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Exam 1 Flashcards

1
Q

calculation of Dq

A

quasi threshold dose
a large Dq can more easily cover than a cell with low Dq
the dose at which the straight portion of the cell survival curve extrapolated backward cut the dose axis drawn through a surviving fraction of one

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2
Q

If Do= D1

A

n will equal 0

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3
Q

variations in radiation sensitivities

A

low let RT shows a wide range of sensitivity these differences are reduced when it comes to Hi-Let radiation. This difference is due to the size of the shoulder

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4
Q

Intrinsic cell radio sensitivity

A

increasing Do indicates more resistant cells

cells from tumors have a broad range of radiosensitivities

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5
Q

Cell classifications

A

Vegetative inter-mitotic
differentiating inter mitotic
reverting post mitotic
fixed post mitotic

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6
Q

vegetative inter mitotic

A

produce cells like themselves, go through mitosis regularly

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7
Q

differentiating inter mitotic

A

divide regularly, some differentiation

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8
Q

reverting post mitotic

A

dont divide regularly, but can if needed

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9
Q

fixed post mitotic

A

do not divide, highly differentiated

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10
Q

plating efficiency (PE)

A

percentage of untreated seeded cells that grow into a colony

PE= (number of colonies)/(number of cells plated) x 100

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11
Q

Survival fraction (SF)

A

Fraction of cells surviving a given dose is determined by counting macroscopic colonies and allowing for plating efficiency
SF = (colonies survived from radiation)/ (total cells initially seeded x (PE/100))

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12
Q

High LET cell survival curves

A

Straight on semi-log plot

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13
Q

Low LET cell survival curves

A

have slope, shoulder and subsequent straight region

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14
Q

Linear quadratic relationship

A

S= e^(aD+bD^2)
a= initial slope
b= quadratic component
ratio of a/b is dose at which linear and quadratic components are equal

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15
Q

Cell mitotic death

A

majority of tumor cells have mitotic death as dominant feature, thus follows linear-guadratic model

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16
Q

Apoptic death

A

if apoptosis dominates, cells are radiosensitive if absence radio resistant

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17
Q

Cell death

A

for cells in G0 it is the loss of function

for cells in M it is the loss of capacity to divide

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18
Q

in context of radiobiology

A

if a cell losses its capacity to divide indefinitely and cant produce a colony it is considered dead

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19
Q

types of cell deaths

A

apoptosis
mitotic death
autophagy
senescence

cause cell to lose ability to proliferate indefinitely

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20
Q

apoptotic death (programmed cell death

A

radiosensitive
lymphoid cells
majority of cells NO apoptosis upon radiation

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21
Q

Mitotic death (passive)

A

most common form of cell death from radiation exposure

death due to damaged chromosomes

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22
Q

how to measure RT induced cell death

A
  1. In Vitro
  2. In Vivo (in situ)
  3. in Vivo ( ex situ or ex vivo)
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23
Q

In Vitro

A

COLOGENIC ASSAY

trypan blue exclusion assay

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24
Q

In Vivo (In Situ)

A

skin (pig skin) intestinal crypt cells, testes kidney tubules

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25
In Vivo (ex situ or ex vivo)
SPLEEN COLONY ASSAY | tumor transplant
26
Cologenic Assay
``` tissue culture techniques- specimen taken from organism chopped into small pieces single cell suspension prepared by use of enzyme trypsin cell plated onto culture dish ```
27
Increasing LET survival curves
increases slope of survival curve results in more linear curve shoulder disappears due to increase of killing by single events
28
Relevant doses
100gy - destroys cell function in non-proliferating systems (nerve, muscle cells) 2gy mean lethal dose for loss of proliferative capacity (blood)
29
features of survival curve
low doses -shoulder intermediate doses- region where survival curve bends and survival shows greater change with increasing dose high dose- region where survival falls rapidly with dose
30
general survival models
multi target model- based on hitting the target linear-quadratic model- dual radiation actions 1- cell killing is proportional to dose 2. cell killing is proportional to square of dose
31
factors regulate therapeutic ratio
1. TUMOR SIZE 2. DOSE RATE EFFECT 3. TIME INTERVAL 4. LET of radiation 5. PResence of radio-sentizers/ protectors 6. Plan design and precision of implementation
32
cell cycle resistant stages
S phase most resistant | G2 and M most sensitive
33
4 r's
1. REPAIR 2. REDISTRIBUTION 3. REPOPULATION 4. REOXYGENATION 5. radiosensitivity
34
operational classification of radiation damage
1. lethal damage 2. potentially lethal damage 3. sublethal damage
35
lethal damage
irreversible, irreparable
36
potentially lethal damage
modified by post irradiation environment conditions
37
sublethal damage
can be repaired under normal circumstances
38
types of dna damage
``` abasic site base damage bulky base damage single strand break double strand break interstrand cross-link ```
39
types of simple repair
chemical repair direct reversal of damage 1. photolyase- revert UV induced pyrimidine dimers by using visible light 2. methyl transferase- removes methyl group from damage base and adds it to itself
40
excision repair
base excision repair nucleotide excision repair mismatch repair
41
base excision repair
DNA glycosylase cuts out damage base- dna polymearse fills the gap. (single nucleotide cut out)
42
nucleotide excision repair
large strand removed and replaced
43
mismatch repair
proofreading of replication endunuclease makes a cut in the newly synthsized strand
44
Repair of DNA strand breaks
A. DNA single strand break repair | B. DNA double strand break repair
45
DNA single strand repair
exonuclease extends the gap- DNA poylmerase fills in the gap- dna ligase seals the strands- part of the base excision repair machinery
46
DNA double strand break repair
1. non-homologous end joining- error prone | 2. homologous recombination repair - error free
47
Lack of DNA repair
mutagenesis chromosome aberrations microsatellite cell death
48
mutagenesis
if DNA damage not repaired before S-phase - DNA polymerase may put in wrong base mutations: silent, frameshift, deletions
49
chromosome aberrations
IR; errors in repair most chemicals: complications during replication of damaged template
50
microsatellite instability
loss of mismatch repair- slippage errors during replication
51
cell death
``` if cell is not able to resolve blocked transcription or blocked replication cell death- premature aging apoptosis autophagy necrosis mitotic catastrophy ```
52
carcinogenesis
initiation-> promotion-> transformation-> progression
53
genes involved in carcinogenesis
proto-oncogenes-> oncogenes tumor suppressor genes (gatekeepers)(p53,Rb) DNA stability genes(caretakers)
54
autophagy
genetically controlled, formation of double membrane casuoles in cytoplasm sequestering mitochondria and ribosomes
55
apoptosis
suicide, genetically controlled, executed by caspases and nucleases, cell shrinkage, dna degradation
56
necrosis
'murder' passively occurring, cell swelling
57
mitotic castastrophy
caused by mis-segregation of chromosomes, often form "micronuclei', 'giant' cells or multinucleate cells, could induce apoptosis
58
spurs
<100eV
59
blob
100-500eV
60
short track
<5000eV
61
branch track
>5000eV
62
direct action of radiation
radiation absorbed directly by the target
63
indirect action of radiation
radiation energy absorb in non-target molecule that then becomes reactive and attacks the target
64
the hydroxyl radical
``` one unpaired electron uncharged very reactive can damage dna if formed close to dna molecule major contributor to indirect IR ```
65
radical scavengers
give up electorns to radicals | can also donate hydrogens to radicals leading to chemical repair

Rad Bio (1 decks)

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