Chronic Disease - Cancer Flashcards
what are the most common cancers
breast, lung, prostate, bowel
recent increase in incidence of cancers linked to lifestyle - kidney, liver, skin, oral
what age is cancer most common in
1/3 of cancers are in those aged 75+
incidence of cancer on SES
higher incidence in those living in more deprived areas - especially smoking-related cancers
outline geographical variation of cancer
due to ethnic differences - genetic factors
environmental exposures - infections
lifestyle - diet, smoking, alcohol
demographic factors - age, sex, SES
what is cancer?
clonal disease with ability to metastasize
solid tumours or leukemias
why is cancer screening important
breast, colon, prostate and cervical cancer screening
for public health, detectability, early intervention
what is the risk of cancer at age 14 and 24
14 = 1 in 600
24 = 1 in 300
what are the main cancers in childhood
leukemia/lymphoma
brain
what are the main cancers in men
big groups are lung cancer, prostate and colorectal
does childhood cancer affect more boys or girls
more boys
what % of childhood cancer can be attributed to genetic factors
5%
what are congenital conditions associated with childhood cancer
downs syndrome
neurofibromatosis
fanconis anaemia
what does the greater incidence of childhood cancer suggest
something to do with better detection but there is still an increase, so suggests a change in environment
what is an example for an environmental cause of leukemia
clustering in seascale village and new towns on leukemia and brain tumours
what were aetiological candidates of the seascale environment in causing leukemia
it is located near a nuclear plant so radiation, population mobility, occupation exposures and EMF (power lines)
outline how X rays affect pregnancy
increased risk of leukaemia and solid tumours by 30%
X ray therapy increases risk of malignancy - 4 fold increase
what case control study tried to get to the bottom of the seascale cluster
Gardner et al - paternal preconceptional occupational radiation
107 cases but the case study was flawed - did not select controls well
court case found no sufficient evidence for the association and there was no biological plausibility given the amount of radiation
what was other evidence for paternal exposure in the seascale cluster
consistent findings of increased risk for leukeamias in children of men employed in radiation industry and petrochemical industry
what did the exposure of fathers not explain in seascale?
commuters
evacuees
which all were shown to have high rates of leukemia
special population movements
what was the population mixing hypothesis for the seascale cluster and leukeamia
linekd increased risk with population movement
more incomers = more risk
what was Kinlens hypothesis in regard to population mixing for seascale cluster
when populations mix for first time there is an exchange of infectious agents for which the previously isolated (susceptible) populations do not have herd immunity
results in childhood infection which can manifest as leukeamia
what was Kinlens hypothesis based on and why is this problematic
communities where mixing occurred like new towns, commuter towns and places used for war time evacuation
but ww2 evacuation was based on mortality data not incidence data so not a good measure BUT there was less treatments at the time so maybe mortality was best analyses back then
outline population mixing and childhood leukemia in Cumbria
evidence shows higher rates of childhood leukaemia for children of non-Cumbrian parents, especially in early childhood, age 1-6
demonstrated population mixing could explain the higher rates
what did the study conclude about population mixing in Cumbria
it increases risk of childhood leukaemia by a factor of 2.5 in children of non-Cumbrian parents and accounts for 58% of cases
what did the Cumbria leukaemia study summarise
children of radiation workers have higher rate of leukeamia - 2/3 due to population mixing and 1/3 due to fathers radiation exposure
there is a dose-response relationship not accounted for by population
risk is higher for seascale children but dose response not the same
what was the Greaves hypothesis of infection and childhood leukaemia
it is normal for children to encounter many infections in early first year - but this is for immune protection or dose limitation from mothers antibodies/breast milk
so said it was due to a reduction in breastfeeding
Greaves : in what 3 ways do lifestyles compromise evolutionary adaptation of the immune system?
pregnant mothers not being exposed
reduction in breastfeeding
reduction and delay of infection
what infections did evidence show in solid tumours
space-time clustering of brain tumours
EBV, measles and influenza
but this is not consistent
what are some dietary requirements factors of potentially greater risk to childhood leukaemia
flavonoids - fruits and veg
catechins - tea, cocoa, wine
what does evidence show about alcohol consumption and leukaemia
higher number of drinks in pregnancy conferred greater risk of AML leukaemia
outline herbicides/pesticides as risk for leukaemia
gene-environment interaction
indoor use of insectisides and pesticide use in garden is a risk
mothers with CYP1A1m1 mutation during pregnancy or child exposed -> risk
outline prenatal exposure to EMF causing leukaemia
maternal occupational exposure to extremely low frequency magnetic fields during pregnancy increased risk of leukaemia MODERATELY
highest odds ratio was 1.2-5.0
how could we minimise childhood ALL leukaemia?
encourage protracted breastfeeding
avoid known leukemogens in pregnancy
encourage early social contact - play groups
identify at-risk individuals
