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5 Apr 2011
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LECTURE โ€“ April 4th, 2011
๎€20-25% based on first semester material; rest based on second semester material
AE courses
๎€Register on ROSI; email sent to you to provide more info on filling out priority
ranking forms
oTo match you to courses you really want
GENETICS OF CANCER
๎€Cancer cells diff from normal cells
Cancer
๎€Results from mutations in different types of genes
oIe. in proto-oncogenes
๎€Cells grow out of control, destroying healthy tissue
๎€Failure in mechanisms controlling cell growth, proliferation, and death
oResult from DNA damage from mutations, or types of altered gene
expression
Chjanges found in cancer cells
๎€Promote or produce uncontrolled growth
๎€Normal cell makes decision whether or not to divide based on signals received
from neightbouring cells
oPositive or stimulatory signals to divide
oNegative signals so stop dividing
๎€Cancer cells either insensitive to negative signals or produce own stimulatory
signals
oAutocrine stimulation
๎€Lack of contact inhibition in tumour cells
๎€Normal cells when proliferate, when come in contact with normal cells, stop
dividing
oOne cell layer only โ€“ if plate normal cells
๎€Contact inhibition
oTumour cells different โ€“ donโ€™t receive or listen to signals from
neighbouring cells
๎€Contact inhibition does not occur
๎€Disorganized pattern seen in tumour tissue different from
organized pattern in normal tissue
๎€Another factor producing uncontrolled growth is insensitivity to cell death cues
oIf damaged, if cannot be repaired โ€“ cells undergo programmed cell death
oIf damaged, can still proliferate
๎€So proflierate damaged cells
๎€Lack of gap junctions in tumour cells
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oLittle holes in cellmembrane, allowing for passage of small molecules btw
cells
oSmall molecules necessary for regulating cell growth and proliferation
oGap junctions lost โ€“ cells cannot communicate, leading to uncontrolled
growth and division
๎€Thus 4 examples leading to uncontrolled growth
Leading to genomic instability
๎€Spontaneous mismatch in replication
oIn normal cell โ€“ corrected by repair enzymes โ€“ genome replicated
faithfully
oIn cancer cells, mismatches not corrected โ€“ genome not corrected
faithfully โ€“ mutations accumulate โ€“ tumourgenic
Potential for immortality
๎€Most normal cell types โ€“ do not divide indefinitely โ€“ will divide x times and stop
dividing spontaneously and die
๎€Many cancer cell types are immortal
oKeep dividing
oTumour and cancer cells have potential for immortality
Have ability to disrupt local tissues โ€“ cancer cells
๎€In normal cells, patterning is consistent
๎€Present I specific region and do not move โ€“ stable
๎€In cancer cells, start moving
oMovement leads to disruption and invasion of distant tissues
oAka metasthesis
oCan be circulated through blood and invade different tissues
Blood vessels
๎€Normally in adult human โ€“ blood vessels โ€“ set number โ€“ unless wound healing,
new vessels will nto form
๎€Tumour cells secrete substances that draw vessels towards them
oBlood vessels can now be used as routes for metasthesis
oAnd as sources for nutrients โ€“ so can grow and keep dividing
How do tumours form?
๎€Multi-hit model developed 40 years ago
๎€Model says that formation of cancer arises by successive mutation in clonal
๎€One clonal descendents receive mutation โ€“ a hit
oAnd as descendents progressively divide and divide
oSuccessive mutations will be accumulated in clonal descendents
oProgressive mutation will lead to malignant cells
๎€Normally occurs in somatic cells
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Document Summary

20-25% based on first semester material; rest based on second semester material. register on rosi; email sent to you to provide more info on filling out priority ranking forms: to match you to courses you really want. results from mutations in different types of genes: ie. in proto-oncogenes. cells grow out of control, destroying healthy tissue. Failure in mechanisms controlling cell growth, proliferation, and death: result from dna damage from mutations, or types of altered gene expression. normal cell makes decision whether or not to divide based on signals received from neightbouring cells: positive or stimulatory signals to divide, negative signals so stop dividing. cancer cells either insensitive to negative signals or produce own stimulatory signals: autocrine stimulation. normal cells when proliferate, when come in contact with normal cells, stop dividing: one cell layer only if plate normal cells. contact inhibition: tumour cells different don"t receive or listen to signals from neighbouring cells.

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