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Dr Catherine Hogan
- Available for postgraduate supervision
Teams and roles for Catherine Hogan
Lecturer
School of Biosciences
Overview
Research overview
Epithelial homeostasis is fundamental to health and survival. Tissue health is maintained via processes that regulate the number and fitness of cells in tissues. This ensures that aberrant or mutant cells - which would otherwise cause disease - are removed. Cell competition describes a general 'quality control' process that leads to the elimination of 'loser' cells. Therefore, only cells of the highest quality contribute to a tissue.
Our research shows that cell competition occurs in epithelia of the adult pancreas and this protects against cancer. We are currently investigating the mechanisms that determine competition outcomes in vivo. Our research suggests that cancer is initiated when cell competition fails or when the balance of competition tips in favour of the mutant cells. By defining what regulates cell competition in healthy tissues, we can determine how tumour cells override this process to trigger tumorigenesis.
Publication
2025
- Salvador-Barbero, B. et al. 2025. KRASG12D cells override homeostatic cell elimination mechanisms in adult pancreas via Wnt5a and cell dormancy. Gastroenterology 169 (5), pp.983-999. (10.1053/j.gastro.2025.02.042)
2024
- Badder, L. et al. 2024. The αvβ6 integrin specific virotherapy, Ad5NULL-A20.FCU1, selectively delivers 2 potent “in-tumour” chemotherapy to Pancreatic Ductal Adenocarcinoma. British Journal of Cancer 131 , pp.1694-1706. (10.1038/s41416-024-02869-3)
- Williams, J. S. et al., 2024. Enhanced bacterial cancer therapy delivering therapeutic RNA interference of c-Myc. Cell & Bioscience 14 (38)(10.1186/s13578-024-01206-8)
2022
- Woolley, T. , Hill, W. and Hogan, C. 2022. Accounting for dimensional differences in stochastic domain invasion with applications to precancerous cell removal. Journal of Theoretical Biology 541 111024. (10.1016/j.jtbi.2022.111024)
- D'Ambrogio, J. , Hill, L. and Hogan, C. 2022. Cell competition: Clonal competition protects against early tumorigenesis. Current Biology 32 (1), pp.PR52-R54. (10.1016/j.cub.2021.11.029)
2021
- Hill, W. et al. 2021. EPHA2-dependent outcompetition of KRASG12D mutant cells by wild-type neigbors in the adult pancreas. Current Biology 31 (12), pp.2550-2560. E5. (10.1016/j.cub.2021.03.094)
2019
- Hill, W. and Hogan, C. 2019. Normal epithelial cells trigger EphA2-dependent RasV12 cell repulsion at the single cell level. Small GTPases 10 (4), pp.305-310. (10.1080/21541248.2017.1324940)
2016
- Porazinski, S. et al. 2016. EphA2 drives the segregation of Ras-transformed epithelial cells from normal neighbors. Current Biology 26 (23), pp.3220-3229. (10.1016/j.cub.2016.09.037)
- Turingan, R. S. et al., 2016. Rapid DNA analysis for automated processing and interpretation of low DNA content samples. Investigative Genetics 7 (1) 2. (10.1186/s13323-016-0033-7)
2012
- Hogan, C. 2012. Impact of interactions between normal and transformed epithelial cells and the relevance to cancer. Cellular and Molecular Life Sciences 69 (2), pp.203-213. (10.1007/s00018-011-0806-3)
2011
- Hogan, C. et al. 2011. Interactions between normal and transformed epithelial cells: Their contributions to tumourigenesis. The International Journal of Biochemistry & Cell Biology 43 (4), pp.496-503. (10.1016/j.biocel.2010.12.019)
2010
- Kajita, M. et al., 2010. Interaction with surrounding normal epithelial cells influences signalling pathways and behaviour of Src-transformed cells. Journal of Cell Science 123 (2), pp.171-180. (10.1242/jcs.057976)
2009
- Hogan, C. et al. 2009. Characterization of the interface between normal and transformed epithelial cells [Letter]. Nature Cell Biology 11 (4), pp.460-467. (10.1038/ncb1853)
2007
- Dupre-Crochet, S. et al., 2007. Casein Kinase 1 Is a novel negative regulator of E-cadherin-based cell-cell contacts. Molecular and Cellular Biology 27 (10), pp.3804-3816. (10.1128/MCB.01590-06)
- Hosking, C. R. et al., 2007. The transcriptional repressor Glis2 Is a novel binding partner for p120 catenin. Molecular biology of the cell 18 (5), pp.1918-1927. (10.1091/mbc.E06-10-0941)
2006
- Fujita, Y. , Hogan, C. and Braga, V. M. M. 2006. Regulation of cell–cell adhesion by Rap1. Methods in Enzymology 407 , pp.359-372. (10.1016/S0076-6879(05)07030-8)
2004
- Hogan, C. et al. 2004. Rap1 regulates the formation of E-Cadherin-based cell-cell contacts. Molecular and Cellular Biology 24 (15), pp.6690-6700. (10.1128/MCB.24.15.6690-6700.2004)
2003
- Jones, G. E. et al., 2003. Requirement for PI 3-kinase γ in macrophage migration to MCP-1 and CSF-1. Experimental Cell Research 290 (1), pp.120-131. (10.1016/S0014-4827(03)00318-5)
Articles
- Salvador-Barbero, B. et al. 2025. KRASG12D cells override homeostatic cell elimination mechanisms in adult pancreas via Wnt5a and cell dormancy. Gastroenterology 169 (5), pp.983-999. (10.1053/j.gastro.2025.02.042)
- Badder, L. et al. 2024. The αvβ6 integrin specific virotherapy, Ad5NULL-A20.FCU1, selectively delivers 2 potent “in-tumour” chemotherapy to Pancreatic Ductal Adenocarcinoma. British Journal of Cancer 131 , pp.1694-1706. (10.1038/s41416-024-02869-3)
- Williams, J. S. et al., 2024. Enhanced bacterial cancer therapy delivering therapeutic RNA interference of c-Myc. Cell & Bioscience 14 (38)(10.1186/s13578-024-01206-8)
- Woolley, T. , Hill, W. and Hogan, C. 2022. Accounting for dimensional differences in stochastic domain invasion with applications to precancerous cell removal. Journal of Theoretical Biology 541 111024. (10.1016/j.jtbi.2022.111024)
- D'Ambrogio, J. , Hill, L. and Hogan, C. 2022. Cell competition: Clonal competition protects against early tumorigenesis. Current Biology 32 (1), pp.PR52-R54. (10.1016/j.cub.2021.11.029)
- Hill, W. et al. 2021. EPHA2-dependent outcompetition of KRASG12D mutant cells by wild-type neigbors in the adult pancreas. Current Biology 31 (12), pp.2550-2560. E5. (10.1016/j.cub.2021.03.094)
- Hill, W. and Hogan, C. 2019. Normal epithelial cells trigger EphA2-dependent RasV12 cell repulsion at the single cell level. Small GTPases 10 (4), pp.305-310. (10.1080/21541248.2017.1324940)
- Porazinski, S. et al. 2016. EphA2 drives the segregation of Ras-transformed epithelial cells from normal neighbors. Current Biology 26 (23), pp.3220-3229. (10.1016/j.cub.2016.09.037)
- Turingan, R. S. et al., 2016. Rapid DNA analysis for automated processing and interpretation of low DNA content samples. Investigative Genetics 7 (1) 2. (10.1186/s13323-016-0033-7)
- Hogan, C. 2012. Impact of interactions between normal and transformed epithelial cells and the relevance to cancer. Cellular and Molecular Life Sciences 69 (2), pp.203-213. (10.1007/s00018-011-0806-3)
- Hogan, C. et al. 2011. Interactions between normal and transformed epithelial cells: Their contributions to tumourigenesis. The International Journal of Biochemistry & Cell Biology 43 (4), pp.496-503. (10.1016/j.biocel.2010.12.019)
- Kajita, M. et al., 2010. Interaction with surrounding normal epithelial cells influences signalling pathways and behaviour of Src-transformed cells. Journal of Cell Science 123 (2), pp.171-180. (10.1242/jcs.057976)
- Hogan, C. et al. 2009. Characterization of the interface between normal and transformed epithelial cells [Letter]. Nature Cell Biology 11 (4), pp.460-467. (10.1038/ncb1853)
- Dupre-Crochet, S. et al., 2007. Casein Kinase 1 Is a novel negative regulator of E-cadherin-based cell-cell contacts. Molecular and Cellular Biology 27 (10), pp.3804-3816. (10.1128/MCB.01590-06)
- Hosking, C. R. et al., 2007. The transcriptional repressor Glis2 Is a novel binding partner for p120 catenin. Molecular biology of the cell 18 (5), pp.1918-1927. (10.1091/mbc.E06-10-0941)
- Fujita, Y. , Hogan, C. and Braga, V. M. M. 2006. Regulation of cell–cell adhesion by Rap1. Methods in Enzymology 407 , pp.359-372. (10.1016/S0076-6879(05)07030-8)
- Hogan, C. et al. 2004. Rap1 regulates the formation of E-Cadherin-based cell-cell contacts. Molecular and Cellular Biology 24 (15), pp.6690-6700. (10.1128/MCB.24.15.6690-6700.2004)
- Jones, G. E. et al., 2003. Requirement for PI 3-kinase γ in macrophage migration to MCP-1 and CSF-1. Experimental Cell Research 290 (1), pp.120-131. (10.1016/S0014-4827(03)00318-5)
Research
Research programme
My lab has pioneered innovative cell and tissue systems and interdisciplinary approaches to study cell competition in mammalian epithelia. We have also developed novel in vivo mouse models of spontaneous pancreatic and lung cancers. Our experimental models recapitulate more accurately human cancer development because we switch on cancer-causing mutations in low numbers of cells. This approach allows us to define the molecular cell biology underlying how genetically mutant cells expand and grow while surrounded by healthy cells and in a complex 3D tissue. We combine mouse models with cutting-edge 3D tissue imaging, quantitative cell biology, transcriptomics, including spatial transcriptomics and computational biology.
Cell competition in epithelial health and disease
We identified EPHA2 (a receptor tyrosine kinase of the Eph-ephrin family of bidirectional signals) as an evolutionarily conserved signal that triggers the expulsion of RAS mutant cells from epithelial tissues in vitro and in vivo. We recently showed that WNT5A signalling is also an important regulator of RAS mutant cell fate. Upregulation of WNT5A signalling allows RAS mutant cells to avoid cell elimination and survive in the tissues.
Current BBSRC/UKRI funded projects are investigating whether and how tissue location determines RAS mutant cell fate and whether cell auonomous and non-autonomous factors predict RAS cell fate.
Unravelling the biology of early pancreatic cancer
Pancreatic cancer is a devastating disease because we are unable to detect it at early stages when clinical intervention would vastly improve patients’ lives. Early detection is vital to improve patient prognosis and save lives.
Pancreatic tumours start from cells expressing oncogenic KRAS mutations. Our research demonstrates that KrasG12D cells are outcompeted and eliminated from healthy pancreas tissues in vivo and this is tumour preventative. However, elimination mechanisms are inefficient and some KRAS cells avoid cell elimination and instead survive in tissues as dormant and stem-like cells. Our goals are to identify factors that enable RAS mutant cells to avoid cell elimination. Equally, our focus is to uncover signals/factors that promote RAS mutant cell expansion during early stages of pancreatic cancer.
Current team members
Dr Non Williams (postdoc)
Dr Ella Reed (computational postdoc)
Shadid Salehin (MRes)
Alumni
Dr Beatriz Barbero-Salvador (former CRUK postdoc and Pancreatic Cancer UK Career Foundation Fellow)
Cherish Lukwago (former MSc student)
Liam Hill (former PhD student)
Joshua D’Ambrogio (former PhD student)
Jacob Morris (former MSc student)
Dr Markella Alatsatianos (former Technician)
Ellis Jones (former CITER MSc student)
Isabelle Parker (former MRes student)
Dr Andreas Zaragkoulias (former postdoc)
Dr Ana Padilha (former Technician)
William Hill (former PhD student)
Dr Sean Porazinski (former postdoc)
Former Integrated Masters students, 2018-2025:
Non Williams,
Aishling Larkin,
Megan Coslett,
Ioanna Kontou,
Ellie McCracken,
Katy Mumford,
Rebecca Samuel,
Molly Sharp
Collaborators:
Dr Renata Jurkowska (BIOSI)
Dr Fisun Hamaratoglu (BIOSI)
Professor Richard Clarkson (ECSCRI).
Professor Alan Parker (MEDIC).
Dr Thomas Woolley (MATHS).
Dr Ian Fallis (CHEMY).
Dr Maria Secrier (UCL).
Professor Owen Sansom (CRUK Scotland Institute).
Professor Jennifer Morton (CRUK Scotland Institute).
Professor Daniel Murphy (CRUK Scotland Institute).
Professor Anne Grapin-Botton (Max Plank Institute MCBG, Dresden).
Dr Joaquin de Navascués (Essex University).
Teaching
Lecturer in Biomedical sciences:
Year 1 Skills for Science.
Year 2 Cell biology.
Year 2 Developmental and Stem Cell Biology.
Year 3 Cancer: Cellular and molecular mechanisms and therapeutics.
Research skills, including integrated masters, Mres, MSc, PhD.
Biography
Lecturer in Biomedical Sciences, School of Biosciences since Sept 2020. I joined the European Cancer Stem Cell Research Institute (ECSCRI) as Research Fellow in 2013. Postdoctoral training in the laboratory of Dr Yasuyuki Fujita at MRC Laboratory for Molecular Cell Biology (LMCB), University College London. I carried out my PhD training in the laboratory of Professor Gareth Jones at the Randall Division of Cell and Molecular Biophysics, King's College London.
Professional memberships
Ambassador for British Society of Cell Biology (BSCB)
Committees and reviewing
Grant reviewer: UKRI (MRC, BBSRC, Springboard), CRUK, Pancreatic Cancer UK, Breast Cancer Now, Dutch Research Council.
Journal reviewer: Science, Current Biology, Nature Communications, Developmental Biology, Disease Models & Mechanisms, Scientific reports, Breast Cancer Research, Biochemical journal, eLife, EMBO.
Supervisions
Epithelial cell biology;
Quantitative image analysis and computational biology;
Early tumorigenesis in epithelial tissues.
Epithelial cell biology;
Quantitative image analysis and computational biology;
Early tumorigenesis in epithelial tissues.
News articles
Contact Details
Research themes
Specialisms
- Cancer cell biology
- Cell competition
- normal-mutant cell-cell interactions
- pancreatic cancer
- Lung cancer
