Martin John Evans (1941– )

Sir Martin John Evans researched developmental biology in the United Kingdom during the twentieth and early twenty-first centuries. He was among the first to isolate and grow embryonic stem cells in the lab. Embryonic stem cells have the ability to develop into many different cell types. Using those cells, Evans and his colleagues developed methods for introducing changes to the DNA of early mouse embryos. He found that when he introduced those modified embryos into foster mothers, the genetic alterations also appeared in subsequent generations. That finding helped him produce some of the first living mice with desired genetic changes, later dubbed knockout mice. In 2007, Evans received the Nobel Prize in Physiology or Medicine along with Mario Capecchi and Oliver Smithies for their work on introducing specific gene modifications in mice using embryonic stem cells. Evans’s scientific contributions have permitted scientists to better understand the roles of different genes in both embryological development and disease.

1. Early Life and Education
2. Professional Career
3. Legacy and Impact

Early Life and Education

Evans was born on 1 January 1941 in Gloucestershire, England. In Evans’s Nobel Prize autobiography, he recounts that his first memories date from his time living in Wareside, England, during World War II. As a child, Evans saw a narrow trench in front of his house that soldiers used as an emergency shelter. He also reports seeing prisoners of war tilling local fields. Evans’s father had a mechanical workshop where they manufactured military transport vehicles and helped run local communication for the Home Guard, which was responsible for guarding coastal areas and factories from invasion. Around that same time, at approximately age three, Evans conducted his first experiment, mixing sand and cement with water to understand how water could make sand and cement solidify. Evans also spent time with his father in the family’s mechanical workshop, where he learned to operate a lathe. With that training, Evans began to make cannons. In Evans’s aforementioned autobiography, he writes that he developed an early passion for chemistry from mixing different chemicals together to create improved explosives for his rockets.

Evans reports that when he entered middle school at St Dunstan’s College in London, England, he was keen on both chemistry and physics. Following his fourth-year math exam, Evans dropped his math classes in favor of biology courses such as botany and zoology. He later won a scholarship to attend Christ’s College, University of Cambridge, in Cambridge, England. In 1963, Evans graduated with a Bachelor of Arts in Natural Science. However, Evans was unable to complete his final examinations due to developing glandular fever, more commonly called mononucleosis, or mono, which limited his postgraduate opportunities. In 1966, he received a Master of Arts in Biochemistry. During his time at Cambridge, Evans met his future wife, Judith Claire Williams, and they married in 1966.

After receiving his master’s, Evans moved to University College London, in London. There, he took a position as a research assistant for Elizabeth Deuchar, who, at that time, was studying biochemical aspects of amphibian development. Evans began studying how teratogens, substances that interfere with normal fetal development, influence the embryonic development of a type of clawed frog. Evans eventually completed a doctoral thesis at University College London entitled Studies on the Ribonucleic Acid of Early Amphibian Embryos and received his PhD in 1969.

In his Nobel Prize autobiography, Evans states that he faced technological limitations using amphibians as a model system to study development. In the late 1960s, Evans talked to Robin Weiss, a professor of viral oncology at University College London, about pursuing a more tractable system for studying developmental biology. Weiss suggested he explore the use of mouse teratocarcinoma stem cells. Teratocarcinoma is a form of cancer that develops primarily in the gonads, the testes or ovaries, from malignant stem cells. Stem cells are cells that are capable of replicating indefinitely and differentiating into new types of cells. Teratocarcinoma stem cells resemble embryonic stem cells in that they are capable of dividing and turning into many different cell types, including cells making up the three embryonic germ layers. For that reason, they are a good model system for studying early development. Evans states in his Nobel autobiography that he decided to pursue using mice as a model organism over amphibians due to mice having a more tractable developmental system and the amount and variety of cells that stem cells can differentiate into.

Professional Career

In 1969, Evans began his career as a lecturer and researcher in the anatomy and embryology department at University College London. As a lecturer, Evans taught both graduate and undergraduate students while simultaneously conducting his own research. Evans began working with mouse teratocarcinoma cells after receiving mouse strain 129 from Leroy Stevens, a researcher at The Jackson Laboratory in Bar Harbor, Maine. Stevens developed strain 129 mice, which had a higher incidence of spontaneous testicular teratocarcinoma than other strains and many tissue types.

In 1972, Evans followed up on Stevens’s work and published his first paper, in which he demonstrated that injecting teratoma cells from mouse strain 129 into other mice caused those cells to produce a fully differentiated tumor. Three years later, he showed that under suitable conditions, teratocarcinoma cells growing in a dish could turn into a variety of different cell types. Those findings demonstrated that it was possible for cells to give rise to various cell types without using a host organism. During his time at University College London, Evans continued to publish his work on teratocarcinoma cell lines and their fate in journals including Cell and Nature. In 1978, Evans left University College London to continue his career as an assistant lecturer and researcher in the genetics department at the University of Cambridge. There, Evans taught a molecular developmental biology course.

In 1980, Evans began working with Matthew Kaufman, who was studying mouse development at Cambridge. In 1981, Evans and Kaufman published a paper in Nature in which they reported that they had established some of the first pluripotent stem cell lines from mouse embryos. Pluripotent stem cells are cells that have the potential to develop into many different cell types. They derive from the inner cell mass of an early-stage embryo called a blastocyst. A cell line is a continuously dividing populations of cells that can be grown in a dish and maintained in the laboratory for an extended period of time. To establish pluripotent stem cell lines, Evans and Kaufman first recovered mouse embryos at the blastocyst stage from mouse strain 129. Next, they grew the blastocysts in petri dishes. After forty-eight hours, they removed the inner cell mass cells from the blastocytes and grew those separately. Those were the pluripotent stem cell lines. They further showed that the pluripotent stem cell lines could differentiate into different cells types, either in a dish or in a living animal. Later that same year, Gail Martin, a biologist working independently at the University of California in San Francisco, California, also created pluripotent stem cell lines from the inner cell mass cells of a mouse blastocyst. The Royal Society credits Martin with coining the term embryonic stem cells.

Before Evans and Kaufman’s and Martin’s findings, having a continuously growing culture of embryonic stem cells in vitro was not possible. Once researchers had cultures of those cells, they could use them to transfer mutated genes into a mouse embryo. That has enabled scientists to study the role of different genes by creating mice with either a mutated version of a gene or mice lacking the gene completely, so-called knockout mice. In 1984, Evans and Kaufman, alongside Allan Bradley and Elizabeth Robertson, two of Evans’s students, showed that the mutations introduced into mice were able to be maintained through subsequent generations.

Evans continued his work on embryonic stem cells following Kaufman’s departure to Edinburgh. In 1987, Evans published an article in Nature that described an experiment in which he created mice with a mutation in their HRPT gene as a potential animal model for Lesch-Nyhan Syndrome, a condition that in humans causes impaired kidney function, arthritis, and self-mutilation behavior. In the 1990s, Evans became a fellow and maintained his own research lab at Cambridge University’s St. Edmund’s College.

Evans recounts that his move to Cambridge was initially difficult, but ultimately was a good decision for his family and research lab. When he moved to Cambridge, Evans’s sons had not started secondary school, and his daughter Clare was four and about to start primary school. Additionally, Evans’s wife, who initially worked in family planning while in London, became a general practice nurse due to limited family planning jobs in Cambridge. His wife helped set up and train local nursing groups. Evans reports having an excellent lab while at Cambridge, having students including Robin Lovell-Badge, David Latchman, and Allan Bradley, all of whom went on to have research careers of their own.

In 1993, Evans’s lab used gene targeting technology to create mutated mice with severe cystic fibrosis, a disease that causes thick mucus to build up in the body, causing breathing and digestive problems. Those mutated mice demonstrated how researchers could use gene targeting to test novel therapeutics, including gene therapy, a form of medical intervention where scientists modify or introduce genes into cells to prevent or treat illness. In 1999, Evans left Cambridge and accepted a job offer to become a professor of mammalian genetics and director of Cardiff University’s School of Biosciences in Cardiff, Wales. During his time at Cardiff University, he continued to earn recognition for his contributions to embryology and medical research.

In 2001, Evans shared the Albert Lasker Basic Medical Research Award with Mario Capecchi, a Howard Hughes Medical Institute Investigator at the University of Utah, in Salt Lake City, Utah, and Oliver Smithies, a professor of pathology and laboratory medicine at the University of North Carolina, in Chapel Hill, North Carolina. Evans, Capecchi, and Smithies received the Lasker Award for their work on creating gene-targeting technology capable of creating mice that model human diseases. In 2007, Evans, Capecchi, and Smithies won the Nobel Prize in Physiology or Medicine for those same scientific advancements.

After winning the Nobel, Evans retired from being a professor at the end of 2007, taking on greater leadership roles at Cardiff University. In 2009, Evans became the president of Cardiff University and later the chancellor of the same university. As chancellor, the university’s most senior position, Evans oversaw Cardiff University’s court and participated in the graduation ceremonies. In 2013, due to Evans’s scientific accomplishments and help with establishing the university’s engagement in biomedical research, Cardiff University renamed the building that houses the School of Bioscience to the Sir Martin Evans Building in his honor. In 2017, Evans stepped down from being chancellor but remained a part of the university as an emeritus professor.

Legacy and Impact

Over the span of Evans’s scientific career, he contributed to the advancement of embryology, genetics, and medical research due to his isolation and culturing of embryonic stem cells. That work led to the development of a mutated mouse model organism possessing genetic alterations, which became known as a knockout mouse. Scientists have since used knockout mice to study the reproduction, function, and pathology of genetically induced diseases, providing different applications in fields such as cancer biology and embryology. For example, scientists used knockout mice to help determine the function of the p53 gene, the mutated version of which has been associated with more than half of all human cancers. Through their use of knockout mice, researchers determined that the function of non-mutated p53 is to prevent the development of tumors.

For his contributions to developmental biology and biomedical research, Evans has received numerous recognitions and awards. In 1990, Evans became a member of the European Molecular Biology Organization. In 1993, the Cambridge Philosophical Society awarded him the William Bate Hardy Prize. That same year, he was elected a fellow of the Royal Society. In 1998, Evans became a founding fellow of the Academy of Medical Sciences, an organization based in the United Kingdom. In 1999, he received the March of Dimes Prize, a prize awarded to researchers who contribute profound advancements to the understanding of prenatal development, birth, and pregnancy. In 2001, he received the Lasker Award. In 2004, Evans was knighted for the contributions he made to medical research. In 2007, he received the Nobel Prize in Physiology or Medicine. In 2009, he received the Gold Medal of the Royal Society of Medicine, the Baly Medal from the Royal College of Physicians, and the Copley Medal from the Royal Society, which is the Royal Society’s oldest award.

As of 2025, Evans is eighty-four years old and resides in Cardiff with his wife.

Sources

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