BIOL 201 Lecture 14: Lecture 14 notes

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29 Jul 2016
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Monday, May 30, 2016
Lecture 14: Cancer Genetics
Cancer incidence in Canada
-Cancer is biggest killer in Canada (1/4 Canadians will die from cancer)
-If you make it beyond 14 yrs, you’re not going to have cancer until you’re old
children’s cancer: brain, leukaemia
cancer is a disease of old people (not significant before because people are living
longer now)– making it past 70
-ovarian, pancreatic, prostate – you don’t know you have it until really late
-lung cancer kills more people each year than breast, colon and prostrate cancers
combined; 70% of lung cancers are smoking associated
Cell Cycle and Cancer
-Cell Cycle General Overview:
G0– spend most of the time being in stasis: not really dividing
G1 prep phase– making stuff the cell needs to divide (nucleotides and DNA
polymerase); have 2n DNA
S-phase, DNA synthesis– by the end of the DNA you have a 2 2n complement
G2 prep phase– condense chromosomes and get ready to get to M phase
M-phase– MITOSIS
-If you begin the cell cycle, you cannot stop the cell if it’s
past the “go” point aka restriction point
growth factors make a difference in G1 phase
-growth factors will bind to cell, transduce signal
through the membrane and tell the nucleus it’s
time to divide
-growth factors have to be present before the DNA
damage checkpoint
!1
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Monday, May 30, 2016
-there is a constant growth inhibition signal– ie: when cells touch, don’t divide
-There are DNA Damage Checkpoints
@S-phase– if the DNA is screwed up, the machinery that recognizes mispaired or
damaged DNA will stop things and going further
@G2 phase– if all the chromosomes don’t get condense properly/DNA doesn’t get
properly synthesized (ie: ssDNA all around), cells won’t go through DNA synthesis
-2 questions for those who study cancer
how do cells systematically proceed from one stage to the next?
what are the checkpoints involved in most cancers?
-the regulation of these checkpoints is the reason most cancers happen
-G’ cells enter cell cycle when they sense presence of growth factors + lack of growth
inhibition factors
Cyclins: cofactors that bind to enzymes (kinases)
and leads to massive increase of catalytic activity
have multiple cyclins involved in mitosis– each turns
the other one on: information pathway where
signal gets passed on
-Cdk4-cyclin D, Cdk6-cyclin D —> Cdk2-cyclin E
> Cdk2-cyclin A —> Cdk1-cyclin A, Cdk1-cyclin B
-one doesn’t get activated unless the other is
activated– ie: Cdk1-cyclin A is a target of Cdk2-
cyclin A
-get a unidirectional travel
-Apoptosis
ie: fingers– programmed cell death happening so that we don’t get webbed fingers
you get signals to go through apoptosis
cancer cells have screwed up regulatory processes– problems with preventing
things from going “rogue”
!2
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Monday, May 30, 2016
-proliferative cues typically need certain things in order to proliferate; in cancer
cells, proliferation happens
without needing these things
ie: proliferation cue that
requires a ligand in order to
proliferate ended up
becoming ligand
independent– kept telling
the cell to proliferate
cancer calls can make their
own growth factors and
internal molecules in the
pathway never get shut off =
uncontrolled proliferation
-aberrant survive signals– cell
should be dying but the
mutation is making it go
survive survive survive
Properties of the cancer cell:
-Transformation: Cell transformed to a cancer-like properties (1 or more of the
properties mentioned above)
-Contact Inhibition: when a cell touches its neighbour, it’s a signal to stop dividing
if you get more than 1 cell layer in alveoli, you suffocate
!3
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