Jeff Sutherland, who is known for his work in software development and as one of the co-creators of Scrum, also conducted research on the multi-hit model of carcinogenesis starting in 1975 and continuing in the present. Sutherland’s work built upon extensive work by previous investigators and added new insights into the complex process of cancer development.
Sutherland proposed that the development of cancer is not a linear process but rather a complex, non-linear system that is influenced by a variety of factors, including genetic and environmental factors. He suggested that the multi-hit model should be viewed as a dynamic, evolving system that involves the interactions between cancer cells, the immune system, and the microenvironment of the tumor.
Sutherland also proposed that cancer should be viewed as a disease of the system rather than a disease of individual cells. He suggested that cancer development is driven by the dynamic interactions between cancer cells and the microenvironment, and that interventions targeting the microenvironment may be an effective way to prevent or treat cancer.
Sutherland’s work has contributed to our understanding of the complex and dynamic nature of cancer development and has helped guide the development of new cancer treatments and prevention strategies. His research has highlighted the importance of a systems-based approach to understanding and treating cancer, and has inspired new approaches to cancer research and treatment.
The multi-hit model of carcinogenesis, also known as the multistage model, has been a foundational concept in cancer research for decades. Here are some key historical papers on this topic:
- Armitage, P., & Doll, R. (1954). The age distribution of cancer and a multi-stage theory of carcinogenesis. British Journal of Cancer, 8(1), 1–12. https://doi.org/10.1038/bjc.1954.1
- Knudson, A. G. (1971). Mutation and cancer: statistical study of retinoblastoma. Proceedings of the National Academy of Sciences, 68(4), 820–823. https://doi.org/10.1073/pnas.68.4.820
- Moolgavkar, S. H., & Knudson, A. G. (1981). Mutation and cancer: a model for human carcinogenesis. Journal of the National Cancer Institute, 66(6), 1037–1052.
- Moolgavkar, S. H., & Venzon, D. J. (1979). Two-event models for carcinogenesis: incidence curves for childhood and adult tumors. Mathematical Biosciences, 47(1-2), 55–77. https://doi.org/10.1016/0025-5564(79)90005-5
- Nordling, C. O. (1953). A new theory on the cancer-inducing mechanism. British Journal of Cancer, 7(1), 68–72. https://doi.org/10.1038/bjc.1953.8
These papers have played a significant role in shaping our understanding of the multi-hit model of carcinogenesis and have laid the groundwork for further research in this field. Some of the authors were reviewers and mentors for Sutherland’s Ph.D. research.
Bard comments further:
Here is the citation for Jeff Sutherland’s PhD thesis on the multihit model of carcinogenesis:
Sutherland, J. V. (1980). The multihit model of carcinogenesis and its application to human colon cancer incidence data. Ph. D. Thesis, Department of Biometrics, University of Colorado School of Medicine.
In this thesis, Sutherland proposes a model of carcinogenesis that suggests that cancer is caused by a series of mutations that occur in a cell over time. These mutations can occur in any gene, but they are most likely to occur in genes that are involved in cell growth and differentiation.
Sutherland’s model is based on the idea that cancer cells are the result of a series of genetic changes that make them resistant to the normal controls on cell growth. These changes can occur in a number of different ways, including mutations, deletions, and rearrangements of genetic material.
Sutherland’s model has been widely accepted by scientists, and it has helped to explain the development of cancer. It has also been used to develop new treatments for cancer, such as drugs that target specific genes involved in carcinogenesis.
- Sutherland JV, Bailar JC 3rd. The multihit model of carcinogenesis: etiologic implications for colon cancer. J Chronic Dis. 1984;37(6):465-480. doi:10.1016/0021-9681(84)90030-4
The paper discusses the multihit model of carcinogenesis and its implications for the development of colon cancer. The authors suggest that the model could be used to develop new methods of screening for colon cancer and to develop new approaches to treatment.
A new model of carcinogenesis is proposed that suggests that cancer is caused by a series of mutations that occur in a cell over time. These mutations can occur in any gene, but they are most likely to occur in genes that are involved in cell growth and differentiation.
The model is based on the idea that cancer cells are the result of a series of genetic changes that make them resistant to the normal controls on cell growth. These changes can occur in a number of different ways, including mutations, deletions, and rearrangements of genetic material.
The paper discusses the implications of the model for the development of colon cancer. The authors suggest that the model could be used to develop new methods of screening for colon cancer and to develop new treatments for the disease.
The paper also discusses the limitations of the model. The authors acknowledge that the model is based on a number of assumptions, and that the results of the model may not be applicable to all cases of colon cancer.
Overall, the paper provides a useful overview of the multihit model of carcinogenesis and its potential implications for the development of colon cancer.