Dr Catherine Hogan
Lecturer
- Available for postgraduate supervision
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 process whereby cells compete with its neighbour for space and survival and ‘loser’ cells are eliminated. Therefore, only cells of the highest quality contribute to a tissue. We currently lack a clear understanding of how healthy cells identify and detect ‘loser’ cells, particularly in highly organised complex tissues. Our research suggests that early tumour formation only occurs when cell competition fails or when the balance of the competition tips in favour of the tumour cells. Our goal is to define what regulates cell competition in healthy epithelial tissues and determine how tumour cells override this process to form a tumour. Our research will improve our understanding of the biology underlying how epithelial tissues maintain health. Equally, we will gain new insights into the biology and timing of early tumorigenesis. Together, this new knowledge will underpin the development of early detection cancer strategies and improve patient prognosis.
Publication
2025
- Salvador-Barbero, B., Alatsatianos, M., Morton, J. P., Sansom, O. J. and Hogan, C. 2025. KRASG12D cells override homeostatic cell elimination mechanisms in adult pancreas via Wnt5a and cell dormancy. Gastroenterology
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, article number: 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., article number: 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., Vasantgadkar, S., Palombo, L., Hogan, C., Jiang, H., Tan, E. and Selden, R. F. 2016. Rapid DNA analysis for automated processing and interpretation of low DNA content samples. Investigative Genetics 7(1), article number: 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., Kajita, M., Lawrenson, K. and Fujita, Y. 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., Alatsatianos, M., Morton, J. P., Sansom, O. J. and Hogan, C. 2025. KRASG12D cells override homeostatic cell elimination mechanisms in adult pancreas via Wnt5a and cell dormancy. Gastroenterology
- 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, article number: 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., article number: 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., Vasantgadkar, S., Palombo, L., Hogan, C., Jiang, H., Tan, E. and Selden, R. F. 2016. Rapid DNA analysis for automated processing and interpretation of low DNA content samples. Investigative Genetics 7(1), article number: 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., Kajita, M., Lawrenson, K. and Fujita, Y. 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
We combine innovative and powerful in vitro epithelial cell systems, ex vivo organoid models and in vivo mouse models of cancer. We employ cutting-edge immunofluorescence techniques, including Lightsheet imaging of cleared tissues, and image analysis platforms to generate powerful 3D landscapes of labelled tissues. We combine these technologies with transcriptomics to uncover transcriptional signatures of cell competition in tissues. Through interdisciplinary collaboration, we apply mathematical modelling to test hypotheses and gain mechanistic insight and use Drosophila melanogaster models to scrutinise the role of key signalling pathways at the genetic level in vivo.
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-transformed cells from tissues in vivo. Current projects in the lab are exploring the generality of this EphA2-dependent mechanism in epithelial tissues where oncogenic RAS is a key driver mutation. We also investigate the molecular mechanisms downstream of EphA2 as a regulator of epithelial tissue health.
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. Pancreatic tumours start from cells expressing oncogenic Kras mutations (KRasG12D). Our research demonstrates that KrasG12D cells are outcompeted and eliminated from healthy pancreas tissues in vivo and this is tumour preventative. Current projects in the lab are investigating how KRasG12D cells override cell competition mechanisms, avoid cell elimination and remain in tissues to drive early disease.
Team members
Dr Beatriz Salvador
Dr Markella Alatsatianos
Liam Hill (PhD student)
Joshua D’Ambrogio (PhD student)
Anna Richards (PhD student; co-supervisor)
Collaborators:
Professor Richard Clarkson (ECSCRI).
Professor Alan Parker (MEDIC).
Professor Ann Ager (MEDIC).
Dr Thomas Woolley (MATHS).
Dr Ian Fallis (CHEMY).
Dr Lee Parry (ECSCRI).
Professor Paul Dyson (Swansea University).
Professor Owen Sansom (CRUK Beatson Institute, Glasgow).
Professor Jennifer Morton (CRUK Beatson Institute, Glasgow).
Professor Daniel Murphy (CRUK Beatson Institute, Glasgow).
Professor Eric O’Neill (Oxford University).
Professor Anne Grapin-Botton (Max Plank Institute MCBG, Dresden).
Dr Joaquin de Navascués (Essex University).
Teaching
Lecturer in Biomedical sciences.
Cell biology.
Cancer: Cellular and molecular mechanisms and therapeutics.
Advanced Research Methods & Project.
Contributor to Concepts in Disease and Skills for Science
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.
Committees and reviewing
Grant reviewer: UKRI (MRC, BBSRC), CRUK, Breast Cancer Now.
Journal reviewer: Current Biology, Nature Communications, Developmental Biology, Disease Models & Mechanisms, Scientific reports, Breast Cancer Research, Biochemical journal.
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.
Contact Details
+44 29206 88505
Hadyn Ellis Building, Room European Cancer Stem Cell Research Institute, Cardiff School of BiosciencesHadyn Ellis Building, Maindy Road, Cardiff CF24 4HQ, Maindy Road, Cardiff, CF24 4HQ