Cancer cells and meiosis Flashcards

1
Q

size of organ depends on total cell mass dependent o

A

total number of cells and their size

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2
Q

processes regulated

A

cell growth, cell division, cell survival

by intracellular programmes and extracellular signal molecules

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3
Q

3 external factors to reach cell from outside - affects progression of cell cycle

A

mitogen
growing factors
survival factors

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4
Q

mitogen function

A

stimulate cell division by triggering waves of G1/S-Cdk activity - relieves intracellular negative control

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5
Q

growing factor

A

stimulate cell growth by promoting protein synthesis and other macromolecules and inhibiting their degradation

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6
Q

survival factors

A

promote cell survival - suppressing the form of programmed cell death(apoptosis)

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7
Q

social control of cell

A

tells how cells act

from outside - extracellular signals

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8
Q

cancer cells

A

cells that no longer respond to social signals

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9
Q

cancer progression

A

evolutionary process driven by gene mutation(providing cell with competitive advantage)

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10
Q

mechanism of mutated cells

A

suppresses mechanism of apoptosis

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11
Q

evolution of cancer

A

initial clone of cancerous cells - additional mutation increase causing generation of diverse sub clones forming cancer cells

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12
Q

Hall marks of cancer cells

A

organising principles of rationalising complexities of neoplastic disease

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13
Q

hall marks includes

A

sustaining proliferative signalling, evading growth suppressors etc

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14
Q

hallmarks genome instability

A

generates genetic diversity that expedites acquisition, inflammation which fosters multiple hallmark functions

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15
Q

features of cancer cells of mutation

A
  • display altered control growth
  • contain and accumulate somatic mutation
  • single mutation - not enough to change normal cells into cancerous cell
    have abnormal to survive stress and DNA damage
  • create own microenvironment(niche) - evolve
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16
Q

feature of cancer cells of control and spread

A
  • can bypass normal proliferation control - independence of mitogens
  • colonise other tissues
  • develop gradually from increasingly aberrant cells
  • altered sugar metabolism
  • genetically unstable
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17
Q

2 genes where mutation stimulates tumour progression

A

oncogene and tumour suppressor gene

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18
Q

oncogene

A

act in dominant manner

gain of function

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19
Q

oncogene function

A

promote cancer - protooncogene - overactive/overproduced

- regulate cell growth, division, survival or differentiation

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20
Q

tumour suppressor gene function

A

normally restrain cell proliferation or tumour - loss of gene increases causing cancer formation

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21
Q

example of oncogene

A

activation via mitogen stimulation

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22
Q

process of activation via mitogen stimulation

A
  • mitogens bind to cell surface receptor = initiate intracellular signalling pathway
  • activation of small GTPas.Ra which activates MAP kinase cascade, increasing expression of numerous intermediate early genes including gene encoding transcription regulatory protein Myc
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23
Q

Myc in example of oncogene

A

increase expression of delayed response gene expression which increases G1-Cdk activity which triggers phosphorylation of Rb family of protein

24
Q

inactivation of Rb proteins

A

freeing gene regulatory protein E2F

activating G1/S gene transcription including genes for G1/S-cyclin and S-cyclin

25
activating G1/S gene transcription
enhances Rb protein phosphorylation = positive feedback loop
26
E2F protein stimulate transcription of their genes after Rb protein phosphorylation
positive feedback loop formed as well
27
tumour suppressor gene
actin submissive manner | loos of function
28
defects that contribute to cancer
signalling pathways cell cycle control apoptosis regulation
29
example of tumour suppressor
p53 - cellular stress sensor
30
p53 function
responds to hyper-proliferation signals, DNA damage, hypoxia, telomere shortening and various stresses
31
mutation of p53
enables cancer cells to survive and proliferate despite stress and DNA damage even with DNA damage the cell cycle will continue = cancer as cell cycle cannot be arrested
32
cell cycle is mis regulated in multiple cancers
change in genes which encodes cell cycle regulator - identified in human cancer cells
33
most cancers have unstable genomes
``` genetic (genomic) instability chromosomal instability (CIN) ```
34
genetic (genomic) instability
abnormal increases in rate at which genes and chromosomes are mutated, rearranged or lost
35
chromosomal instability (CIN)
abnormally high incidence of defects in chromosome number of chromosome structure
36
meiosis
nuclear division leading to generation of haploid cells in gametes many control systems and molecular mechanisms are shared with mitotic division
37
meiosis I
time taken longer than meiosis II especially prophase | homologous chromosome recognise each other and associate
38
meiosis I structure
2 closely aligned duplicate homologs - bivalent
39
meiosis I - synaptonemal complex (SC)
protein complex usually joining to homologs
40
prophase I stages
leptotene, zygotene, pachytene, diplotene
41
leptonene
homologous chromosomes condense partially, pair and genetic recombination begin
42
sygotene
SC start to assemble; synapsis and recombination are taking place
43
pachytene
SC complete and recombination finishes are very tightly linked
44
diplotene
disassembly of SC, condensation and shortening of chromosomes
45
after chiasmata are visible
homologies can segragate
46
SC
each homolog is organised around protein axial core and SC form when these homolog axes are linked by rod shaped transverse filaments
47
axial cores of each homolog
interacts with cohesin complexes that hold the sister chromatids together
48
location of SC
between sister chromatid especially during crossover | uses cohesin
49
homolog synapsis and desynapsis during different stage of prophase
2 sister chromatids coalesce and chromatid loops extend out from common axial core
50
assembly of synaptonemal complex begins
in early zygotene and complete in pachytene | complex disassembles in diplotene
51
SC under electron microscope
from meiotic cell at pachytene in lily flower
52
cross over
chiasmata
53
chiasmata
crossover seen as thin connection between homologs
54
chiasmata in late stage bivalent
single crossover occurs between non sister chromatids | when SC disassembles and separate a little at end of prophase I
55
difference in meiosis I to mitosis
- both sister kinetochores remain attached to same spindle pole - chiasmata keep homologs together which allows bi-orientation - centromeric cohesin on sister chromatid remains bound through anaphase