Benign and malignant tumours
Not all tumours are cancer. Tumours are tissue growths beyond the required tissue growth for healthy functioning. Benign tumours are local and cannot spread. Mostly they pose no direct health risk, and only require medical interventions such as surgery if they interfere with organ, nerve or blood vessel function by their presence (i.e. increasing local pressure).
The ability of tumour cells to spread beyond the local tumour is called metastasis and defines malignant tumours which are the basis of cancer. This is also the primary source of death related to tumours.
Benign growths keep to themselves and cannot spread through the blood system or lymphatic system. Cancer on the other hand poses a big risk to unrelated areas of the body by carrying cancer cells via the bloodstream. Therefore, a local cancer in the breast tissue can extend to the bones or liver.
The differences between benign and malignant tumours, respectively, in their appearance and behaviour include:
-slower growth versus faster growth
-capsule versus lack of capsule
-lack of necrosis versus necrosis
-lack of vessel invasion versus vessel invasion
Cancer is primarily an environmental/lifestyle disease, with a minority of cancer types being inheritable or caused genetically. However, the effects of the environment upon cells results in clear pathways of genetic changes such as mutation as well as epigenetic changes such as methylation.
There are multiple separate events that lead to cancer. Often they interact with and exacerbate one another. Oncogenes and tumour suppressor genes are key players that regulate the cell cycle.
Oncogenes promote cell growth and division, while tumour suppressor genes suppress cell division and survival. Combinations of events involving these can lead to cancer.
Oncogenes can be duplicated, or existing oncogenes can be expressed too much. Tumour suppressor genes can be inactivated. These epigenetic events can be controlled via simple methylation.
A series of cell regulation failures ends up in malignant tumours.
Sometimes, the effects are not caused by genetic expression directly. Sex hormones have been shown to be involved in the development of some types of cancer such as breast and prostate cancer, because they promote cell division. In women whose mothers got certain breast cancers, but did not have the increased susceptibility variants BRCA1 and BRCA2, higher levels of oestrogen and progesterone were found.
Knowledge of these different gene regulation pathways leading to cancer can help in finding treatments.