Dr Ruth Thompson
Clinical Medicine, School of Medicine and Population Health
Royal Society Dorothy Hodgkin Research Fellow
+44 114 215 9235
Full contact details
Clinical Medicine, School of Medicine and Population Health
GU34
The Medical School
Beech Hill Road
Sheffield
S10 2RX
- Profile
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For enquiries, please contact - iicd-om-operational@sheffield.ac.uk
2018 - present
Royal Society Dorothy Hodgkin Research Fellow
School of Medicieneand Popuoation Health, University of Sheffield, Sheffield, UK.2016 - 2018
JG Graves Academic Fellow
Unit of Molecular Oncology, University of Sheffield, Sheffield, UK.
2013 - 2015
Post-doctoral Researcher
Division of Haematology and Medical Oncology, Mount Sinai Hospital, New York, USA.
2010 - 2013
Post-doctoral Researcher
Geisel School of Medicine, Dartmouth College, New Hampshire, USA.
2006 - 2010
PhD
YCR Institute for Cancer Studies, University of Sheffield, Sheffield, UK.
2003 - 2006
BSc
Genetics, University of Sheffield, Sheffield, UK.Current PhD Opportunities
- Research interests
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It is commonly understood that DNA damage is largely sensed and repaired in interphase and it is proposed that DNA repair is largely repressed during mitosis due to the risk of telomere fusion.
Cancer treatments such as chemo and radiotherapy induce massive amounts of DNA damage leading to cell death of rapidly dividing cells. Some cancers have developed resistance to these agents by repairing the damage prior to cell division. For this reason, drugs which target the well-known interphase DNA repair pathways are rapidly being developed for use in the clinic. Drugs such as these could be substantially less effective if there was also a DNA damage checkpoint in mitosis.
The aim of my research is to understand what happens when a cell with damaged DNA arrives in mitosis due to dysfunctional interphase checkpoints. I want to understand which signalling proteins are involved and hope to discover the mechanism by which DNA damage is sensed and targeted for repair in mitosis.Understanding and inhibiting this pathway could lead to sensitization of tumours to standard cancer agents and thus represents a novel site of therapeutic intervention.
- Publications
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Show: Featured publications All publications
Featured publications
Journal articles
- An IRAK1–PIN1 signalling axis drives intrinsic tumour resistance to radiation therapy. Nature Cell Biology, 21(2), 203-213. View this article in WRRO
- NPM1 directs PIDDosome-dependent caspase-2 activation in the nucleolus. The Journal of Cell Biology, 216(6), 1795-1810. View this article in WRRO
- A mitosis-sensing caspase activation platform? New insights into the PIDDosome. Molecular & Cellular Oncology, 3(3), e1059921-e1059921.
- A subset of cancer cell lines is acutely sensitive to the Chk1 inhibitor MK-8776 as monotherapy due to CDK2 activation in S phase. Oncotarget, 7(2), 1380-1394. View this article in WRRO
- An Inhibitor of PIDDosome Formation. Molecular Cell, 58(5), 767-779.
- Suppression of Apoptosis by PIF1 Helicase in Human Tumor Cells. Cancer Research, 71, 4998-5008.
- Treatment with the Chk1 inhibitor G�6976 enhances cisplatin cytotoxicity in SCLC cells. International Journal of Oncology.
- The Mre11 Nuclease Is Critical for the Sensitivity of Cells to Chk1 Inhibition. PLoS ONE, 7(8), e44021-e44021.
All publications
Journal articles
- Modification of Seurat v4 for the development of a phase assignment tool able to distinguish between G2 and mitotic cells. International Journal of Molecular Sciences, 25(9). View this article in WRRO
- FANCI functions as a repair/apoptosis switch in response to DNA crosslinks. Developmental Cell, 56(15), 2207-2222.e7.
- Poly(ADP-Ribose) glycohydrolase (PARG) vs. poly(ADP-Ribose) polymerase (PARP) – function in genome maintenance and relevance of inhibitors for anti-cancer therapy. Frontiers in Molecular Biosciences, 7. View this article in WRRO
- How cells handle DNA breaks during mitosis : detection, signaling, repair, and fate choice. Cells, 8(9).
- An IRAK1–PIN1 signalling axis drives intrinsic tumour resistance to radiation therapy. Nature Cell Biology, 21(2), 203-213. View this article in WRRO
- Assessment of haemodynamic disturbance. British Journal of Hospital Medicine, 78(5), C74-C77.
- Treatment of haemodynamic disturbance. British Journal of Hospital Medicine, 78(5), C78-C80.
- NPM1 directs PIDDosome-dependent caspase-2 activation in the nucleolus. The Journal of Cell Biology, 216(6), 1795-1810. View this article in WRRO
- A mitosis-sensing caspase activation platform? New insights into the PIDDosome. Molecular & Cellular Oncology, 3(3), e1059921-e1059921.
- A subset of cancer cell lines is acutely sensitive to the Chk1 inhibitor MK-8776 as monotherapy due to CDK2 activation in S phase. Oncotarget, 7(2), 1380-1394. View this article in WRRO
- An Inhibitor of PIDDosome Formation. Molecular Cell, 58(5), 767-779.
- Sensitization of human cancer cells to gemcitabine by the Chk1 inhibitor MK-8776: cell cycle perturbation and impact of administration schedule in vitro and in vivo. BMC Cancer, 13(1).
- The cancer therapeutic potential of
Chk1 inhibitors: how mechanistic studies impact on clinical trial design. British Journal of Clinical Pharmacology, 76(3), 358-369. - Abstract 3413: Dissecting the combination of gemcitabine and the Chk1 inhibitor MK-8776 in vitro and in vivo: cell cycle perturbation and the impact of administration schedule.. Cancer Research, 73(8_Supplement), 3413-3413.
- Suppression of Apoptosis by PIF1 Helicase in Human Tumor Cells. Cancer Research, 71, 4998-5008.
- CD9 co-operation with syndecan-1 is required for a major staphylococcal adhesion pathway. mBio. View this article in WRRO
- Treatment with the Chk1 inhibitor G�6976 enhances cisplatin cytotoxicity in SCLC cells. International Journal of Oncology.
- The Mre11 Nuclease Is Critical for the Sensitivity of Cells to Chk1 Inhibition. PLoS ONE, 7(8), e44021-e44021.
Preprints
- Modification of Seurat v4 for the development of a phase assignment tool able to distinguish between G2 and Mitotic cells, Cold Spring Harbor Laboratory.
- A SOD1-dependent mitotic DNA damage checkpoint, Cold Spring Harbor Laboratory.