Dr Ruth Thompson

Clinical Medicine, School of Medicine and Population Health

Royal Society Dorothy Hodgkin Research Fellow

R.H.Thompson@Sheffield.ac.uk
+44 114 215 9235

GU34, The Medical School

Full contact details

Dr Ruth Thompson
Clinical Medicine, School of Medicine and Population Health
GU34
The Medical School
Beech Hill Road
Sheffield
S10 2RX

Profile

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

Understanding the mitotic DNA damage checkpoint in order to develop new cancer treatments

Research interests

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

Show: Featured publications All publications

Featured publications

Journal articles

Liu PH, Shah RB, Li Y, Arora A, Ung PM-U, Raman R, Gorbatenko A, Kozono S, Zhou XZ, Brechin V , Barbaro JM et al (2019) An IRAK1–PIN1 signalling axis drives intrinsic tumour resistance to radiation therapy. Nature Cell Biology, 21(2), 203-213. View this article in WRRO
Ando K, Parsons MJ, Shah RB, Charendoff CI, Paris SL, Liu PH, Fassio SR, Rohrman BA, Thompson R, Oberst A , Sidi S et al (2017) NPM1 directs PIDDosome-dependent caspase-2 activation in the nucleolus. The Journal of Cell Biology, 216(6), 1795-1810. View this article in WRRO
Shah RB, Thompson R & Sidi S (2016) A mitosis-sensing caspase activation platform? New insights into the PIDDosome. Molecular & Cellular Oncology, 3(3), e1059921-e1059921.
Sakurikar N, Thompson R, Montano R & Eastman A (2015) 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
Thompson R, Shah RB, Liu PH, Gupta YK, Ando K, Aggarwal AK & Sidi S (2015) An Inhibitor of PIDDosome Formation. Molecular Cell, 58(5), 767-779.
Gagou ME, Ganesh A, Thompson R, Phear G, Sanders CM & Meuth M (2011) Suppression of Apoptosis by PIF1 Helicase in Human Tumor Cells. Cancer Research, 71, 4998-5008.
Thompson R () Treatment with the Chk1 inhibitor Gï¿½6976 enhances cisplatin cytotoxicity in SCLC cells. International Journal of Oncology.
Thompson R, Montano R & Eastman A () The Mre11 Nuclease Is Critical for the Sensitivity of Cells to Chk1 Inhibition. PLoS ONE, 7(8), e44021-e44021.

All publications

Journal articles

Shah RB, Kernan JL, van Hoogstraten A, Ando K, Li Y, Belcher AL, Mininger I, Bussenault AM, Raman R, Ramanagoudr-Bhojappa R , Huang TT et al (2021) FANCI functions as a repair/apoptosis switch in response to DNA crosslinks. Developmental Cell, 56(15), 2207-2222.e7.
Harrision D, Gravells P, Thompson R & Bryant HE (2020) 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
Thompson R, Gatenby R & Sidi S (2019) How cells handle DNA breaks during mitosis : detection, signaling, repair, and fate choice. Cells, 8(9).
Liu PH, Shah RB, Li Y, Arora A, Ung PM-U, Raman R, Gorbatenko A, Kozono S, Zhou XZ, Brechin V , Barbaro JM et al (2019) An IRAK1–PIN1 signalling axis drives intrinsic tumour resistance to radiation therapy. Nature Cell Biology, 21(2), 203-213. View this article in WRRO
Ando K, Parsons MJ, Shah RB, Charendoff CI, Paris SL, Liu PH, Fassio SR, Rohrman BA, Thompson R, Oberst A , Sidi S et al (2017) NPM1 directs PIDDosome-dependent caspase-2 activation in the nucleolus. The Journal of Cell Biology, 216(6), 1795-1810. View this article in WRRO
Shah RB, Thompson R & Sidi S (2016) A mitosis-sensing caspase activation platform? New insights into the PIDDosome. Molecular & Cellular Oncology, 3(3), e1059921-e1059921.
Sakurikar N, Thompson R, Montano R & Eastman A (2015) 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
Thompson R, Shah RB, Liu PH, Gupta YK, Ando K, Aggarwal AK & Sidi S (2015) An Inhibitor of PIDDosome Formation. Molecular Cell, 58(5), 767-779.
Gagou ME, Ganesh A, Thompson R, Phear G, Sanders CM & Meuth M (2011) Suppression of Apoptosis by PIF1 Helicase in Human Tumor Cells. Cancer Research, 71, 4998-5008.
Thompson R () Treatment with the Chk1 inhibitor Gï¿½6976 enhances cisplatin cytotoxicity in SCLC cells. International Journal of Oncology.
Thompson R, Montano R & Eastman A () The Mre11 Nuclease Is Critical for the Sensitivity of Cells to Chk1 Inhibition. PLoS ONE, 7(8), e44021-e44021.

Preprints

Watson S, Porter H, Sudbery I & Thompson R (2022) Modification of Seurat v4 for the development of a phase assignment tool able to distinguish between G2 and Mitotic cells, Cold Spring Harbor Laboratory.
Gatenby R, Li N, Lata P, Walne T, Tufail A, Breitweiser A & Thompson R (2022) A SOD1-dependent mitotic DNA damage checkpoint, Cold Spring Harbor Laboratory.