Acquired MYC rearrangement potentially associated with ibrutinib resistance in mantle cell lymphoma.

Chang-Tsu Yuan, Li-Yu Sun, Chieh-Lung Cheng, Ming Yao, Bor-Sheng Ko, Wei-Li Ma

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Article in Virchows Archiv : an international journal of pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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6 authors.

Chang-Tsu YuanDepartment and Graduate Institute of Pathology, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.ORCID http://orcid.org/0000-0003-1438-9187

Li-Yu SunDepartment and Graduate Institute of Pathology, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.

Chieh-Lung ChengDivision of Hematology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.

Ming YaoDivision of Hematology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.

Bor-Sheng KoDepartment of Hematological Oncology, National Taiwan University Cancer Center, Taipei, Taiwan.

Wei-Li MaDepartment of Oncology, National Taiwan University Hospital, No.7, Chung Shan S. Rd, Zhongzheng Dist, Taipei, 100225, Taiwan. excellent0667@gmail.com.ORCID http://orcid.org/0000-0002-6840-2976

Funding

College of Medicine, National Taiwan University NTUCCS-112-07National Science and Technology Council 112-2320-B-040-

6 · The paper itself

Abstract

Mantle cell lymphoma (MCL) is a subtype of mature B-cell lymphoma characterized by the expression of CD5, cyclin D1, and SOX11, along with the IGH::CCND1 rearrangement. While the introduction of ibrutinib, a Bruton tyrosine kinase inhibitor, has significantly improved outcomes, resistance remains a challenge. The role of MYC rearrangement in ibrutinib resistance remains unclear. We investigated the pathological features and the status of MYC, BCL2, and BCL6 rearrangements in ibrutinib-resistant versus ibrutinib-responsive MCL tumors. Among the 31 specimens from 27 patients, 7 tumors (23%) were resistant to ibrutinib. A comparison between ibrutinib-resistant and ibrutinib-responsive tumors revealed a significant difference in c-Myc expression (median 25 vs. 5%, p = 0.008) and MYC rearrangement (43 [3/7] vs. 0% [0/23], p = 0.009). All MYC rearrangements were acquired, and these tumors demonstrated intrinsic resistance to ibrutinib. Furthermore, MYC-rearranged tumors exhibited blastoid or pleomorphic cytomorphology, CD10 expression, elevated c-Myc expression, and a high Ki-67 proliferative index. In conclusion, our findings suggest that c-Myc overexpression and MYC rearrangement are associated with ibrutinib resistance in MCL. Detecting MYC rearrangement in selected MCL cases could be critical for optimizing treatment strategies and improving patient outcomes.

Indexed as

AdenineDrug Resistance, NeoplasmGene RearrangementLymphoma, Mantle-CellProtein Kinase InhibitorsProto-Oncogene Proteins c-mycPyrazolesPyrimidinesAgedAged, 80 and overBiomarkers, TumorFemaleHumansMaleMiddle AgedPiperidinesAdenineBiomarkers, TumoribrutinibMYC protein, humanPiperidinesProtein Kinase InhibitorsProto-Oncogene Proteins c-mycPyrazolesPyrimidinesBCL2 rearrangementBCL6 rearrangementDouble-hitIbrutinib resistanceMantle cell lymphomaMYC rearrangement

Identifiers

PMID41339992

DOI10.1007/s00428-025-04364-3

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.