Although “cancer” is talked about as if it were a single disease, it is an umbrella concept covering numerous different diseases that share a common biological logic. Frequently heard cancer types such as breast, lung, colon, prostate or thyroid meet in the idea of “uncontrolled multiplication”. Despite this, they can differ markedly in terms of where they start from, how they behave, at what speed they can progress and which biological weak points they carry.<\/p>\n
In this article, we address, within a general framework, the basic common features that cancer types share and why they differ, without distorting the logic behind clinical decisions. The content is for general information purposes and does not replace a medical assessment.<\/p>\n
The most basic common feature of cancer is that the cells partially or completely stretch the rules they should normally comply with. In healthy tissue, cell division is kept in balance through mechanisms such as damage control, immune surveillance and harmony with the surrounding tissue. In cancer, on the other hand, the cell can, with the accumulation of genetic and epigenetic changes, turn this balance in its own favour.<\/p>\n
One dimension of this commonality is the disruption of the control of growth signals. Cancer cells can become more sensitive to growth signals or can produce their own growth signal. This situation is, in some tumours, associated with disruptions occurring in the intracellular communication networks. In clinical practice, an approach such as “the same pathway is disrupted in every patient” is not correct; biomarkers and pathology findings help to understand which mechanism may be more prominent.<\/p>\n
Another common mechanism is the tendency to avoid cell death. A normal cell, when it takes serious damage, prevents bigger problems by destroying itself. A cancer cell, on the other hand, can disable these “brake” systems. In this way, a damaged cell line can over time gain an advantage and continue to multiply.<\/p>\n
As the tumour grows, its need for nutrients and oxygen increases. For this reason, in many cancer types, processes that increase blood vessel formation can come into play. Saying that this occurs “in the same way in every cancer” is not correct; the microenvironment of the tumour, the tissue it is in and its biology affect this picture markedly.<\/p>\n
One of the most critical common headings from a clinical standpoint is the potential for spread to surrounding tissues and metastasis. Saying that every cancer metastasises is not correct. However, in many cancer types, the risk of progression to the surrounding tissue and attachment to distant organs over time can come into consideration. How much this risk is and how it is monitored varies according to the type and subtype of the cancer.<\/p>\n