A Systems Theory of Small-Cell Lung Cancer

摘要

At some critical threshold value of cigarette comsumption between 20 and 40 per day, we can see a transition from a simple probability of tumor development to a non-zero tumor cell population. In the 20 cigarettes per day run, we are left with a greater risk of developing cancer -it transitions from the 3.95e-29 that comes with normal aging given our model to 2.50e-26, a value indicating a cancer risk more than 1000 times higher in the given tissue.In the consumption value range that develops a growing tumor, we find that the cancer population grows exponentially at first expanding into any available free blood supply capacity and by replacing peripheral cells (specifically differentiated cells) that have a shorter lifespan and therefore lower population expansion rate. Once the replacement processes and the equilibration of populations based on birth and death rates is done, the tumor population grows linearly as the blood supply finishes expanding at the maximum allowed rate. All of this behaviour is in line with what little is known about the initial growth phases of a primary tumor - that it will expand based on it's indicated population growth rate (difference between division and death rates) until it reaches the resource limit for the tissue, and that it will then grow based on it's angiogenic ability and the local tissue angiogenic rate maxima until it reaches the maximum blood supply capacity for the locality. Further growth is dependent on ability to grow and invade into the surrounding periphery.The tumor population is growing even as it's starving and though initially cells are drifting towards compensating for the nicotine and toxic waste clearance load by increasing blood supply, the development of even one tumor cell soon leads to explosive tumor growth irrelevant of the metabolic checks on its growth. This process of growing in toxic surroundings also gives the tumor cells a competitive edge in replacing the differentiated cells surrounding them.