This is not a hallmark as such, but rather an 'enabling feature'
The ability of malignant cells to develop a wide array of mutations in multiple oncogenes and tumour suppressor genes suggests a much higher rate of mutation than is seen in normal cells. Malignant cells have been shown to downregulate the normal cellular mechanisms that detect and prevent mutation, allowing them to accelerate the rate of mutation acquisition.
This helps to explain the ability of tumours to adapt to therapies such as chemotherapy or radiotherapy through a process of natural selection - the cells with the ability to mutate (or with mutations that have already been acquired) their genome to avoid destruction are those which survive and reproliferate the tumour.
Patients with congential mutations in tumour suppressor genes (e.g. TP53) have much higher rates of malignancy. Once the other, normal gene is mutated, cells are able to acquire mutations much more rapidly.
Links
-
Old R04: Advanced Cell Biology
- R4.1: Major Cell Cycle Regulators
- R4.2: Signal Transduction
- R4.3: Molecular Response to Ionising Radiation
- R4.4: Tumour Kinetics
-
R4.5: Hallmarks of Cancer
- R4.5a: Self Sufficiency In Growth Signals
- R4.5b: Insensitivity To Growth Inhibition
- R4.5c: Resisting Cell Death
- R4.5d: Immortality
- R4.5e: Angiogenesis
- R4.5f: Invasion and Metastasis
- R4.5g: Deregulation of Cellular Energetics
- R4.5h: Immune Avoidance
- R4.5i: Genomic Instability
- R4.5j: Tumour Promoting Inflammation
- R4.6: In Vitro Features Of Transformed Cells
- R4.7: Mouse Models Of Tumour Initiation And Promotion