Allard, David - University of Exeter

个人简介

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.

研究领域

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.

近期论文

查看导师新发文章（温馨提示：请注意重名现象，建议点开原文通过作者单位确认）

Jiang J, Azevedo-Pouly AC, 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 Abstract. Author URL. Full text. Article has an altmetric score of 1 Azevedo-Pouly ACP, Sutaria DS, Jiang J, Elgamal OA, Amari F, Allard D, Grippo PJ, Coppola V, Schmittgen TD (2016). 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, 1-10. Abstract. Full text. Article has an altmetric score of 2 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. Article has an altmetric score of 51 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.