ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012
Mutated BCR-ABL generates immunogenic T-cell epitopes in CML patients.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Beyond cold to hot: oncolytic virotherapy as the next cornerstone of immuno-oncology.Nature reviews. Clinical oncology · 2026Review
- T cell receptors specific for an imatinib-induced mutation in BCR-ABL for adoptive T cell therapy.Frontiers in immunology · 2025Article
- On the peptide binding affinity changes in population-specific HLA repertoires to the SARS-CoV-2 variants Delta and Omicron.Journal of autoimmunity · 2022Article
- Identification of neoantigens for individualized therapeutic cancer vaccines.Nature reviews. Drug discovery · 2022Review
- Allogeneic Tumor Antigen-Specific T Cells for Broadly Applicable Adoptive Cell Therapy of Cancer.Cancer treatment and research · 2022Article
- Pan-Cancer Analysis RevealedJournal of oncology · 2022Article
- Evolution of CD8Cells · 2021Review
- Personal neoantigen vaccines induce persistent memory T cell responses and epitope spreading in patients with melanoma.Nature medicine · 2021Article
- Article
- Therapeutic applications of the selective high affinity ligand drug SH7139 extend beyond non-Hodgkin's lymphoma to many other types of solid cancers.Oncotarget · 2020Article
- Personal tumor antigens in blood malignancies: genomics-directed identification and targeting.The Journal of clinical investigation · 2020Review
- Integrative -omics and HLA-ligandomics analysis to identify novel drug targets for ccRCC immunotherapy.Genome medicine · 2020Article
- The Immunogenic Potential of Recurrent Cancer Drug Resistance Mutations: AnFrontiers in immunology · 2020Article
- Neoantigens in Hematologic Malignancies.Frontiers in immunology · 2020Review
- Neoantigens and genome instability: impact on immunogenomic phenotypes and immunotherapy response.Genome medicine · 2019Review
- Antigen Targets for the Development of Immunotherapies in Leukemia.International journal of molecular sciences · 2019Review
- Neoantigens in Hematological Malignancies-Ultimate Targets for Immunotherapy?Frontiers in immunology · 2019Review
- Neoantigen vaccine generates intratumoral T cell responses in phase Ib glioblastoma trial.Nature · 2019Article
- Chromosome Y-encoded antigens associate with acute graft-versus-host disease in sex-mismatched stem cell transplant.Blood advances · 2018Article
- Generation of TCR-Expressing Innate Lymphoid-like Helper Cells that Induce Cytotoxic T Cell-Mediated Anti-leukemic Cell Response.Stem cell reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
purposeCharacterization of an approach to identify leukemia neoantigens arising in the context of drug resistance. EXPERIMENTAL
designWe assessed whether leukemia neoantigens could be generated from drug-resistant mutations in BCR-ABL after imatinib relapse in patients with chronic myelogenous leukemia (CML).
resultsWe computationally predicted that approximately 70 peptides derived from 26 BCR-ABL mutations would bind eight common alleles of MHC class I (IC(50) < 1,000 nmol/L). Seven of nine imatinib-resistant CML patients were predicted to generate at least 1 peptide that binds autologous HLA alleles. We predicted and confirmed that an E255K mutation-derived peptide would bind HLA-A3 with high affinity (IC(50) = 28 nmol/L), and showed that this peptide is endogenously processed and presented. Polyfunctional E255K-specific CD8+ T cells were detected in two imatinib-resistant HLA-A3+ CML patients concurrent with an effective anti-CML response to further therapy.
conclusionsOur in vitro studies support the hypothesis that leukemia-driven genetic alterations are targeted by the immune system in association with a clinical response, and suggest the possibility of immunizing relapsed patients with CML against newly acquired tumor neoantigens.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.