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Lecture

Lecture 23- Genetics of Cancer

4 Pages
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Department
Human Biology
Course Code
HMB265H1
Professor
Stephen Wright

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HMB265H1S- Lecture 23- Genetics of Cancer April 5th, 2011
How cancer cells differ from normal cells
Cancer results from mutations from different types of genes; cells grow out of
control- failures in mechanisms that control cell proliferation, cell death, cell growth
Changes in cancer cells:
ouncontrolled growth;
insensitive to signals or produce own signals for stimulation therefore
proliferate more rapidly, therefore produce cancer
Lack of contact inhibition-normal cells form one cell layer only in petri
dish- contact inhibition
Tumour cells dont listen or receive or receive signals from
neighbouring cells- cells keep piling up- much different from the
pattern of normal cells
Insensibility to cell death cues; mutagens- cell cannot be correct
therefore dies- programmed cell death b/c dont want them to
proliferate
Tumour cells insensitive to cell death cues- proliferation of damaged
cells
Lack of gap junctions in tumour cells- cells cannot communicate
oGenomic instability- in normal cell, can be corrected (mismatches); in cancer
cells, not corrected- cancer cells arise
oPotential for immortality- normal cells only divide set amount of times; many
cancer cells keep dividing- immortal; cancer cells have ability to disrupt
normal tissues
oTumour cells start moving; leads to disruption and invasion of normal
tissues- circulation through blood vessels- metastasis
Blood vessels- in adult, stop forming; tumour cells secrete certain
substances, draw blood vessels towards them; use them as roots for
metastasis and/or nutrients
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Description
th HMB265H1S- Lecture 23- Genetics of Cancer April 5 , 2011 How cancer cells differ from normal cells Cancer results from mutations from different types of genes; cells grow out of control- failures in mechanisms that control cell proliferation, cell death, cell growth Changes in cancer cells: o uncontrolled growth; insensitive to signals or produce own signals for stimulation therefore proliferate more rapidly, therefore produce cancer Lack of contact inhibition-normal cells form one cell layer only in petri dish- contact inhibition Tumour cells dont listen or receive or receive signals from neighbouring cells- cells keep piling up- much different from the pattern of normal cells Insensibility to cell death cues; mutagens- cell cannot be correct therefore dies- programmed cell death bc dont want them to proliferate Tumour cells insensitive to cell death cues- proliferation of damaged cells Lack of gap junctions in tumour cells- cells cannot communicate o Genomic instability- in normal cell, can be corrected (mismatches); in cancer cells, not corrected- cancer cells arise o Potential for immortality- normal cells only divide set amount of times; many cancer cells keep dividing- immortal; cancer cells have ability to disrupt normal tissues o Tumour cells start moving; leads to disruption and invasion of normal tissues- circulation through blood vessels- metastasis Blood vessels- in adult, stop forming; tumour cells secrete certain substances, draw blood vessels towards them; use them as roots for metastasis andor nutrients www.notesolution.com
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