Chris Marshall (1949–2015)

Chris Marshall Chris Marshall, who died on August 8 at age 66, was a world-renowned cell biologist best known for his pioneering contributions to oncogene research and to cell signaling via GTPases, especially to our understanding of tumor cell signaling through the Ras-Raf-Mek-Erk pathway. He spent the whole of his independent research career at the Chester Beatty Laboratories of the Institute of Cancer Research (ICR) in London, where he was Professor of Cell Biology and Head of the Division of Cancer Biology. Not long after his arrival at ICR in 1980, he established a close and superbly successful research partnership with Alan Hall, who predeceased him by three months (Cell 161, pp. 1239–1240, 2015). It is poignant that Chris, who spoke so eloquently at Alan’s funeral, was to follow so soon and that he succumbed to colon cancer, one of the tumors that most frequently carries RAS mutations. The international cancer research community keenly feels the dual loss of Chris and Alan. Christopher John Marshall was born in Birmingham on January 19, 1949 to James and Lillian Marshall and later lived in Coventry, where he attended King Henry VIII School. His father was a works manager for Massey-Ferguson, the tractor manufacturers, and there was not a strong science tradition in his family. He won a scholarship to Churchill College, Cambridge to study natural sciences, specializing in genetics. As a graduate student, he joined Henry Harris’s laboratory at the Sir William Dunn School of Pathology in Oxford, where he gained his DPhil in 1973. His doctoral studies concerned somatic cell genetics of hybrids between human and murine cells after Harris and Watkins developed an efficient method of cell fusion using inactivated Sendai virus. He used species-specific chromosome banding to examine chromosome segregation and studied the control of expression of ribosomal RNA in heterokaryons. His experience of somatic cell genetics served him well when he joined Sammy Franks’ experimental pathology laboratory at the Imperial Cancer Research Fund Laboratories (now part of the Francis Crick Institute) and became interested in suppression of the malignant phenotype in normal-tumor cell hybrids and in markers of neoplastic transformation in human carcinomas. He continued this interest in tumor suppression during a second post-doctoral position with Ruth Sager at the Dana-Farber Cancer Center at Harvard Medical School. Chris Marshall’s illustrious career took off in 1980, when he joined the ICR to establish his own team. With the grant that he won from the Cancer Research Campaign, now part of Cancer Research UK (CRUK), he planned to continue studies of tumor suppression, which was still a nascent field. However, he soon joined forces with Alan Hall in Robin Weiss’s laboratory to study oncogenes instead. Alan introduced the relatively new recombinant DNA techniques to the ICR, and the two of them embarked on a project searching for human oncogenes by DNA transfection into murine NIH 3T3 cells. This technique had recently been shown to work for murine tumors, and it was the natural next step to apply it to human tumors. Marshall and Hall tried DNA transfer from many human neoplastic cell lines without success and were on the point of abandoning the project when they obtained transformed cells using DNA from two human sarcoma cell lines. They successfully cloned the human gene responsible for cell transformation to reveal a novelmember of theRASoncogene family,NRAS.HRAS andKRASwere originally identified as retroviral onco-