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Targets of Genetic Damage
3 classes of normal regulatory genes:
Oncogenes: growth promoting
Anti-oncogenes (tumour supressing genes): growth suppressing P53 - commonest target for genetic alteration in human cancer
Apoptosis-regulating genes: pre-programmed cell death
Karyotypic Changes
1. Balanced translocations - Philadelphia chromosome in CML
2. Deletions - Solid tumors - retinoblastoma
3. Gene amplification - Breast cancer –; c-erb2
4. Loss or gain of whole chromosomes
Carcinogenesis is a multi-step process at both phenotypic and genotypic levels
latent period before become clinically detectable usually YEARS
mass of 1 cm = 1 billion cells, we can detect disease at 3-5 mm but still represents millions of cells
by the time a solid tumor is clinically detected, it has already completed a major portion of its life cycle
once clinically detectable average doubling time 2-3 months (range < 1 month (childhood cancers) to years (salivary gland tumours)
without vascularization tumour nodules cannot grow larger than 1-2 mm
vascularization needed for: oxygen, nutrients
correlation between angiogenesis and metastatic potential
