Bio 256 Exam 2 Flashcards
Epiidemiology
Study of frequency of distribution of disease in human populations
Random Fluctuation and what is its connection to p values and the chi square test
need to have a large sample size to rule this out
p values and chi square test
the difference between what was observed and what expected was actually due to a real difference not random
Confounding variables
a factor that affects the rink of developing cancer and is linked in some way to the factor being investigated
ie. age or smoking
Detection bias
failure to use consistent and equivalent procedures to measure incidence rates
Publication bias
journals don’t punich the absence of relationships or lack of cause-effect. So we don’t see that data
Experimenter bias
the scientist isn’t remaining objective
ie. viewing data thru rose tinted glasses
Selection bias
nonrandom volunteers
Retrospective Studies
what is it and whats its other name
Assess past exposure of people already with cancer
aka: “case-control studies”
Prospective Studies
and its other name
Follow people into the future to see who develops cancer
aka: cohort studies
a “disease free cohort” following them to see what reasons they might develop cancer
- need a large sample size
- some people will refuse to participate after a while
recall bias
and what studies are susceptible to this
people may not remember what happened to them
retrospective studies are susceptible to this bias
post hoc fallacy
conflating correlation with causation
How to demonstrate cause and effect
Show statistical significance
Demonstrate dose-response relationship
Demonstrate magnitude (it has to at least double the rate of cancer)
Randomized trials
why is it a problem on humans. who is it used on?
not ethical in humans it will kill them
is for animals because rats cant feel lol
Ames test
effective way of finding cause and effect
rapid screening test of possible chemical carcinogens
Main risk for human cancer
Age
Environmental and lifestyle (diet smoking eating)
alcohol
food choices
pesticides in our daily foods
synthetic and natural alike
red meats saturated fats
radiation exposure
oncogenic virus
viruses that cause cancer
rouse sacarcoma, hpv, epstein barr, hepatitis b and c
3 principles of chemical carciongens
-exposure — delay —– cancer
-dose dependence
-chemical carcinogens have organ specificity
workplace carcinogen
cancer causes agents the work place
asbestos is the big one
asbestos penetrates the lung and lodges in the mesothelial cells
modelsof dose cancer relationship
linear: increase dose - increase rate
threshold: no risk low, linear after threshold met
hormetic: u-shaped, low doeses decrease rate while high doses increase
Polycyclic aromatic hydrocarbons (PAHs)
Mechanism of Chemical Carcinogenesis
fused benzene rings
coal tars, soots, oils when not completely burned
Mechanism of Chemical Carcinogenesis
Aromatic amines
Mechanism of Chemical Carcinogenesis
n-nitroso
Mechanism of Chemical Carcinogenesis
nitrites nitrates
may be converted into carcinogens in stomach
in fruits, an pacakged meat
akylating agents
Mechanism of Chemical Carcinogenesis
add akyl groups to a chemcial
in plastics, making antifreeze
Some carcinogens must be activated by the liver
precarcinogens
Some carcinogens interact directly with DNA
converted in liver to electrophilic molecules
so binds DNA and breaks gydogen bonds
“free radicals”
Three stages of chemical carcinogenesis
(so cancer you get from chemicals)
- initiation
carcinogen is activated
dna damage occurs
precancerous cells made - promotion
selection for cells that divide autonomously
promotors: alchol, asbestos - progression
selection for rapid growth
Epigenetics
cancer cells turn on/off expression of unmutated genes, and change cell behavior
SO there isn’t a mutation of the genes but it is still being expressed wrong or different
Incomplete carcinogen
chemical is either an initiator or a promotor
complete carcinogen
chemical acts as both initiator and promotor
potency
size of dose necessary to cause cancer
reasons:
some are more electrophilic and induse more mutations
Why doesn’t everyone who is exposed to carcinogens develop cancer?
The type of carcinogen:
High potency or low
how long exposed
luck
Types of radiation
Sunlight (UVA and UVB)
Ionizing Radiation such as
X rays, nuclear (radon, polonium, radium)
(short wavelengths are more dangerous)
What percent of newcancers are caused to sunlight exposure
1/2
Sunlight is composed of
electromagnetic radiaton
-infrared - visible - utraviolet (UV)
UVA
longest wave, lowest energy
causes skin ages
UVB
higher energy (most dangerous)
causes sunburn, tanning and cancer
partially absorbed by ozone
UVC
highest energy
absorbed by the ozone
artificial sources cause cancer such as germicidal lamps
p53 and DNA damage
When mutated p54 doesn’t stop the cell cycle and cells continue to proliferate (how quickly a cancer cells copies its dna and divides)
BERT:
Background equivalent radiation time
how long long it takes a person to get an equivalent amount of radiation from natural sources
a mammogram is wort 3 months of background radiation
smoking per year is worth 10 years of background radiation
Nuclear Explosions and massive doeses of ionizing radiation
bombs in japan
Ionizing radiation and free radicals
DNA damage
free radicals form (ions that have extra elections which can destry DNA)
remove base
or break dna
Pathogen:
disease producing agent
4 criteria for proving a pathogen
kochs potsulates
present in deseased tissue
isolated in grown from diseased tissue
grown pathogen can then cause diesease in new tissue
newly isolated pathogen must be identical to original
first oncogenic viruses found
epstein barr (EBV)
oncogenic virus
often are latent
HTVL-1 and HIV
HTVL-1 direct cancer rink (virus directly mutates DNA)
HIV: indirect cancer risk thru weakening immune system
3 types of viruses
DNA
RNA
Retroviruses
All trigger cancer thru
A: indirect (things like weakening immune system)
B: direct (damage DNA)
Episome
Viral DNA that are seperate from the host DNA (independently replicated)
Latent virus
viruses are in the cells but not acting yet not triggering immune ststem
Retroviruses (the unique one)
RNA as genetic material
reverese transcribed
integrase (helps insert RNA)
once inside it is a Provirus
it is unique because it is direct it can alter DNA directly
V-src
is an oncogene
viral copy of onc protein
