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Allan Bradley
Wellcome Trust Sanger Institute
368Publications
112H-index
58.7kCitations
Publications 368
Newest
#1Gabriel Balmus (University of Cambridge)H-Index: 11
#2Domenic Pilger (University of Cambridge)H-Index: 2
Last.Stephen P. Jackson (University of Cambridge)H-Index: 118
view all 24 authors...
Mutations in the ATM tumor suppressor gene confer hypersensitivity to DNA-damaging chemotherapeutic agents. To explore genetic resistance mechanisms, we performed genome-wide CRISPR-Cas9 screens in cells treated with the DNA topoisomerase I inhibitor topotecan. Thus, we here establish that inactivating terminal components of the non-homologous end-joining (NHEJ) machinery or of the BRCA1-A complex specifically confer topotecan resistance to ATM-deficient cells. We show that hypersensitivity of A...
#1Julia Weber (TUM: Technische Universität München)H-Index: 7
#2Jorge de la Rosa (Wellcome Trust Sanger Institute)H-Index: 7
Last.Roland RadH-Index: 37
view all 41 authors...
B-cell lymphoma (BCL) is the most common hematologic malignancy. While sequencing studies gave insights into BCL genetics, identification of non-mutated cancer genes remains challenging. Here, we describe PiggyBac transposon tools and mouse models for recessive screening and show their application to study clonal B-cell lymphomagenesis. In a genome-wide screen, we discover BCL genes related to diverse molecular processes, including signaling, transcriptional regulation, chromatin regulation, or ...
#1Amy T. Y. YeungH-Index: 9
Last.Gordon DouganH-Index: 102
view all 0 authors...
ABSTRACT A genome-scale CRISPR knockout library screen of THP-1 human macrophages was performed to identify loss-of-function mutations conferring resistance to Salmonella uptake. The screen identified 183 candidate genes, from which 14 representative genes involved in actin dynamics (ACTR3, ARPC4, CAPZB, TOR3A, CYFIP2, CTTN, and NHLRC2), glycosaminoglycan metabolism (B3GNT1), receptor signaling (PDGFB and CD27), lipid raft formation (CLTCL1), calcium transport (ATP2A2 and ITPR3), and cholesterol...
#1Alina Rudorf (University Medical Center Freiburg)
#2Tony Andreas Müller (University Medical Center Freiburg)H-Index: 1
Last.Anna Lena IllertH-Index: 7
view all 16 authors...
Activating mutations in FLT3 and NPM1 are most frequent alterations in acute myeloid leukemia (AML) and often coincidental. The mutational status of NPM1 has strong prognostic relevance to patients with point mutations of the FLT3 tyrosine kinase domain (TKD), but the biological mechanism underlying this effect remains unclear. In the present study, we investigated the impact of the coincidence of NPM1c and FLT3-TKD. While expression of FLT3-TKD is not sufficient to induce a disease in mice, co-...
#1Jian Yang (Wellcome Trust Sanger Institute)H-Index: 81
#2Sandeep S. Rajan (University of Cambridge)
Last.Emmanouil Metzakopian (University of Cambridge)H-Index: 1
view all 10 authors...
Summary Primed epiblast stem cells (EpiSCs) can be reverted to a pluripotent embryonic stem cell (ESC)-like state by expression of single reprogramming factor. We used CRISPR activation to perform a genome-scale, reprogramming screen in EpiSCs and identified 142 candidate genes. Our screen validated a total of 50 genes, previously not known to contribute to reprogramming, of which we chose Sall1 for further investigation. We show that Sall1 augments reprogramming of mouse EpiSCs and embryonic fi...
#1Mathias Friedrich (Wellcome Trust Sanger Institute)H-Index: 9
#2Iraad F. Bronner (Wellcome Trust Sanger Institute)H-Index: 5
Last.Roland Rad (DKFZ: German Cancer Research Center)H-Index: 37
view all 5 authors...
#1Katharina Boroviak (Wellcome Trust Sanger Institute)H-Index: 5
#2Beiyuan Fu (Wellcome Trust Sanger Institute)H-Index: 26
Last.Allan Bradley (Wellcome Trust Sanger Institute)H-Index: 112
view all 5 authors...
#1Konstantinos Tzelepis (Wellcome Trust Sanger Institute)H-Index: 7
#2Etienne De Braekeleer (Wellcome Trust Sanger Institute)H-Index: 3
Last.George S. Vassiliou (University of Cambridge)H-Index: 27
view all 35 authors...
We recently identified the splicing kinase gene SRPK1 as a genetic vulnerability of acute myeloid leukemia (AML). Here, we show that genetic or pharmacological inhibition of SRPK1 leads to cell cycle arrest, leukemic cell differentiation and prolonged survival of mice transplanted with MLL-rearranged AML. RNA-seq analysis demonstrates that SRPK1 inhibition leads to altered isoform levels of many genes including several with established roles in leukemogenesis such as MYB, BRD4 and MED24. We focu...
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