cancer is a well-established point (Melo et al. 2013; Bertolaso 2016; Plutynski
2018). First, cancers found in humans are quite diverse. Solid tumors (e.g.,
a carcinoma, a cancer that develops from epithelial cells, which constitutes the
most frequent form of cancer) differ from liquid tumors (e.g., leukemia, a cancer
that develops from bone marrow–derived cells). Cancers also differ from organ
to organ: for example, a breast cancer can be quite unlike a skin cancer (this is
called intertumor heterogeneity) (Melo et al. 2013). Cancers affecting a given
organ, such as the breast for example, can have different characteristics
(Zardavas et al. 2015). Moreover, a cancerous tumor can exhibit a high level
of internal heterogeneity (“intratumoral heterogeneity”)(Fisher et al. 2013).
Last but not least, some tumors are benign, as they do not invade other body
parts. Second, beyond humans, cancers exist in a great number of multicellular
organisms, which further increases the diversity of cancer types and character-
istics. If cancer is defined as a breakdown of multicellular cooperation that
manifests itself by uncontrolled proliferation, inappropriate cell survival,
resource monopolization, deregulated differentiation, and degradation of the
environment, then it is found in many different groups, including starfish, hydra,
insects, and plants (Aktipis et al. 2015).
Despite the diversity and heterogeneity of cancers, the immune system has
been shown to be implicated in cancer progression in a large range of cancer
types in various vertebrates (and also, if perhaps more speculatively given the
limited number of studies, in invertebrates (Pastor-Pareja et al. 2008; Robert
2010)). Because of the publicity around cancer immunotherapies, most people
are now aware that the immune system plays a role in cancer. Yet much remains
to be done to understand the detailed mechanisms underlying this process.
Study of the interactions between cancer and the immune system has undergone
major transformations in the last two decades. To understand why the immune
system can participate in the rupture of cohesion that characterizes cancer, it is
essential to understand the nature of these recent transformations.
The history of the study of how the immune system influences cancer
progression is itself illuminating. In the 1890s William Coley (Coley 1893)
took advantage of the observation that spontaneous tumor regression could
follow infection with a pathogen to develop a killed bacterial vaccine for cancer,
a phenomenon in which immune components were thought to play a role (Cann
et al. 2003). At the beginning of the twentieth century, Paul Ehrlich suggested
that the immune system could recognize and eliminate malignant cells (Ehrlich
1909). In the mid-1950s, Lewis Thomas (at a symposium held in 1957, and
published two years later (Thomas 1959)) and Macfarlane Burnet (Burnet 1957)
argued that cellular immunity was, in the words of Thomas,“designed as
a useful and effective mechanism for the early sensing and early elimination
Philosophy of Immunology 31