, 義行 高橋, Szabolcs Tarapcsák, Kerry A. Rogers, Shrilekha Misra, John C. Byrd, Gábor Marth, Deborah M. Stephens, Jennifer A. Woyach,
Tópico(s)Lymphoma Diagnosis and Treatment
ResumoLetter to Blood| July 28, 2022 Subclonal evolution of CLL driver mutations is associated with relapse in ibrutinib- and acalabrutinib-treated patients Clinical Trials & Observations Gage S. Black, Gage S. Black Department of Human Genetics, University of Utah, Salt Lake City, UT; Utah Center for Genetic Discovery, School of Medicine, University of Utah, Salt Lake City, UT; https://orcid.org/0000-0003-2086-5266 Search for other works by this author on: This Site PubMed Google Scholar Xiaomeng Huang, Xiaomeng Huang Department of Human Genetics, University of Utah, Salt Lake City, UT; Utah Center for Genetic Discovery, School of Medicine, University of Utah, Salt Lake City, UT; Search for other works by this author on: This Site PubMed Google Scholar Yi Qiao, Yi Qiao Department of Human Genetics, University of Utah, Salt Lake City, UT; Utah Center for Genetic Discovery, School of Medicine, University of Utah, Salt Lake City, UT; Search for other works by this author on: This Site PubMed Google Scholar Szabolcs Tarapcsak, Szabolcs Tarapcsak Department of Human Genetics, University of Utah, Salt Lake City, UT; Utah Center for Genetic Discovery, School of Medicine, University of Utah, Salt Lake City, UT; https://orcid.org/0000-0001-7182-0135 Search for other works by this author on: This Site PubMed Google Scholar Kerry A. Rogers, Kerry A. Rogers Division of Hematology, Department of Internal Medicine, The Ohio State University, Columbus, OH; https://orcid.org/0000-0001-5748-7874 Search for other works by this author on: This Site PubMed Google Scholar Shrilekha Misra, Shrilekha Misra Division of Hematology, Department of Internal Medicine, The Ohio State University, Columbus, OH; Search for other works by this author on: This Site PubMed Google Scholar John C. Byrd, John C. Byrd Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH; and Search for other works by this author on: This Site PubMed Google Scholar Gabor T. Marth, Gabor T. Marth Department of Human Genetics, University of Utah, Salt Lake City, UT; Utah Center for Genetic Discovery, School of Medicine, University of Utah, Salt Lake City, UT; Search for other works by this author on: This Site PubMed Google Scholar Deborah M. Stephens, Deborah M. Stephens Division of Hematology and Hematologic Malignancies, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT https://orcid.org/0000-0001-9188-5008 Search for other works by this author on: This Site PubMed Google Scholar Jennifer A. Woyach Jennifer A. Woyach Division of Hematology, Department of Internal Medicine, The Ohio State University, Columbus, OH; Search for other works by this author on: This Site PubMed Google Scholar Blood (2022) 140 (4): 401–405. https://doi.org/10.1182/blood.2021015132 Article history Submitted: December 12, 2021 Accepted: April 13, 2022 First Edition: April 27, 2022 Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Request Permissions Cite Icon Cite Search Site Citation Gage S. Black, Xiaomeng Huang, Yi Qiao, Szabolcs Tarapcsak, Kerry A. Rogers, Shrilekha Misra, John C. Byrd, Gabor T. Marth, Deborah M. Stephens, Jennifer A. Woyach; Subclonal evolution of CLL driver mutations is associated with relapse in ibrutinib- and acalabrutinib-treated patients. Blood 2022; 140 (4): 401–405. doi: https://doi.org/10.1182/blood.2021015132 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBlood Search Subjects: Clinical Trials and Observations, Lymphoid Neoplasia TO THE EDITOR: Bruton’s tyrosine kinase (BTK) is a common target for therapeutic intervention in patients with chronic lymphocytic leukemia (CLL).1,2 Ibrutinib is a first-generation BTK inhibitor (BTKi) that covalently binds to BTK to disrupt the B-cell receptor signaling pathway.3,4 Although BTKis are known to be an effective therapy for CLL, treatment-related toxicities can lead to the discontinuation of therapy.5,6 Acalabrutinib is a second-generation BTKi developed to reduce off-target toxicities.7,8 Though BTKis have improved the management of CLL, some patients experience clinical resistance and relapse during treatment due to mutations in arising clonal cell populations.9,10 This clonal evolution occurs when a dividing cell develops a new mutation that results in a greater competitive advantage compared with the surrounding cells.11-13 Clonal evolution can lead to treatment resistance when an expanding subclone contains a mutation that... REFERENCES 1.Herman SEM, Gordon AL, Hertlein E, et al. Bruton tyrosine kinase represents a promising therapeutic target for treatment of chronic lymphocytic leukemia and is effectively targeted by PCI-32765. Blood. 2011;117(23):6287-6296.Google ScholarCrossrefSearch ADS PubMed 2.Woyach JA, Johnson AJ, Byrd JC. The B-cell receptor signaling pathway as a therapeutic target in CLL. Blood. 2012;120(6):1175-1184.Google ScholarCrossrefSearch ADS PubMed 3.Davids MS, Brown JR. Ibrutinib: a first in class covalent inhibitor of Bruton’s tyrosine kinase. Future Oncol. 2014;10(6):957-967.Google ScholarCrossrefSearch ADS PubMed 4.Burger JA, Tedeschi A, Barr PM, et al; RESONATE-2 Investigators. Ibrutinib as initial therapy for patients with chronic lymphocytic leukemia. N Engl J Med. 2015;373(25):2425-2437.Google ScholarCrossrefSearch ADS PubMed 5.Mato AR, Nabhan C, Thompson MC, et al. Toxicities and outcomes of 616 ibrutinib-treated patients in the United States: a real-world analysis. Haematologica. 2018;103(5):874-879.Google ScholarCrossrefSearch ADS PubMed 6.Maddocks KJ, Ruppert AS, Lozanski G, et al. Etiology of ibrutinib therapy discontinuation and outcomes in patients with chronic lymphocytic leukemia. JAMA Oncol. 2015;1(1):80-87.Google ScholarCrossrefSearch ADS PubMed 7.Byrd JC, Harrington B, O’Brien S, et al. Acalabrutinib (ACP-196) in relapsed chronic lymphocytic leukemia. N Engl J Med. 2016;374(4):323-332.Google ScholarCrossrefSearch ADS PubMed 8.Barf T, Covey T, Izumi R, et al. Acalabrutinib (ACP-196): a covalent bruton tyrosine kinase inhibitor with a differentiated selectivity and in vivo potency profile. J Pharmacol Exp Ther. 2017;363(2):240-252.Google ScholarCrossrefSearch ADS PubMed 9.Komarova NL, Burger JA, Wodarz D. Evolution of ibrutinib resistance in chronic lymphocytic leukemia (CLL). Proc Natl Acad Sci USA. 2014;111(38):13906-13911.Google ScholarCrossrefSearch ADS 10.Woyach JA, Furman RR, Liu T-M, et al. Resistance mechanisms for the Bruton’s tyrosine kinase inhibitor ibrutinib. N Engl J Med. 2014;370(24):2286-2294.Google ScholarCrossrefSearch ADS PubMed 11.Burrell RA, McGranahan N, Bartek J, Swanton C. The causes and consequences of genetic heterogeneity in cancer evolution. Nature. 2013;501(7467):338-345.Google ScholarCrossrefSearch ADS PubMed 12.Ferrando AA, López-Otín C. Clonal evolution in leukemia. Nat Med. 2017;23(10):1135-1145.Google ScholarCrossrefSearch ADS PubMed 13.Gerlinger M, Swanton C. How Darwinian models inform therapeutic failure initiated by clonal heterogeneity in cancer medicine. Br J Cancer. 2010;103(8):1139-1143.Google ScholarCrossrefSearch ADS PubMed 14.Burger JA, Landau DA, Taylor-Weiner A, et al. Clonal evolution in patients with chronic lymphocytic leukaemia developing resistance to BTK inhibition. Nat Commun. 2016;7:11589.Google ScholarCrossrefSearch ADS PubMed 15.Ahn IE, Underbayev C, Albitar A, et al. Clonal evolution leading to ibrutinib resistance in chronic lymphocytic leukemia. Blood. 2017;129(11):1469-1479.Google ScholarCrossrefSearch ADS PubMed 16.Leeksma AC, Taylor J, Wu B, et al. Clonal diversity predicts adverse outcome in chronic lymphocytic leukemia. Leukemia. 2019;33(2):390-402.Google ScholarCrossrefSearch ADS PubMed 17.Landau DA, Tausch E, Taylor-Weiner AN, et al. Mutations driving CLL and their evolution in progression and relapse. Nature. 2015;526(7574):525-530.Google ScholarCrossrefSearch ADS PubMed 18.Woyach JA, Ruppert AS, Guinn D, et al. BTKC481S-mediated resistance to ibrutinib in chronic lymphocytic leukemia. J Clin Oncol. 2017;35(13):1437-1443.Google ScholarCrossrefSearch ADS PubMed 19.Liu T-M, Woyach JA, Zhong Y, et al. Hypermorphic mutation of phospholipase C, γ2 acquired in ibrutinib-resistant CLL confers BTK independency upon B-cell receptor activation. Blood. 2015;126(1):61-68.Google ScholarCrossrefSearch ADS PubMed 20.Landau DA, Sun C, Rosebrock D, et al. The evolutionary landscape of chronic lymphocytic leukemia treated with ibrutinib targeted therapy. Nat Commun. 2017;8(1):2185.Google ScholarCrossrefSearch ADS PubMed 21.Gángó A, Alpár D, Galik B, et al. Dissection of subclonal evolution by temporal mutation profiling in chronic lymphocytic leukemia patients treated with ibrutinib. Int J Cancer. 2020;146(1):85-93.Google ScholarCrossrefSearch ADS PubMed 22.Rendeiro AF, Krausgruber T, Fortelny N, et al. Chromatin mapping and single-cell immune profiling define the temporal dynamics of ibrutinib response in CLL. Nat Commun. 2020;11(1):577.Google ScholarCrossrefSearch ADS PubMed 23.Woyach J, Huang Y, Rogers K, et al. Resistance to acalabrutinib in CLL is mediated primarily by BTK mutations. Blood. 2019;134:504.Google ScholarCrossrefSearch ADS 24.Zenz T, Kröber A, Scherer K, et al. Monoallelic TP53 inactivation is associated with poor prognosis in chronic lymphocytic leukemia: results from a detailed genetic characterization with long-term follow-up. Blood. 2008;112(8):3322-3329.Google ScholarCrossrefSearch ADS PubMed 25.Chakraborty S, Martines C, Porro F, et al. B-cell receptor signaling and genetic lesions in TP53 and CDKN2A/CDKN2B cooperate in Richter transformation. Blood. 2021;138(12):1053-1066.Google ScholarCrossrefSearch ADS PubMed © 2022 by The American Society of Hematology2022 © 2022 by The American Society of Hematology2022 You do not currently have access to this content. Sign in via your Institution
Referência(s)