Allan Balmain

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Allan Balmain
Allan-Balmain-FRS.jpg
Allan Balmain at the Royal Society admissions day in London, July 2015
Alma mater University of Glasgow (BSc, PhD)
Awards
Scientific career
Fields
Institutions
Thesis Studies in the diterpenoid field  (1969)
Website

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]

Contents

Education

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]

Awards and honours

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]

Related Research Articles

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.

Benign tumor Mass of cells which cannot spread throughout the body

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.

KDM1A

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

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.

FANCD2

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.

BAP1 Protein-coding gene in the species Homo sapiens

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 Protein-coding gene in the species Homo sapiens

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 J. Patel

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).

Stephen D. M. Brown

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.

Mouse Models of Human Cancer database

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.

References

  1. 1 2 3 "Professor Allan Balmain FRS". London: The Royal Society. Archived from the original on 2 May 2015.
  2. 1 2 3 4 5 "Allan Balmain, PhD, FRSE". University of California, San Francisco. Archived from the original on 6 February 2013.
  3. ↑ Balmain, A; Gray, J; Ponder, B (2003). "The genetics and genomics of cancer". Nature Genetics . 33 Suppl (3s): 238–44. doi:10.1038/ng1107. PMID   12610533. S2CID   8379885.
  4. ↑ Quigley, D. A.; To, M. D.; Kim, I. J.; Lin, K. K.; Albertson, D. G.; Sjolund, J.; Pérez-Losada, J. S.; Balmain, A. (2011). "Network analysis of skin tumor progression identifies a rewired genetic architecture affecting inflammation and tumor susceptibility" (PDF). Genome Biology . 12: R5. doi:10.1186/gb-2011-12-1-r5. PMC   3091303 . PMID   21244661. Open Access logo PLoS transparent.svg
  5. ↑ Cui, W.; Fowlis, D. J.; Bryson, S.; Duffie, E.; Ireland, H.; Balmain, A.; Akhurst, R. J. (1996). "TGFβ1 Inhibits the Formation of Benign Skin Tumors, but Enhances Progression to Invasive Spindle Carcinomas in Transgenic Mice". Cell. 86 (4): 531–542. doi: 10.1016/S0092-8674(00)80127-0 . PMID   8752208. S2CID   18065761.
  6. ↑ Merritt, A. J.; Potten, C. S.; Kemp, C. J.; Hickman, J. A.; Balmain, A; Lane, D. P.; Hall, P. A. (1994). "The role of p53 in spontaneous and radiation-induced apoptosis in the gastrointestinal tract of normal and p53-deficient mice". Cancer Research. 54 (3): 614–7. PMID   8306319.
  7. ↑ Derynck, R; Akhurst, R. J.; Balmain, A (2001). "TGF-beta signaling in tumor suppression and cancer progression". Nature Genetics. 29 (2): 117–29. doi:10.1038/ng1001-117. PMID   11586292. S2CID   9923320.
  8. ↑ Quintanilla, M; Brown, K; Ramsden, M; Balmain, A (1986). "Carcinogen-specific mutation and amplification of Ha-ras during mouse skin carcinogenesis". Nature. 322 (6074): 78–80. Bibcode:1986Natur.322...78Q. doi:10.1038/322078a0. PMID   3014349. S2CID   4353576.
  9. ↑ Allan Balmain's publications indexed by the Scopus bibliographic database. (subscription required)
  10. ↑ Balmain, A.; Barrett, J. C.; Moses, H.; Renan, M. J. (1993). "How many mutations are required for tumorigenesis? Implications from human cancer data". Molecular Carcinogenesis. 7 (3): 139–146. doi:10.1002/mc.2940070303. PMID   8489711. S2CID   29456469.
  11. ↑ Balmain, A.; Ramsden, M.; Bowden, G. T.; Smith, J. (1984). "Activation of the mouse cellular Harvey-ras gene in chemically induced benign skin papillomas". Nature. 307 (5952): 658–660. Bibcode:1984Natur.307..658B. doi:10.1038/307658a0. PMID   6694757. S2CID   4254723.


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