Nonetheless in present day cancer research there is a marked
Nonetheless, in present-day cancer research there is a marked tendency to overlook the role of the immune system.
The increase in cancer incidence with age indicates that cancer is the result of a multistep accumulation of cellular changes; if caused by one-step changes, cancer would occur with same likelihood at any moment in life.
However, if (as is likely) the immune system becomes less effective with age, then a mutation occurring in old age will have a greater impact. As a matter of fact, there are many infectious diseases whose likelihood also increases with age.
One of the main goals of the present paper is to estimate the capacity of the immune system to identify and eliminate cancer cells. It will be seen that the comparison with TB will guide us in this task.
1.2. Possible role of stem cell mutations in TB
It has been recognized for more than a century that some organs (and the corresponding tissue types) give rise to cancers much more frequently than others. Mutations can occur at three levels: (i) genes (ii) stem ATPγS tetralithium salt (in diverse degrees of differentiation) (iii) Differentiated cells in specific organs, an assumption in line with the classical somatic mutation ‘‘theory’’ of cancer.
Thanks to the work of Miguel Lopez-Lazaro (see ) we know that gene mutations play only a small role in explaining differential cancer risk across organs.
In recent years there has been renewed interest in this question in relation with a better understanding of mutations arising during DNA replication in stem cells. In a pioneering work Cristian Tomasetti and Bert Vogelstein (, Fig. 1) showed that the likelihood of cancer across organs is compatible with the number of stem cell divisions which is itself a proxy for the number of mutations. This explanation is also supported by the great variability in degrees of differentiation observed in high malignancy cancer cells .
The parallel between tuberculosis and cancer developed in the present paper includes the responses of organs respectively to the two diseases. As, at first sight, the role of mutations seems less obvious for TB than it is for cancer, such correlations would tend to emphasize organ-specific idiosyncrasies of the immune system rather than the role of mutations. The bulk of this paper was written without having in mind the stem cell mechanism. In order to make our observation consistent with this mechanism, a natural conjecture is that predisposition to TB is also somehow connected with the number of stem cell mutations. This conjecture would extend the role of this mechanism beyond cancer per se.
What in the title is meant by the expression ‘‘a physicist view’’ is that our investigation relies on reasoning by comparison and analogy. Nowadays, researchers seem reluctant to use this approach, perhaps because it is not found sufficiently ‘‘scientific’’. However, as shown in the Appendix, it appears that historically this form of exploration has played a key-role in the development of physics. Although analogies alone cannot solve a problem, they can suggest conjectures which may turn out to be essential steps.
Moreover, the concepts that we introduce, e.g. learning curve, endogenous versus exogenous intruders, comparison to animal species, are certainly uncommon in papers written by biologists.
1.4. Sharp contrast in death rate changes
In the early 20th century in Europe and the United States tuberculosis (TB) was the first cause of death. Cancer came only in fourth position after cardiovascular and cerebrovascular diseases. In 1900 in the United the death rate of TB (all forms) was 194 per 1000 whereas for cancer it was only 64 per 1000. Nowadays, although remaining a substantial cause of death in old age, tuberculosis has been virtually eliminated in young and middle-aged patients. In contrast, despite intensive research, progress in cancer treatment was very limited.2