Allan Balmain | |
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Alma mater | University of Glasgow (BSc, PhD) |
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Scientific career | |
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Thesis | Studies in the diterpenoid field (1969) |
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Allan Balmain FRS [1] FRSE is Barbara Bass Bakar Distinguished Professor of Cancer Genetics [2] at the University of California, San Francisco (UCSF). [7] [8] [9] [10] [11]
Balmain was educated at the University of Glasgow where he was awarded a Bachelor of Science degree in chemistry in 1966, followed by a PhD on the organic chemistry of terpenoids in 1969. [2]
Balmain was elected a Fellow of the Royal Society (FRS) in 2015. His certificate of election reads:
Allan Balmain has pioneered the use of the mouse as a model system for understanding the complexity of cancer at a genetic, molecular and cellular level. Through his novel and creative experiments he established the first molecular link between cancer initiation and carcinogen exposure, identified how specific genetic events lead to malignant progression and made major advances in our understanding of cancer susceptibility. Balmain's wide-ranging, innovative use of mouse genetics has generated new approaches for visualizing the genetic architecture of cancer pathways and the roles of complex network interactions in determining an individual's cancer susceptibility. [1]
Balmain was also elected a Fellow of the Royal Society of Edinburgh (FRSE) in 1995. [2]
The Institute of Cancer Research is a public research institute and a member institution of the University of London in London, United Kingdom, specialising in oncology. It was founded in 1909 as a research department of the Royal Marsden Hospital and joined the University of London in 2003. It has been responsible for a number of breakthrough discoveries, including that the basic cause of cancer is damage to DNA.
A benign tumor is a mass of cells (tumor) that lacks the ability either to invade neighboring tissue or metastasize. When removed, benign tumors usually do not grow back, whereas malignant tumors are cancerous and sometimes do. Unlike most benign tumors elsewhere in the body, benign brain tumors can be life-threatening. Benign tumors generally have a slower growth rate than malignant tumors and the tumor cells are usually more differentiated. They are typically surrounded by an outer surface or stay contained within the epithelium. Common examples of benign tumors include moles and uterine fibroids.
Sir Walter Fred Bodmer is a German-born British human geneticist.
Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer cells. The process is characterized by changes at the cellular, genetic, and epigenetic levels and abnormal cell division. Cell division is a physiological process that occurs in almost all tissues and under a variety of circumstances. Normally, the balance between proliferation and programmed cell death, in the form of apoptosis, is maintained to ensure the integrity of tissues and organs. According to the prevailing accepted theory of carcinogenesis, the somatic mutation theory, mutations in DNA and epimutations that lead to cancer disrupt these orderly processes by interfering with the programming regulating the processes, upsetting the normal balance between proliferation and cell death. This results in uncontrolled cell division and the evolution of those cells by natural selection in the body. Only certain mutations lead to cancer whereas the majority of mutations do not.
Lysine-specific histone demethylase 1A (LSD1) also known as lysine (K)-specific demethylase 1A (KDM1A) is a protein in humans that is encoded by the KDM1A gene. LSD1 is a flavin-dependent monoamine oxidase, which can demethylate mono- and di-methylated lysines, specifically histone 3, lysines 4 and 9. This enzyme can have roles critical in embryogenesis and tissue-specific differentiation, as well as oocyte growth. KDM1A was the first histone demethylase to be discovered though more than 30 have been described.
CHEK2 is a tumor suppressor gene that encodes the protein CHK2, a serine-threonine kinase. CHK2 is involved in DNA repair, cell cycle arrest or apoptosis in response to DNA damage. Mutations to the CHEK2 gene have been linked to a wide range of cancers.
Caretaker genes encode products that stabilize the genome. Fundamentally, mutations in caretaker genes lead to genomic instability. Tumor cells arise from two distinct classes of genomic instability: mutational instability arising from changes in the nucleotide sequence of DNA and chromosomal instability arising from improper rearrangement of chromosomes.
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.
Fanconi anemia group D2 protein is a protein that in humans is encoded by the FANCD2 gene. The Fanconi anemia complementation group (FANC) currently includes FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ, FANCL, FANCM, FANCN and FANCO.
BRCA1 associated protein-1 is a deubiquitinating enzyme that in humans is encoded by the BAP1 gene. BAP1 encodes an 80.4 kDa nuclear-localizing protein with a ubiquitin carboxy-terminal hydrolase (UCH) domain that gives BAP1 its deubiquitinase activity. Recent studies have shown that BAP1 and its fruit fly homolog, Calypso, are members of the polycomb-group proteins (PcG) of highly conserved transcriptional repressors required for long-term silencing of genes that regulate cell fate determination, stem cell pluripotency, and other developmental processes.
Mouse models of colorectal cancer and intestinal cancer are experimental systems in which mice are genetically manipulated, fed a modified diet, or challenged with chemicals to develop malignancies in the gastrointestinal tract. These models enable researchers to study the onset, progression of the disease, and understand in depth the molecular events that contribute to the development and spread of colorectal cancer. They also provide a valuable biological system, to simulate human physiological conditions, suitable for testing therapeutics.
Somatic evolution is the accumulation of mutations and epimutations in somatic cells during a lifetime, and the effects of those mutations and epimutations on the fitness of those cells. This evolutionary process has first been shown by the studies of Bert Vogelstein in colon cancer. Somatic evolution is important in the process of aging as well as the development of some diseases, including cancer.
CYP2A7 is a protein that in humans is encoded by the CYP2A7 gene.
Sir Michael Rudolf Stratton, is a British clinical scientist and the third director of the Wellcome Trust Sanger Institute. He currently heads the Cancer Genome Project and is a leader of the International Cancer Genome Consortium.
Sir Bruce Anthony John Ponder FMedSci FRS is an English geneticist and cancer researcher. He is Emeritus Professor of Oncology at the University of Cambridge and former director of the Cancer Research UK Cambridge Institute.
Studies with protons and HZE nuclei of relative biological effectiveness for molecular, cellular, and tissue endpoints, including tumor induction, demonstrate risk from space radiation exposure. This evidence may be extrapolated to applicable chronic conditions that are found in space and from the heavy ion beams that are used at accelerators.
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.
Ketan Jayakrishna Patel is a British-Kenyan scientist who is Director of the MRC Weatherall Institute of Molecular Medicine and the MRC Molecular Haematology Unit at the University of Oxford. Until 2020 he was a tenured principal investigator at the Medical Research Council (MRC) Laboratory of Molecular Biology (LMB).
Steve David Macleod Brown is director of the Medical Research Council (MRC) Mammalian Genetics Unit, MRC Harwell at Harwell Science and Innovation Campus, Oxfordshire, a research centre on mouse genetics. In addition, he leads the Genetics and Pathobiology of Deafness research group.
The laboratory mouse has been instrumental in investigating the genetics of human disease, including cancer, for over 110 years. The laboratory mouse has physiology and genetic characteristics very similar to humans providing powerful models for investigation of the genetic characteristics of disease.