USP7 inhibition alters homologous recombination repair and targets CLL cells independently of ATM/p53 functional status

Author:

Agathanggelou Angelo1,Smith Edward1,Davies Nicholas J.1,Kwok Marwan12,Zlatanou Anastasia1,Oldreive Ceri E.1,Mao Jingwen1,Da Costa David1,Yadollahi Sina1,Perry Tracey1,Kearns Pamela1,Skowronska Anna1,Yates Elliot1,Parry Helen12,Hillmen Peter3,Reverdy Celine4,Delansorne Remi4,Paneesha Shankara5,Pratt Guy12,Moss Paul12,Taylor A. Malcolm R.1,Stewart Grant S.1,Stankovic Tatjana1

Affiliation:

1. Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom;

2. Centre for Clinical Haematology, Queen Elizabeth Hospital Birmingham, Birmingham, United Kingdom;

3. Section of Experimental Haematology, Leeds Institute of Cancer and Pathology, University of Leeds, Leeds, United Kingdom;

4. Hybrigenics Services, Paris, France; and

5. Heartlands Hospital, Birmingham, United Kingdom

Abstract

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.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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