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SL32113 - Molecular Biology > Cancer Stem Cells > Flashcards

Cancer Stem Cells Flashcards

(85 cards)

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1
Q

Name the 3 different factors which the development of an organism relies on

A

Differentiation
Proliferation (growth)
Apoptosis (death)

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2
Q

What is self-renewal in stem cells?

A

Self-renewal refers to the ability of stem cells to continuously replicate and produce many identical copies of themselves.

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3
Q

Why is self-renewal important?

A

It is key for tissue maintenance and repair.

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4
Q

What happens to stem cells as they differentiate?

A

As stem cells move to a more differentiated state, their rate of proliferation generally goes down.

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5
Q

What characterizes cancer cells?

A

Cancer cells are unmature and differentiated, leading to rapid proliferation.

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6
Q

What is an example of cancer affecting cell structure?

A

Leukemias in the bone marrow do not have the same structure and function as functional white blood cells.

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7
Q

What is the goal regarding cancer cells and proliferation?

A

The goal is to push cancer cells away from the proliferation status.

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8
Q

What is the relationship between differentiation and proliferation?

A

More differentiation leads to less proliferation.

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9
Q

What happens to cells as they mature?

A

As cells mature, they typically lose their ability to divide.

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10
Q

What can stem cells do?

A

Stem cells can differentiate to become specialized cells (e.g., liver, brain) and proliferate to increase cell numbers.

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11
Q

What is cancer?

A

Cancer is a proliferative disease where cells divide uncontrollably.

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12
Q

How do cancer cells typically behave?

A

Cancer cells are often undifferentiated, immature, and lack specialized functions.

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13
Q

What is a characteristic of cancer cells compared to normal cells?

A

Cancer cells behave more like stem/progenitor cells in an uncontrolled way.

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14
Q

What does it mean that cancer cells are clonal?

A

Cancer cells arise from a single cell and are caused by the accumulation of mutations in that cell.

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15
Q

Why do most cells not become cancerous?

A

Most cells have a finite lifetime and do not live long enough to acquire 3 mutations.

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16
Q

What is necessary for a cell to acquire mutations?

A

Cells need to be growing fast to acquire mutations and pass them on to daughter cells.

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17
Q

What is a critical mutation in cancer development?

A

A critical mutation pushes a cell from benign growth to malignant invasive growth.

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18
Q

How many mutations are needed for a cell to become cancerous?

A

At least 3 mutations within a cell are needed to make it cancerous.

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19
Q

What are the therapeutic goals for cancer treatment?

A

Shift cancer cells away from a proliferative state, promote differentiation, and maintain a balance between renewal and specialization.

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20
Q

What is the normal role of proliferation in the body?

A

Normal proliferation replaces damaged or worn-out cells and is essential in wound healing, immune response, and general homeostasis.

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21
Q

What are embryonic stem cells?

A

Pluripotent cells that can become various different cell types.

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22
Q

What are the characteristics of stem cells?

A

They are unspecialised, capable of self-renewal (indefinite division), and can generate specialised cells.

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23
Q

What are progenitor/precursor cells?

A

Intermediate stage between stem cells and fully differentiated cells.

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24
Q

What are specialised (differentiated) cells?

A

Cells that perform specific functions and usually cannot divide.

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25
What is terminal differentiation?
Typically irreversible and regulated by transcriptional and epigenetic mechanisms.
26
What are adult stem cells?
Small number of residual stem cells identified in adult tissues.
27
What is the role of adult stem cells?
Required for normal cell turnover and normal repair.
28
In which tissues are adult stem cells found?
Include blood, intestine, skin, muscle, liver, and brain.
29
What is the role of stem cells in bone marrow?
Stem cells required for normal cell turnover.
30
What is the role of stem cells in liver and muscle?
Stem cells involved in healing.
31
How many adult stem cells are typically present?
Only present in very small numbers; proliferation normally suppressed.
32
What is a challenge associated with adult stem cells?
Difficult to identify and isolate.
33
What happens to a population of cells that grow faster but are not differentiated?
They cannot carry out normal tissue function and exhibit characteristics of stem cells.
34
Where do adult stem cells reside?
In the tissue surrounded by niche cells.
35
What is the role of niche cells in relation to adult stem cells?
They secrete factors to suppress the growth of adult stem cells and keep them under control.
36
What occurs when growth suppression of adult stem cells is relieved?
The adult stem cells start to divide and produce more daughter cells, becoming more differentiated, but their proliferative capacity decreases.
37
What is a key factor in cancer related to adult stem cells?
Either the suppression of adult stem cells fails, or they do not switch off their proliferative status.
38
Why do stem cells have more opportunity for mutations to accumulate?
They are long-lived, unlike most differentiated cells which do not live long enough to acquire many mutations.
39
What are stem cells known for?
Stem cells are long lived and self-renewing, giving more opportunity for mutations to accumulate.
40
What does the asymmetric division of stem cells contribute to?
The asymmetric division of stem cells may account for the heterogenicity of the tumour mass.
41
Where are adult stem cells found and what is their ability?
Adult stem cells are present at low numbers in tissues but have been shown to have the ability to recolonise.
42
What is the relationship between self-renewal pathways and cancer cells?
Many of the signalling pathways involved in self-renewal have been shown to be matured in cancer cells.
43
How is stem cell proliferation normally regulated?
Stem cell proliferation is normally regulated (suppressed) by niche cells.
44
What role do niche cells play in stem cell regulation?
Niche cells secrete factors which suppress or stimulate stem cells to proliferate.
45
What happens to cancer stem cells in relation to niche cells?
Cancer stem cells can become 'niche-independent' or under control of a different niche.
46
What are the two potential fates of stem cells?
Stem cells can self-renew or differentiate.
47
How are pathways controlling stem cell behavior regulated?
Pathways are controlled by transcription factors that upregulate or suppress self-renewal or differentiation genes.
48
What happens when self-renewal genes are activated?
When self-renewal genes are activated and transcribed, stem cells grow.
49
What occurs when differentiated genes are activated?
When differentiated genes are activated and transcribed, stem cells stop growing and become more specialised.
50
What is the stem cell hypothesis in cancer?
Cancer cells arose from mutations in residual adult stem cells.
51
What are some mechanisms by which cancer cells can arise from stem cells?
1. More stem cells and more niches that are suppressed. 2. Switching to different niches with less suppression. 3. Becoming niche dependent with no suppression. 4. Differentiating without switching off proliferative capacity.
52
What is the likely explanation for the mechanisms of cancer cell emergence?
Probably a mixture of all of these.
53
What do targeted therapies aim to do in cancer treatment?
Target pathways and proteins in terminally differentiated cells.
54
What is the effect of chemotherapy on tumor mass?
Chemotherapy kills off about 98% of tumor mass.
55
What happens to the remaining cancer cells after chemotherapy?
About 0.5% remain resistant to chemotherapy, which are adult stem cells.
56
What can happen five years after chemotherapy?
The resistant adult stem cells can start to grow again, leading to cancer recurrence.
57
What are the two main pathways involved in cancer?
Wnt and Hedgehog (Hh) pathways.
58
What is the role of the Wnt pathway in colon cancer?
Wnt helps control cell growth. In ~90% of colon cancers, mutations prevent β-catenin from being destroyed, leading to uncontrolled cell growth.
59
What happens when Wnt binds to its receptor Frizzled?
It blocks GSK-3, allowing β-catenin to build up and enter the nucleus to activate growth genes like c-myc and cyclin D.
60
What is the consequence of losing the APC protein in colon cancer?
The complex cannot form, leading to free β-catenin that drives cyclin D expression and promotes cell proliferation.
61
What are the three types of Hedgehog (Hh) pathways?
Sonic, Desert, and Indian Hedgehog.
62
What is the normal function of the Hedgehog pathway?
Hh binds to the Patched receptor, releasing the inhibition on Smoothened, which activates the transcription factor Gli.
63
What happens if Hedgehog or Gli are overactive?
The pathway becomes stuck in 'ON' mode, which can lead to cancer.
64
What is the role of Gli in the Hedgehog pathway?
Gli enters the nucleus and activates growth genes.
65
How do intestinal villi cells differentiate?
Rapidly dividing cells arise from stem cells and move upwards along the villi, differentiating into specialized cells like absorptive and goblet cells.
66
Is the Wnt pathway activated in wild type somatic differentiated cells?
No, the Wnt pathway is not activated in wild type somatic differentiated cells.
67
Are residual adult stem cells using the Wnt pathway?
Yes, residual adult stem cells are using the Wnt pathway.
68
What is a potential strategy for targeting cancer pathways?
Target the Wnt pathway rather than the epidermal growth factor pathway.
69
What happens if there is a mutation in the APC?
If the mutation is in the APC, there is no point in targeting Wnt and its receptor because it is upstream.
70
What can be targeted if Wnt is overexpressed or its receptor is constitutively active?
If Wnt is overexpressed or its receptor is constitutively active, one might be able to target the Wnt ligand.
71
What is the best place to block Wnt signaling?
The best place to block Wnt signaling depends on where the mutation is.
72
What is one strategy to stop Wnt signal from starting?
Use Porcupine inhibitors to block Wnt ligand production/secretion.
73
What is another strategy to stop Wnt signal from starting?
Use monoclonal antibodies (Mabs) to bind to Wnt ligand or its receptor to block activation.
74
How can Axin levels be stabilized?
Use Tankyrase inhibitors to keep Axin levels high, so it can help break down β-catenin.
75
What is a method to block β-catenin activity?
Prevent β-catenin from acting as a transcription factor to stop it from turning on genes that cause cell growth and self-renewal.
76
What are telomerases?
Telomerases are reverse transcriptase enzymes containing an RNA template to add TTAGGG repeats to chromosome ends.
77
What role do telomeres play in cell division?
Telomeres are tandem repeats found on the end of chromosomes and aid chromosomal replication.
78
Why do telomeres shorten with each cell division?
DNA polymerases cannot copy right to the end of the chromosomes, causing telomeres to shorten on each cell division.
79
What happens when telomeres get too short?
When telomeres get too short, they are recognized as damaged DNA, activating p53 to induce senescence or apoptosis.
80
In which types of cells are telomerases found?
Telomerases are found in rapidly dividing and germ line cells; most somatic cells lack telomerases.
81
How do stem cells utilize telomerases?
Stem cells express telomerases, which repair the ends of chromosomes using RNA templates during cell division.
82
Why do cancer cells express telomerases?
Cancer cells express telomerases, allowing them to repair chromosomes and extend cell life.
83
What is the significance of telomerase and N-myc levels?
Telomerase and N-myc levels are indicative of prognosis; high levels are associated with poor outcomes.
84
What are potential therapeutic strategies targeting telomerases?
Potential strategies include telomerase antisense or telomerase with mutated RNA template.
85
What are some challenges in targeting telomerases for therapy?
Challenges include heterogeneity of tumor mass, 3D/hypoxic nature of tumor mass, potential harm to WT stem cells, and drug resistance from ABC transporters.

SL32113 - Molecular Biology (7 decks)

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