less life-threatening (but disrupt functioning of vital organs)
localised effects
removed by surgery
rarely reoccur after treatment
MALIGNANT
grow large
rapid
larger and darker nucleus
unspecialised cells
metastasis (no adhesion molecules)
no capsule (finger-like projections into tissues)
life-threatening as normal tissue is replaced with abnormal
systemic effects
radiotherapy/ chemotherapy and surgery
reoccur after treatment
WHAT ARE THE TWO GENES THAT PLAY A ROLE IN CANCER?
oncogenes and tumour suppressor genes
ONCOGENES?
mutations of proto-oncogenes (stimulatecell to divide when growth factors attach to protein receptor on cell-surface membrane, activates genes causing DNA replication)
an oncogene is permanently activated because...
receptor protein is permanently activated so cell division is switched on even without a growth factor
oncogene may code for a growth factor so produced in excessive amounts
most mutations are acquired with only a few being inherited
TUMOUR SUPPRESSOR GENES?
slow downcell division, repair mistakes in DNA and controlapoptosis (programmed cell death)
if mutated it is inactivated
stops inhibiting cell division
e.g. TP53, BRCA1, BRCA2
most mutations are acquired with only a few being inherited
ABNORMAL METHYLATION OF GENES?
HYPERMETHYLATION OF TUMOUR SUPPRESSOR GENES
increased methylation
in promoter region
inactivates gene
inhibits transcription of promoter region
gene silenced
increased cell division
e.g. in BRCA1
HYPOMETHYLATION OF ONCOGENES
activation
increased cell division
OESTROGEN CONCENTRATION AND CANCER?
regulatesmenstrual cycle
after menopause, risk of breast cancerincreases
fat cells of breasts produce more oestrogen
develops tumour, further increasesoestrogen concentration
WBCs drawn to tumour, further increases oestrogen concentration