Gerard Evan | |
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Born | [1] | 17 August 1955
Alma mater | St Peter's College, Oxford King's College, Cambridge [1] |
Known for | Disease Models & Mechanisms |
Awards | Fellow of the Royal Society (2004) FMedSci (1999) [2] PhD (1982) |
Scientific career | |
Fields | Cancer [3] [4] [5] [6] [7] [8] Disease biology Myc regulator gene [9] p53 tumour suppressor [10] |
Institutions | University of Oxford University of Cambridge UCSF [1] [11] Cancer Research UK [12] Ensemble Therapeutics |
Thesis | Monoclonal antibodies as reagents for the analysis of cell surfaces (1982) |
Website | www labmed |
Gerard Ian Evan FRS, FMedSci (born 17 August 1955) is a British biologist and, since May 2022, Professor of Cancer Biology at King's College London and a principal group leader in the Francis Crick Institute. Prior to this he was Sir William Dunn Professor of Biochemistry and Head of Biochemistry at the University of Cambridge (2009-2022). [11] [13]
Evan was educated at St Peter's College, Oxford, where he studied Biochemistry, and King's College, Cambridge, where he was awarded his PhD in 1982 for research using Monoclonal antibodies. [1] [14]
Evan does research to the determine the molecular basis of cancer. [15] [16] [17] [18] [19] [20] [21] [22]
Prior to Cambridge, Evan was Royal Society Napier Professor at University College London and the Imperial Cancer Research Fund (1988-99), then Gerson & Barbara Bass Bakar Distinguished Professor of Cancer Biology, at University of California, San Francisco (1999-2011).
p53, also known as Tumor protein P53, cellular tumor antigen p53, or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. The p53 proteins are crucial in vertebrates, where they prevent cancer formation. As such, p53 has been described as "the guardian of the genome" because of its role in conserving stability by preventing genome mutation. Hence TP53 is classified as a tumor suppressor gene.
Bert Vogelstein is director of the Ludwig Center, Clayton Professor of Oncology and Pathology and a Howard Hughes Medical Institute investigator at The Johns Hopkins Medical School and Sidney Kimmel Comprehensive Cancer Center. A pioneer in the field of cancer genomics, his studies on colorectal cancers revealed that they result from the sequential accumulation of mutations in oncogenes and tumor suppressor genes. These studies now form the paradigm for modern cancer research and provided the basis for the notion of the somatic evolution of cancer.
Mouse double minute 2 homolog (MDM2) also known as E3 ubiquitin-protein ligase Mdm2 is a protein that in humans is encoded by the MDM2 gene. Mdm2 is an important negative regulator of the p53 tumor suppressor. Mdm2 protein functions both as an E3 ubiquitin ligase that recognizes the N-terminal trans-activation domain (TAD) of the p53 tumor suppressor and as an inhibitor of p53 transcriptional activation.
Myc is a family of regulator genes and proto-oncogenes that code for transcription factors. The Myc family consists of three related human genes: c-myc (MYC), l-myc (MYCL), and n-myc (MYCN). c-myc was the first gene to be discovered in this family, due to homology with the viral gene v-myc.
N-myc proto-oncogene protein also known as N-Myc or basic helix-loop-helix protein 37 (bHLHe37), is a protein that in humans is encoded by the MYCN gene.
Bcl-2 homologous antagonist/killer is a protein that in humans is encoded by the BAK1 gene on chromosome 6. The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein localizes to mitochondria, and functions to induce apoptosis. It interacts with and accelerates the opening of the mitochondrial voltage-dependent anion channel, which leads to a loss in membrane potential and the release of cytochrome c. This protein also interacts with the tumor suppressor P53 after exposure to cell stress.
MYC proto-oncogene, bHLH transcription factor is a protein that in humans is encoded by the MYC gene which is a member of the myc family of transcription factors. The protein contains basic helix-loop-helix (bHLH) structural motif.
Karen Heather Vousden, CBE, FRS, FRSE, FMedSci is a British medical researcher. She is known for her work on the tumour suppressor protein, p53, and in particular her discovery of the important regulatory role of Mdm2, an attractive target for anti-cancer agents. From 2003 to 2016, she was the director of the Cancer Research UK Beatson Institute in Glasgow, UK, moving back to London in 2016 to take up the role of Chief Scientist at CRUK and Group Leader at the Francis Crick Institute.
Promyelocytic leukemia protein (PML) is the protein product of the PML gene. PML protein is a tumor suppressor protein required for the assembly of a number of nuclear structures, called PML-nuclear bodies, which form amongst the chromatin of the cell nucleus. These nuclear bodies are present in mammalian nuclei, at about 1 to 30 per cell nucleus. PML-NBs are known to have a number of regulatory cellular functions, including involvement in programmed cell death, genome stability, antiviral effects and controlling cell division. PML mutation or loss, and the subsequent dysregulation of these processes, has been implicated in a variety of cancers.
Inhibitor of growth protein 1 is a protein that in humans is encoded by the ING1 gene.
MAX is a gene that in humans encodes the MAX transcription factor.
MAX-interacting protein 1 is a protein that in humans is encoded by the MXI1 gene.
Protein phosphatase 1D is an enzyme that in humans is encoded by the PPM1D gene.
L-myc-1 proto-oncogene protein is a protein that in humans is encoded by the MYCL1 gene.
Protein CIP2A also known as cancerous inhibitor of PP2A (CIP2A) is a protein that in humans is encoded by the KIAA1524 gene.
Joshua T. Mendell is an American molecular biologist who is a professor of molecular biology at the University of Texas Southwestern Medical Center, where he is a Howard Hughes Medical Institute Investigator. Before moving to UT Southwestern, Mendell was a Howard Hughes Medical Institute early career scientist at Johns Hopkins School of Medicine. His molecular biology research examines microRNA (miRNA) regulation and function, with particular emphasis on miRNAs and cancer.
Douglas Green, is an American biologist. He holds the Peter C. Doherty Endowed Chair of Immunology in St. Jude Children's Research Hospital. His research has focused on the process of active cell death and cell survival, extending from the role of cell death in cancer regulation and immune responses in the whole organism to the molecular events directing the death of the cell. Green was editor in chief of the journal Oncogene from 2009-2016, is a Deputy Editor of the journal "Science Advances" and the author of the book Cell Death, Means To An End.
Breast cancer metastatic mouse models are experimental approaches in which mice are genetically manipulated to develop a mammary tumor leading to distant focal lesions of mammary epithelium created by metastasis. Mammary cancers in mice can be caused by genetic mutations that have been identified in human cancer. This means models can be generated based upon molecular lesions consistent with the human disease.
AI-10-49 is a small molecule inhibitor of leukemic oncoprotein CBFβ-SMHHC developed by the laboratory of John Bushweller with efficacy demonstrated by the laboratories of Lucio H. Castilla and Monica Guzman. AI-10-49 allosterically binds to CBFβ-SMMHC and disrupts protein-protein interaction between CBFβ-SMMHC and tumor suppressor RUNX1. This inhibitor is under development as an anti-leukemic drug.
Laura Soucek is a Group Leader at VHIO, Research Professor at ICREA, and CEO of Peptomyc S.L. She works on the Myc oncoprotein, the deregulation of which occurs during almost all cancers. Soucek has designed a dominant negative variant, Omomyc, which allows her to investigate the benefits of inhibiting Myc in cancer.