USP7 inhibition alters homologous recombination repair and targets CLL cells independently of ATM/p53 functional status.
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Key Points: USP7 is overexpressed and regulates HRR in CLL cells. USP7 inhibition is selectively cytotoxic to CLL cells independently of ATM and p53 and synergizes with chemotherapy.
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Many small molecule USP7 inhibitors have been found to inhibit cancer cell growth in vitro and in animal xenograft models.
“While human trials of USP7 inhibitors have yet to be conducted, many of these compounds have been found to inhibit cancer cell growth in vitro, as well as in animal xenograft models (Fan et al., 2013; Agathanggelou et al., 2017; Turnbull et al., 2017; Peng et al., 2019; Zhang et al., 2020).”
From USP7 Is a Master Regulator of Genome Stability (2020) · cites this paper as Agathanggelou et al., 2017
USP7 inhibition with HBX19,818 sensitizes chronic lymphoblastic leukemia cells to cyclophosphamide and mitomycin C in cells with defects in p53 or ATM kinase.
“USP7 inhibition with the compound HBX19, 818, for example, was shown to sensitize chronic lymphoblastic leukemia cells to the chemotherapeutic agents cyclophosphamide and mitomycin C in cells with defects in p53 or the ATM kinase (Agathanggelou et al., 2017; Sampath, 2017).”
From USP7 Is a Master Regulator of Genome Stability (2020) · cites this paper as Agathanggelou et al., 2017
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References 72 · Cited by 75
- Authors
- Agathanggelou, A., Smith, E., Davies, N. J., Kwok, M., Zlatanou, A., Oldreive, C. E., Mao, J., Da Costa, D., Yadollahi, S., Perry, T., Kearns, P., Skowronska, A., Yates, E., Parry, H., Hillmen, P., Reverdy, C., Delansorne, R., Paneesha, S., Pratt, G., Moss, P., Taylor, A. M. R., Stewart, G. S., & Stankovic, T.
- Affiliations
- University of Birmingham (GB)
- Queen Elizabeth Hospital Birmingham (GB)
- Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom;
- University of Leeds (GB)
- Hybrigenics Services, Paris, France; and
- Heartlands Hospital (GB)
- Corresponding author
- Agathanggelou, Angelo
- Smith, Edward
- ORCID
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2017-07-13
- Volume
- 130
- Issue
- 2
- Pages
- 156-166
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2613148757
- Cited by
- 75
- References
- 72
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 7 · 2023: 7 · 2022: 12 · 2021: 10 · 2020: 13 · 2019: 9 · 2018: 7 · 2017: 2
- FWCI
- 4.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- White Rose Research Online (University of Leeds, The University of Sheffield, University of York) (submittedVersion)
- University of Birmingham Research Portal (University of Birmingham) (submittedVersion, other-oa)
- Funders
- European Hematology Association (TRTH114)
- National Institute for Health and Care Research (CL-2016-09-001)
- Topics
- Health Sciences › Medicine › Genetics › Chronic Lymphocytic Leukemia Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- USP7, chronic lymphocytic leukemia, homologous recombination repair, DNA damage response, RAD18, p53, ATM, deubiquitinase, chemoresistance, ibrutinib resistance, DNA damage accumulation, therapeutic target, hematologic malignancies
- MeSH terms
- Ubiquitin-Specific Peptidase 7, Adenine, Animals, Antineoplastic Agents, DNA Damage, Humans, Piperidines, Pyrazoles, Pyrimidines, Signal Transduction, Leukemia, Lymphocytic, Chronic, B-Cell, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Mice, Inbred NOD, Drug Resistance, Neoplasm, Xenograft Model Antitumor Assays, RNA, Small Interfering, Cell Line, Tumor, Mice, Recombinational DNA Repair, Primary Cell Culture, Ataxia Telangiectasia Mutated Proteins, Ubiquitin-Specific Proteases
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