The DOI matches its Crossref record; 83 of the 83 references it cites were found in a registry or an index.
Past, present, and future of Bcr-Abl inhibitors: from chemical development to clinical efficacy
Open accessAbstract
Bcr-Abl inhibitors paved the way of targeted therapy epoch. Imatinib was the first tyrosine kinase inhibitor to be discovered with high specificity for Bcr-Abl protein resulting from t(9, 22)-derived Philadelphia chromosome. Although the specific targeting of that oncoprotein, several Bcr-Abl-dependent and Bcr-Abl-independent mechanisms of resistance to imatinib arose after becoming first-line therapy in chronic myelogenous leukemia (CML) treatment.Consequently, new specific drugs, namely dasatinib, nilotinib, bosutinib, and ponatinib, were rationally designed and approved for clinic to override resistances. Imatinib fine mechanisms of action had been elucidated to rationally develop those second- and third-generation inhibitors. Crystallographic and structure-activity relationship analysis, jointly to clinical data, were pivotal to shed light on this topic. More recently, preclinical evidence on bafetinib, rebastinib, tozasertib, danusertib, HG-7-85-01, GNF-2, and 1,3,4-thiadiazole derivatives lay promising foundations for better inhibitors to be approved for clinic in the near future.Notably, structural mechanisms of action and drug design exemplified by Bcr-Abl inhibitors have broad relevance to both break through resistances in CML treatment and develop inhibitors against other kinases as targeted chemotherapeutics.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
O'Brien, S. G., Guilhot, F., Larson, R. A., Gathmann, I., Baccarani, M., Cervantes, F., Cornelissen, J. J., Fischer, T., Hochhaus, A., Hughes, T., et al. (2003) · New England Journal of Medicine · doi:10.1056/nejmoa022457 · Cited by 3,570
Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells
Druker, B. J., Tamura, S., Buchdunger, E., Ohno, S., Segal, G. M., Fanning, S., Zimmermann, J., & Lydon, N. B. (1996) · Nature Medicine · doi:10.1038/nm0596-561 · Cited by 2,967
A quantitative analysis of kinase inhibitor selectivity
Karaman, M. W., Herrgard, S., Treiber, D. K., Gallant, P., Atteridge, C. E., Campbell, B. T., Chan, K. W., Ciceri, P., Davis, M. I., Edeen, P. T., et al. (2008) · Nature Biotechnology · doi:10.1038/nbt1358 · Cited by 2,466
Borst, O., Walker, B., Münzer, P., Russo, A., Schmid, E., Faggio, C., Bigalke, B., Laufer, S., Gawaz, M., & Lang, F. (2013) · Cellular Physiology and Biochemistry · doi:10.1159/000350110 · Cited by 1,860
Overriding Imatinib Resistance with a Novel ABL Kinase Inhibitor
Shah, N. P., Tran, C., Lee, F. Y., Chen, P., Norris, D., & Sawyers, C. L. (2004) · Science · doi:10.1126/science.1099480 · Cited by 1,796
Structural Mechanism for STI-571 Inhibition of Abelson Tyrosine Kinase
Schindler, T., Bornmann, W., Pellicena, P., Miller, W. T., Clarkson, B., & Kuriyan, J. (2000) · Science · doi:10.1126/science.289.5486.1938 · Cited by 1,780
Shah, N. P., Nicoll, J. M., Nagar, B., Gorre, M. E., Paquette, R. L., Kuriyan, J., & Sawyers, C. L. (2002) · Cancer Cell · doi:10.1016/s1535-6108(02)00096-x · Cited by 1,612
Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl
Weisberg, E., Manley, P. W., Breitenstein, W., Brüggen, J., Cowan-Jacob, S. W., Ray, A., Huntly, B., Fabbro, D., Fendrich, G., Hall-Meyers, E., et al. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.01.007 · Cited by 1,492
Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug
Capdeville, R., Buchdunger, E., Zimmermann, J., & Matter, A. (2002) · Nature Reviews Drug Discovery · doi:10.1038/nrd839 · Cited by 1,389
Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy
Hochhaus, A., Kreil, S., Corbin, A., La Rosée, P., Müller, M., Lahaye, T., Hanfstein, B., Schoch, C., Cross, N., Berger, U., et al. (2002) · Leukemia · doi:10.1038/sj.leu.2402741 · Cited by 906
Cited by
Molecular targeted therapy for anticancer treatment
Min, H.-Y., & Lee, H.-Y. (2022) · Experimental & Molecular Medicine · doi:10.1038/s12276-022-00864-3 · Cited by 569
Properties of FDA-approved small molecule protein kinase inhibitors
Roskoski, R. (2019) · Pharmacological Research · doi:10.1016/j.phrs.2019.03.006 · Cited by 554
Emerging Therapeutic Strategies to Overcome Drug Resistance in Cancer Cells
Garg, P., Malhotra, J., Kulkarni, P., Horne, D., Salgia, R., & Singhal, S. S. (2024) · Cancers · doi:10.3390/cancers16132478 · Cited by 339
Alves, R., Gonçalves, A. C., Rutella, S., Almeida, A. M., De Las Rivas, J., Trougakos, I. P., & Sarmento Ribeiro, A. B. (2021) · Cancers · doi:10.3390/cancers13194820 · Cited by 204
Inhibition of USP1, a New Partner of Bcr-Abl, Results in Decrease of Bcr-Abl Level in K562 Cells
Antonenko, S. V., & Telegeev, G. D. (2023) · Experimental Oncology · doi:10.32471/exp-oncology.2312-8852.vol-42-no-2.14533 · Cited by 19
Metadata
- Authors
- Rossari, F., Minutolo, F., & Orciuolo, E.
- Venue
- Journal of Hematology & Oncology
- Published
- 2018-06-20
- Volume
- 11
- Issue
- 1
- Pages
- 84-84
- ISSN
- 1756-8722 (ISSN-L)
- OpenAlex
- W2808764596
- Cited by
- 371
- References
- 83
- FWCI
- 22.64
- Type
- journal article
- Language
- en
- Open access
- gold
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Past, present, and future of Bcr-Abl inhibitors: from chemical development to clinical efficacy. https://app.cochat.ai/papers/10.1186/s13045-018-0624-2
- The paper
- Rossari, F., Minutolo, F., & Orciuolo, E. (2018). Past, present, and future of Bcr-Abl inhibitors: from chemical development to clinical efficacy. Journal of Hematology & Oncology. https://doi.org/10.1186/s13045-018-0624-2
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
