Blizard Institute - Barts and The London

Cleo Bishop, BSc PhD

Cleo

Non-Clinical Senior Lecturer and Director of Graduate Studies

Email: c.l.bishop@qmul.ac.uk
Telephone: +44 (0)20 7882 2343

Profile

Cleo received her PhD in Biological Sciences from University College London in 2001. She then spent four years as a MRC Career Development Fellow in the laboratory of Prof. Chris Higgins at the MRC Clinical Sciences Centre (now the London Institute of Medical Sciences), Imperial College London, where she developed a keen interest in cancer biology.

In 2006, she moved to the Blizard Institute to pursue her interest in senescence and cancer, spending four years in the laboratory of Prof. David Beach (FRS). During this time, she established our Phenotypic Screening facility, and has used this technology to discover novel regulators of the ageing and senescence biomarker, p16.

In 2010, Cleo was awarded a Lecturership, and promoted to Senior Lecturer in 2016.

Cleo is the Academic Lead for The QMUL Phenotypic Screening Facility, managed by Dr Luke Gammon, and in 2018 became the Director of Graduate Studies for the Blizard Institute. She also organises our cross-campus forums on ‘Senescence and Ageing’ and ‘Extracellular Vesicles’

 

Group Members

Dr Eleanor Tyler

 

PhD Students

Deborah Milligan (BBSRC iCASE)

Ryan Wallis (Professor Derek Willoughby Foundation)

Ugochim (Stefany) Eduputa (BBSRC LIDo)

Hannah Mizen (BBSRC LIDo iCASE)

 

Screening Facility Staff

Dr Luke Gammon

 

Alumni

Dr Madeleine Moore (MRC)

Dr Paul Braker (Barts Charity)

James Newman (iBSc, SSC4)

Arturo Robles (MSc)

Daniel Yee (MRes)

Mateja Sborchia (MRes)

 

We are always interested in hearing from bright, motivated scientist who are interested in joining our team.

Summary

Recent and ongoing research projects:

Advanced age is the main risk factor for most chronic diseases in humans, but the basic machinery that drives ageing remains largely unknown. With the exception of pluripotent embryonic stem cells, primary cells in vitro and in vivo gradually lose the ability to divide. One of the key effectors of this process is p16, a master regulator of the cell cycle whose expression results in cellular senescence. The gradual accumulation of p16 expression during physiological ageing and several ageing-associated diseases promotes p16 as a robust biomarker of human ageing. Its locus, the INK/ARF locus, is intimately involved in the susceptibility to a broad range of ageing-associated diseases, including coronary artery disease and type 2 diabetes. Targeting cellular senescence represents an exciting strategy for promoting healthy ageing.

The regulated cell proliferation that is essential for human longevity contrasts with the uncontrolled growth of cancer cells. During early tumourigenesis, cells harbouring precancerous lesions often respond by activating tumour suppressors, such as p16, and entering a premature cell cycle arrest called oncogene-induced senescence. The establishment of this growth arrest relies on the timely activation of p16, a virtual hallmark of early stage neoplasia, and acts as a vital barrier to cancer progression. By illuminating the fundamental mechanisms that regulate senescence programmes we will further our understanding of how cells sense early carcinogenic events, and the interplay between cancer progression, healthy ageing and cellular rejuvenation.

Keywords

Cellular senescence, oncogene-induced senescence, cancer, ageing, cellular rejuvenation,pro-senescence therapy for cancer, p16, INK/ARF, miRNAs, exosomes.

Teaching

Undergraduate

Course Lecturer: BIO111 Cell Biology

Course Lecturer: BIO115 The Human Cell

MBBS –Problem Based Learning

 

Postgraduate

Module Lead: ICM7141 Cell and Molecular Basis of Regeneration, MSc Regenerative Medicine

Course Lecturer: ICM7142 Stem cell and developmental biology, MSc Regenerative Medicine

Course Lecturer: Research Techniques

 

Personal tutor, MSc Regenerative Medicine

 

http://www.blizard.qmul.ac.uk/study-with-us/postgraduate-taught-courses/900-regen-med.html


Research

Research Interests:

Advanced age is the main risk factor for most chronic diseases in humans, but the basic machinery that drives ageing remains largely unknown. With the exception of pluripotent embryonic stem cells, primary cells in vitro and in vivo gradually lose the ability to divide. One of the key effectors of this process is p16, a master regulator of the cell cycle whose expression results in cellular senescence. The gradual accumulation of p16 expression during physiological ageing and several ageing-associated diseases promotes p16 as a robust biomarker of human ageing. Its locus, the INK/ARF locus, is intimately involved in the susceptibility to a broad range of ageing-associated diseases, including coronary artery disease and type 2 diabetes. Targeting cellular senescence represents an exciting strategy for promoting healthy ageing.

The regulated cell proliferation that is essential for human longevity contrasts with the uncontrolled growth of cancer cells. During early tumourigenesis, cells harbouring precancerous lesions often respond by activating tumour suppressors, such as p16, and entering a premature cell cycle arrest called oncogene-induced senescence. The establishment of this growth arrest relies on the timely activation of p16, a virtual hallmark of early stage neoplasia, and acts as a vital barrier to cancer progression. By illuminating the fundamental mechanisms that regulate senescence programmes we will further our understanding of how cells sense early carcinogenic events, and the interplay between cancer progression, healthy ageing and cellular rejuvenation.

Publications

Key Publications

Remodelling of microRNAs in colorectal cancer by hypoxia alters metabolism profiles and 5-fluorouracil resistance. A Nijhuis, H Thompson, J Adam, A Parker, L Gammon, A Lewis, JG Bundy, T Soga, A Jalaly, D Propper, R Jeffery, N Suraweera, S McDonald, MA Thaha, R Feakins, R Lowe, CL Bishop*, A Silver1* (2017Human Molecular Genetics 26(8):1552-1564.

The Senescent Methylome and its relationship with cancer, ageing, and germline genetic variation in humans. R Lowe, MG Overhoff, DH Beach, VK Rakyan and CL Bishop (2015Genome Biology 16:194.

Low serum levels of MicroRNA-19 are associated with a stricturing Crohn’s disease phenotype. A Lewis, SMehta, LN Hanna, LA Rogalski, R Jeffery, A Nijhuis, T Kumagai, P Biancheri, JG Bundy, CL Bishop, R Feakins, A Di Sabatino, JC Lee, JO Lindsay and A Silver (2015Inflammatory Bowel Disease 21(8):1926-1934.

Isogenic induced pluripotent stem cell lines from an adult with mosaic Down Syndrome model accelerated neuronal ageing and neurodegeneration. A Murray, A Letourneau, C Canzonetta, E Stathaki, S Gimelli, F Sloan-Bena, R Abrehart, P Goh, S Lim, C Baldo, F Dagna-Bricarelli, S Hannan, M Mortensen, D Ballard, D Syndercombe Court, N Fusaki, M Hasegawa, TG Smart, CL Bishop, E Antonarakis, J Groet*, and D Nizetic* (2015Stem Cells 33(6):2077-84.

Cellular senescence mediated by p16INK4A-coupled miRNA pathways. MG Overhoff, JC Garbe, J Koh, MR Stampfer, DH Beach, CL Bishop (2014Nucleic Acids Res. 42(3):1606-18. 

All Publications

Supervision

Dr Madeleine MooreMiss Eleanor Tyler, PhD StudentMiss Deborah Milligan, PhD StudentMr Ryan Wallis, PhD Student AlumniDr Paul BrakerDaniel YeeArturo Robles