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HMB265H1 (300)
Lecture

Notes taken in class


Department
Human Biology
Course Code
HMB265H1
Professor
Stephen Wright

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LECTURE April 4th, 2011
20-25% based on first semester material; rest based on second semester material
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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 if plate normal cells
Contact inhibition
oTumour cells different dont 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 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 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 corrected by repair enzymes genome replicated
faithfully
oIn cancer cells, mismatches not corrected genome not corrected
faithfully mutations accumulate tumourgenic
Potential for immortality
Most normal cell types do not divide indefinitely 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 cancer cells
In normal cells, patterning is consistent
Present I specific region and do not move 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 blood vessels set number 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 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 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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