The crucial pathological features/hallmarks that malignant cells use to growout of control are: sustaining cell proliferation signals; evading cell death; replicative immortality; evading tumour suppressors; inducing or accessing vasculature; and metastasis.
These abnormal capabilities malignant cells use to grow out of control occur by: proliferative signallingbypassingnormallimits for cell proliferation; cells evadingcell death signals; alteredhomeostasis allowing cells to grow & dividefaster than they die; genetic or epigeneticmanipulation of tissue environment to evadeTSG for cell survival; alteredcellular metabolism for vasculatureentry; and cellsescaping from home tissue to proliferate in foreign sites.
Abnormal cell cycle can lead to cells accumulating multiple mutations in TSG & oncogenes by cells proliferating with no 'breaks' or stops. This is because multiple oncogene mutation in one copy of allele is sufficient for gain of function mutation, as these mutations keep promoter proteins (e.g. Ras) in cell cycle active. While multiple TSG mutations in both copies of allele is needed for loss of function mutation, as these mutations prevent suppressor proteins (e.g. Rb) in cell cycle to act as control points.
Abnormalcell cycle control affects cancer development by: abnormal mitogen receptor (i.e. RTK) being constantlyautophosphorylated for constantlyactivedownstream signalling, because mutated RTK would notrequiremitogen/external signalling to activate pathway; and abnormal Ras being constantlyactivated with GTP for constantdownstream signalling, because mutated Ras would notrequiremitogen signalling to activatedownstream effects.
Some current cancer preventionstrategies include: maintaininghealthy body weight; eat healthily; don't smoke; & minimisealcohol.
Some current cancer treatment strategies include: surgery, cuttingcancer out; chemotherapy, drugs to impededcancer growth; & radiotherapy, gamma radiation.
Future possibilities for cancer prevention & treatment include drugs with more selectivity, where it is targetedtowardspreventingcancer cells themselves & nothealthy cells. An example of this is Gleevec drugtargeting the catalytic site of fusion protein BCR-ABL to inhibitpathway activation.