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Dr David Allard

Dr David Allard

Lecturer (E&R)





Dr Allard received a BSc (Hons) in Cellular and Molecular Pathology from the University of Bristol and completed a PhD in Cancer Studies at the University of Liverpool studying the regulation of the metastasis gene S100A4. Subsequently Dr Allard worked as a postdoctoral fellow at the ICRF in Cambridge (Prof Gherardi and Sir Stoker FRS) where he developed his interest in the role of cell-cell interactions in determining cancer progression. An interest in cell-cell interactions in disease settings was developed by postdoctoral studies in the department of Medicine, Cambridge University (Prof Bennett) and the CR:UK Cambridge Research Institute (Prof Tuveson). In 2011, Dr Allard moved to the University of Exeter to set up a group studying the cell biology of disease. Dr Allard’s research interests are in the molecular and cell biology of disease progression, particularly cancer.


BSc (Hons) Bristol

PhD Liverpool


Research group links


Research interests

Cell and Molecular biology of tumour progression.

Although cancer is the second most common cause of death in the UK, there are many mechanisms by which tumour progression is controlled. These include genetic and epigenetic alterations in the cancer cell and interactions between the cancer cell and surrounding cells, the tumour microenvironment. We study the role of the tumour microenvironment in suppressing the growth of tumour cells. A major part of our work is determining the molecular signals at the cell surface through which control of tumour cell fate is determined by the microenvironment. Complementary projects aim to identify the molecules within the tumour cell through which these signals are transmitted to initiate this form of growth arrest.

The approaches we use are both a targeted investigation of candidate genes and unbiased screening (e.g. with shRNA libraries) for functional genes. Gene expression is affected in cells found in the tumour microenvironment and the effect on the growth of surrounding cancer cells evaluated using high-throughput microscopy or next generation sequencing.

These studies are performed in collaboration with Professor Tuveson (CSHL), Professors Georg Klein and Laszlo Szerkely (Karolinska institute, Sweden) and Professor Gherardi (Italy).

Pancreatic beta cell biology.

Diabetes is characterised by the loss of pancreatic beta cell function, either through death of beta cells or through the reduced ability of beta cells to secrete insulin. We aim to identify novel genes that either protect pancreatic beta cells from death or increase insulin secretion. Subsequently, the products of these genes may be amenable to the development of therapeutic intervention strategies. These studies are complemented by functional analysis of SNPs associated with diabetic phenotypes identified in GWAS studies either directly or indirectly through comparison of GWAS and functional screen data.

In collaboration with Professor Tim Frayling (UEMS).

Research projects

Role of cell-cell interactions in tumour initiation and progression

• High throughput microscopic screening for genes involved in non-cell autonomous control of cancer progression 
• Identification of novel genes involved in the tumour microenvironment through next generation sequencing.
• Role of the extracellular matrix enzymes in tumour initiation and progression

Beta cell biology

• Identification of novel genes controlling pancreatic beta cell proliferation and death through next generation sequencing based screening approaches
• Identification of novel genes involved in secretion of insulin from beta cells through high-throughput microscopy
• The role of genes identified by GWAS in pancreatic beta cell function

Research networks

Professor Gherardi (University of Pavia)

Professors Klein and Szekely (Karolinska Institute, Sweden)


Journal articles

Azevedo-Pouly ACP, Sutaria DS, Jiang J, Elgamal OA, Amari F, Allard D, Grippo PJ, Coppola V, Schmittgen TD (2017). miR-216 and miR-217 expression is reduced in transgenic mouse models of pancreatic adenocarcinoma, knockout of miR-216/miR-217 host gene is embryonic lethal. Functional and Integrative Genomics, 17(2-3), 203-212. Abstract.
Jiang J, Azevedo-Pouly ACP, Redis RS, Lee EJ, Gusev Y, Allard D, Sutaria DS, Badawi M, Elgamal OA, Lerner MR, et al (2016). Globally increased ultraconserved noncoding RNA expression in pancreatic adenocarcinoma. Oncotarget, 7(33), 53165-53177. Abstract.  Author URL.
Azevedo ACP, Jiang J, Lee EJ, Gusev Y, Allard D, Tuveson DA, Calin GA, Schmittgen TD (2011). Global increase in ultraconserved non-coding RNA expression in pancreatic adenocarcinoma. CANCER RESEARCH, 71 Author URL.
Olive KP, Jacobetz MA, Davidson CJ, Gopinathan A, McIntyre D, Honess D, Madhu B, Goldgraben MA, Caldwell ME, Allard D, et al (2009). Inhibition of Hedgehog signaling enhances delivery of chemotherapy in a mouse model of pancreatic cancer. Science, 324(5933), 1457-1461. Abstract.  Author URL.
Allard D, Figg N, Bennett MR, Littlewood TD (2008). Akt regulates the survival of vascular smooth muscle cells via inhibition of FoxO3a and GSK3. J Biol Chem, 283(28), 19739-19747. Abstract.  Author URL.
Allard D, Stoker M, Gherardi E (2003). A G2/M cell cycle block in transformed cells by contact with normal neighbors. Cell Cycle, 2(5), 484-487. Abstract.  Author URL.


Allard DJ, Figg N, Bennett MR, Littlewood TD (2007). Akt-mediated inhibition of apotosis in vascular smooth muscle cells.  Author URL.

David_Allard Details from cache as at 2023-10-04 01:04:06

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Dr Allard is a co-module lead on the BSc (Hons) Medical Sciences program for the core final year module (Integrated Clinical Sciences 4), is the theme lead for Cell biology within the Medical School and teaches various aspects of both the BSc (Hons) Medical Sciences and BMBS programs.



Information not currently available

Supervision / Group

Postgraduate researchers

  • Lorena Boquete-Vilarino
  • Ashley Nicholls


  • Emma Dearing underggraduate project
  • Jade Lyons-Rimmer undergraduate project
  • Richard Perryman undergraduate project
  • Katarzyna Wolanska research associate

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