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CBIO02: Cell Signalling in Cancer and Apoptosis Test| Qs & As Latest Update (100% Solution)
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CBIO02: Cell Signalling in Cancer and Apoptosis Test| Qs & As Latest Update (100% Solution)
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CBIO02: Cell Signalling in Cancer andApoptosis Test| Qs & As Latest Update (100%
Solution)
Which processes are cancer cells' genetic changes ultimately linked to? - ✔✔Cancer cells'
genetic changes are ultimately linked to TUMORIGENESIS + CANCER PROGRESSION.
What 4 things can oncogenic mutations potentially cause? - ✔✔Oncogenic mutations can cause...
- SUPPRESSION of negative
regulators. (e.g., tumour suppressors)
- OVEREXPRESSION of affected genes.
- Abnormal proteins w/ ABNORMAL ACTIVITY, by point mutations or chromosomal rearrangement.
- Effects on OTHER LINKED PATHWAYS.
p53
(does it promote or suppress tumour formation? which key cellular mechanism is it involved in? what
is its effect on cytoplasmic signalling?) - ✔✔*tumour suppressor*, commonly mutated gene in
cancer.
- one of the most important *apoptosis-triggering proteins*.
IDENTIFIES IRREPARABLE DNA DAMAGE + signals cell to UNDERGO APOPTOSIS.
,(if lost/defective, cell may not undergo apoptosis + original defect replicated, increasing risk of
further DNA errors)
- can also serve as NEGATIVE REGULATOR of cytoplasmic signalling.
How can gene mutations affect RTKs in cancer? (3 ways) - ✔✔In cancer, RTK gene mutations
can cause...
- RTK activation + clustering despite absence of growth factor/ligand.
- activating mutations in kinase, extracellular, transmembrane + juxtamembrane domains.
- fusion of RTK genes w/ genes making proteins w/ oligomerisation domain.
(i.e., forming oncogenic fusion proteins w/ permanently active kinase)
protein tyrosine phosphatases (PTPases)
(what is their function? how do they relate to RTKs?) - ✔✔highly active enzymes
*dephosphorylating RTK's phosphorylated tyrosines*, CONTROLLING RTK ACTIVITY.
juxtamembrane domain
(where in the RTK is this found?) - ✔✔intracellular region of RTK, *adjacent to
transmembrane domain*, which is *NOT* PART OF KINASE DOMAIN.
Sos
(what role does it have? which signalling pathways, with which receptors, is it involved in?) -
✔✔a *guanine nucleotide exchange factor (GEF)* bound to Grb2 via two SH3 domains.
, REMOVES GDP FROM RAS, allowing GTP to spontaneously bind + activate Ras.
- involved in signalling pathways initiated by RTK activation.
GTPase-activating proteins (GAPs) - ✔✔proteins ENHANCING GTP HYDROLYSIS W/
GTPASES, shortening the time in which Ras is active.
MAP kinase cascade
(triggered by which receptor family + which growth factors? how many kinases involved in cascade?
how is the initial signal amplified? what is the overall result?) - ✔✔(mitogen-activated protein kinase
cascade) one of most common intracellular signalling pathways *triggered by RTKs*, with *many
different growth factors* signalling via this cascade.
involves THREE SERINE-THREONINE KINASES.
- each of them *phosphorylate the other* to activate them (first kinase = MAPKKK, second kinase
= MAPKK, third kinase = MAPK)
- each kinase *phosphorylates several different factors, AMPLIFYING SIGNAL*
ultimately, GENE TRANSCRIPTION altered.
PI3K protein cascade
(triggered by which *two* receptor families? what is the overall result?) - ✔✔(phosphoinositide
3-kinase protein cascade)
a signalling pathway also *triggered by RTKs AND insulin-like growth factor receptors (IGFRs)*.
involves activated Akt protein *inhibiting pro-apoptotic Bcl-2 family members BAD + BAX and others*.
ultimately, APOPTOSIS INHIBITED, promoting cell survival, proliferation + growth.
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