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Paul Nass, British biochemist. He was awarded the Nobel Prize in Physiology or Medicine in 2001, along with Lilan Hartwell and Tim Hunt, for discovering key regulatory factors in the cell cycle. From 2010 to 2015, he served as the President of the Royal Society's National Academy of Sciences, including world-class scientists such as Hawking. In March 2017, Sir Paul began serving as the Chancellor of the University of Bristol, a top university in the UK, awarding degrees to students who graduate each year. In order to welcome Sir Paul's appointment, Buda raised a huge NASA lunar model in the Welsh Hall of the school. In January 1949, Nass was born into a working class family in England. His father was a mechanic and his mother was a cleaner. There were hardly any books at home, but at the age of 8, when he saw Soviet Sputnik 2 flying over London, he became obsessed with science. After graduating from high school, he was rejected by the university due to failing the French exam. Fortunately, a professor persuaded him to make an exception and enter the university. In 1970, Nass obtained a Bachelor's degree in Biochemistry from the University of Birmingham in the United Kingdom, and later transferred to research in yeast genetics and cell biology. In 1973, he obtained a doctoral degree from the University of East Anglia. He worked at the London laboratory of the Imperial Cancer Research Foundation and the University of Oxford, and his research team discovered the cyclic dependent kinase CDK that controls yeast cell division, indicating that humans have the same gene corresponding to this enzyme. The Karolinska School of Medicine commented that the findings of Hartwell, Nass, and Hunter have significant implications for studying cell development, especially for exploring new ways to treat cancer, as defects in cell cycle control can lead to chromosomal mutations in carcinogenic cells. This work allowed Nass and two other scientists to share the 2001 Nobel Prize in Physiology or Medicine. The research results of Paul and others will benefit most biomedical research fields. It will help to understand the instability of chromosomes in tumor cells, that is, how chromosomes or parts of chromosomes are rearranged, lost, or unevenly allocated to offspring cells. This change in chromosomes is likely caused by defects in the cell cycle regulation process. Previous research has shown that CDK molecules and cyclin genes are functionally equivalent to oncogenes that can cause tumors. Moreover, in cell cycle regulation, CDK molecules and cyclins can also act in opposition to tumor suppressor genes and oncogenes. They can inhibit excessive cell proliferation and prevent tumor formation, hence the synergistic effect of tumor suppressor gene products such as p53 and RB. These achievements in the field of cell cycle research will undoubtedly be applied to tumor diagnosis. In human tumors such as breast cancer and brain tumor, the level of CDK molecule and cyclin will sometimes increase. In the long run, this will also open up new avenues for cancer treatment, as people can design drugs that control cell growth and division based on cell cycle regulators to prevent the proliferation of cancer cells. Clinical trials using CDK molecular inhibitors for tumor treatment are currently underway.

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