lecture 5- cancer and stem cells Flashcards

(30 cards)

1
Q

what is an oncogene

A

a gene capable of transforming a normal cell into a tumour cell

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2
Q

what do tumour supressors do

A

restrict proliferation

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3
Q

what are the 2 groups of kinases involved in the cell cycle

A

Cdk
cyclins

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4
Q

which part of division is controlled by Cdk1 and cyclin A/B

A

m phase

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5
Q

which part of the cell cycle is controlled by Cdk 4/6 and cyclin D

A

G1

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6
Q

which part of the cell cycle is controlled by Cdk2 and cyclin E

A

G1/S checkpoint

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7
Q

which part of the cell cycle is controlled by Cdk2 and cyclin A

A

S

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8
Q

what are the 4 main causes of cancer

A

Chemicals
parasites
radiation
viruses

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9
Q

how is intra-tumour heterogeneity achieved in cancer cells

A

differences in:
-differentiation state
-proliferation state
-migratory and invasive
-capacity
-size
-therapeutic response

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10
Q

what is the difference between intra and inter tumour heterogeneity

A

intra- cells within the same tumour
inter-between different tumours

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11
Q

describe the stochastic model for cancer

A

all tumour cells are equipotent

a proportion of them stochastically proliferate to fuel tumour growth while other tumour cells differentiate

fates are random

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12
Q

describe the cancer cell model

A

within a tumour, there exists a small subset of cells with stem cell-like properties. These cancer stem cells are the “drivers” of tumour growth, responsible for initiation, maintenance, metastasis, and recurrence of the cancer.

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13
Q

what are the key differences between the stochastic model and the cancer stem cell model

A

Sto= random cell fate
CSC= predetermined cell fate by stemness

sto= tumour growth driven by random mutations
CSC= tumour growth driven by CSCs

sto= must target all cells
CSC= only need to target CSCs

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14
Q

why can CSCs resist treatment

A

they have a slow cell cycle

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15
Q

what are to 2 similarities between normal stem cells and cancer stem cells

A

self renewal
regulated by WNT

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16
Q

what is the difference in differentiation between normal stem cells and cancer stem cells

A

normal= differentiation for organ functionality

cancer= differentiation for tumour advantage

17
Q

what are the 2 ways a stem cell can be transformed into a cancer stem cell

A

1) a specialised cell accumulates mutations which brings it back to its progenitor state
this allows for reprogramming to a cancer cell

2) oncogenic transformation of pre-existing stem cells

18
Q

what is the in vitro potential of capturing cancer stem cells

A

establishment of cell lines that can self renew and differentiate

19
Q

what is the in vivo potential of capturing cancer stem cells

A

ability to give rise to cancer following transplantation into animals

20
Q

what is acute myeloid leukaemia

A

blood cancer affecting the myeloid lineage

21
Q

how is AML caused

A

clonogenic leukaemic progenitors

22
Q

how can we use stem cells to investigate brain cancer

A

-dissociate cells
-plate on laminin in presence of cytokines FGF2 and EGF

no expression of undifferentiated markers = differentiation to either glia or neurons

23
Q

what are the undifferentiated markers of brain cancer stem cells

24
Q

what are the main approaches of in vitro models of tumourigenesis

A

xenograft models
cancer cell lines
genetically modified animals

25
what are the main limitations of in vitro models of tumourigensis
cant capture the transition is a traceable manner cant track the mechanisms
26
how can iPSCs / hESCs be used to solve issues with in vitro tumour models
can add the cancer stem cells to the iPSCs and watch the differentiation in human cells can take hESCs and introduce oncogenic mutations
27
how are neuroblastomas formed
ectopic overexpression of the transcription factor MYCN in normal neural crest cells
28
how was it proved that neuroblastomas were cause by overexpression of MYCN
hPSCs were grown with WNT and BMP and they formed neural crest cells hECS were growth with WNT, BMP, and MYCN overexpression and these formed the neuroblastoma phenotype
29
which model for cancer stem cells does the leukemia case study support and why
the cancer cell model was found that only a small subset of cells could actually initiate leukemia
30
which markers are used to identify leukemia stem cells
CD34+ CD38-