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Cinzia Allegrucci

Lecturer in Molecular Genetics and Cell Biology, Faculty of Medicine & Health Sciences

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Biography

Cinzia Allegrucci graduated in Chemistry and Pharmaceutical Technologies at the University of Perugia (Italy) in 1995. She obtained her PharmD (EU-qualified) in 1996. Cinzia then attained a PhD (Cum Laude) in Biochemistry from the University of Perugia (Italy) in 2001. She spent two years (2001-2003) as Post-doctoral Fellow at the School of Biosciences (University of Nottingham) and was then appointed as Senior Research Fellow at the School of Human Development (University of Nottingham) for the following four years. In 2007 she joined the Institute of Genetics and spin-out company EvoCell Ltd (University of Nottingham) as Senior Research Fellow. Cinzia received tenure at the University of Nottingham in 2009.

Expertise Summary

Dr Cinzia Allegrucci is a Lecturer in Molecular Genetics and Cell Biology.

Dr Allegrucci is a member of the Centre for Genetics and Genomics at the University of Nottingham.

http://beta.nottingham.ac.uk/Genetics/Research/staff.aspx

Dr Allegrucci is a member of the Cancer Research at Nottingham Centre (CRN).

http://www.cancerresearch.nottingham.ac.uk/index.php?content=researchexpertise

Teaching Summary

Module Convenor: Integrated Oncology and Genetics

Research Summary

My research interests are in Epigenetics and Stem Cell Biology. I am interested in understanding how stem cells are epigenetically regulated during normal tissue homeostasis and in disease. The… read more

Recent Publications

PhD applications are accepted all the year round.

Current Research

My research interests are in Epigenetics and Stem Cell Biology. I am interested in understanding how stem cells are epigenetically regulated during normal tissue homeostasis and in disease. The answer to this biological question is fundamental to understand the basis of diseases characterised by a stem cell dysfunction and for the development of stem cell therapies.

Epigenetic alterations in carcinogenesis

The epigenetic regulation of DNA function is achieved by chromatin remodelling via DNA methylation and histone modifications and RNA interference. These epigenetic modifications play a fundamental role in development and disease. A fundamental question in cancer research is the identification of molecular mechanisms that initiate and sustain tumour growth. The recent identification of founder cells that initiate and sustain tumour growth is opening a new promise for the understanding of tumorigenesis and for the development of novel diagnostic and therapeutic strategies targeted specifically to tumour-initiating cells. My research group is investigating the epigenetic events that initiate cancer formation and how they cooperate with genetic alterations in the progression of cancer. We are studying epigenetic alterations in t humans and and using relevant veterinary species as disease models.

Epigenetic reprogramming of cancer cells

Altered epigenetic regulation of the genome is associated with tumour initiation and progression. Genome-wide DNA hypomethylation and hypermethylation of tumour suppressor genes are hallmark of cancer. Our Lab is focussing on dissecting the epigenetic mechanisms of tumorigenesis by using oocyte extracts and induced pluripotent stem cell (iPSC) technologies to epigenetically reprogram cancer cells.

Pluripotent stem cells and germ cell tumours

The origin of germ cell tumours has puzzled scientists for many years. Our laboratory is investigating the molecular mechanisms of germ cell differentiation and tumourigenesis using human embryonic stem cells, teratocarcinoma cells and induced pluripotent stem cells.

Comparative oncology

A significant challenge in advancing cancer research is the availability of experimental models that accurately recapitulate the complexity of the disease in humans. Many cancer types are currently studied by using a combination of models including cell lines, xenografts and genetically engineered mice. However, existing models show some limitations. We are using companion animals as models because of the similarities of their naturally occurring cancers with humans. Tumour growth in companion animals occur over long periods in the context of a functional immune system. Their cancers share many features with cancers in humans, including histology, genetics, intra- and inter-individual heterogeneity, metastasis to related sites and response to conventional therapies.

Funding

Royal Society, PetPLan, Evocell Ltd, University of Nottingham

Lab Members

Mansi Shah, PhD student

Somsin Petyim, PhD student

Editorial Board member: Frontiers in Epigenomics http://www.frontiersin.org/epigenomics

School of Veterinary Medicine and Science

University of Nottingham
Sutton Bonington Campus
Leicestershire, LE12 5RD

telephone: +44 (0)115 951 6116
fax: +44 (0)115 951 6415
email: veterinary-enquiries@nottingham.ac.uk