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Cell Bio 2020 > Stem Cells and Cancer (L25) > Flashcards

Stem Cells and Cancer (L25) Flashcards

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1
Q

What are four characteristics of most tissues?

A
  1. Have mechanical strength
  2. Import nutrients, export waste
  3. Are connected to nervous system
  4. Are protected by immune system
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2
Q

What three things does the maintenance of tissues rely on?

A
  1. Cell communication
  2. Selective cell adhesion
  3. Cell memory/epigenetics
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3
Q

Do all tissues renew at the same rate?

A

No - different tissues experience different cell turnover rates

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4
Q

What can errors in cell turnover/renewal process lead to?

A

Cancer

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5
Q

What are terminally differentiated cells?

A

Cells that can perform specialized functions that do not divide and will be lost to cell death.

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6
Q

Most cells in tissues are…

A

terminally differentiated

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7
Q

When a stem cell divides, each daughter can either remain a stem cell or can go on to become …

A

terminally differentiated

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8
Q

What types of cells replenish tissues?

A

Stem cells and precursor cells

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9
Q

Are stem cells rare in tissues?

A

Generally yes

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10
Q

What are two important qualities of stem cells?

A
  1. Undifferentiated
  2. Can self-renew
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11
Q

How does tissue renewal work in the intenstine?

A

Stem cells are located at the base of crypts.

They divide and differentiate as they move up the villus. There is no cell division at the villus

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12
Q

What types of pathways maintain stem cell populations?

A

Cell signaling

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13
Q

What signals cell proliferation in the intestinal crypt?

A

Wnt signaling

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14
Q

What is Wnt?

A

A secreted protein made by Paneth cells

It binds a GPCR receptor on neighboring cells and drives cell proliferation in the crypt

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15
Q

Where are stem and precursor cells found in the skin?

A

In the basal layer. Differentiated cells are pushed outward, and dead cells are shed at the skin surface.

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16
Q

Where are differentiated blood cells produced? What types of stem cells do this?

A

In bone marrow

Hematopoietic stem cells

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17
Q

Embryonic stem (ES) cells

A

Are pluripotent

Transcription factors and/or cell signaling pathways direct their differentiation into different cell types

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18
Q

Pluripotent

A

Capable of generating any cell type

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19
Q

Induced pluripotent stem (iPS) cells

A

Created by converting a fibroblast into ES-like cell by removing 3 transcription factors

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20
Q

Organoids

A

Mini 3D collection of tissues formed from proliferation, differentiation, and self-assembly of pluripotent cells in culture

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21
Q

Applications of organoid models

A
  1. Study infectious diseases
  2. Study genetic basis of disease
  3. Toxicology
  4. Personalized medicine
  5. Cancer
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22
Q

Two constants of cancer cell behavior

A
  1. Excessive proliferation
  2. Inappropriate migration
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23
Q

Benign vs malignant cancers

A

Benign do not invade other tissues to form metastases

24
Q

Cancer results from the accumulation of these three variables

A
  1. Heredity
  2. Environment
  3. Random mutations (Replicative)
25
Q

Cancer incidence increases with…

A

Accumulation of mutations

26
Q

What two things contribute to the accumulation of mutations?

A
  1. Age
  2. Faster cell turnover (undergo more cell divisions)
27
Q

Cancers develop in accumulation of somatic or germ-line mutations?

A

Somatic

28
Q

What is a key hallmark of cancer?

A

Genetic instability

29
Q

What are the factors that contribute to genetic instability?

A
  1. Defects in DNA replication
  2. Defects in DNA repair
  3. Defects in cell-cycle checkpoints
  4. Mistakes in mitosis
  5. Abnormal chromosome numbers
30
Q

What is genetic instability?

A

An increased rate of mutation caused by other defects in replication and maintenance of the genome

31
Q

What is the main timeline of cancer evolution?

A
  1. Random mutations occur and can give cells a growth advantage
  2. Mutated cells survive and proliferate
  3. Subsequent mutations give further advantages
  4. Dangerous cell survival and proliferation yields cells that can invade neighboring tissues
32
Q

What are the two main cancer-related genes?

A
  1. Oncogenes
  2. Tumor suppressor genes
33
Q

Dominant mutation

A

Gain of function - oncogenes

34
Q

Recessive mutation

A

Loss of function - tumor suppressor genes

35
Q

How do oncogenes arise?

A
  1. Coding sequence mutations
  2. Gene amplification
  3. Chromosomal rearrangement

Lead proto-oncogenes to mutate into oncogene

36
Q

Tumor-suppressor genes are removed via

A

Epigenetic changes - both copies of the suppressor gene must be lost/inactivated

37
Q

Why don’t elephants get cancer?

A

Have lots of p53 (tumor suppressing gene) that coordinates DNA repair and causes apoptosis if there is too much damage. More p53 means harder to mutate all of them as each copy may respond to different stressors.

38
Q

What are the six hallmarks of cancer?

A
  1. Evading apoptosis
  2. Self sufficiency in growth signals
  3. Insensitivity to anti-growth signals
  4. Tissue invasion and metastasis
  5. Limitless replicative potential
  6. Sustained angiogenesis
39
Q

What are five other hallmarks of cancer?

A
  1. Abnormally invasive
  2. Generate ATP via glycolysis
  3. Survival in abnormal locations
  4. Generation of own microenvironment
  5. Genetic instability
40
Q

Commonly impacts pathways in cancer:

A
  1. Cell proliferation
  2. DNA Damage responseh
41
Q

Outline the progression of colon cancer (a genetic cancer)

A
  1. Inactivation of both copies of tumor suppressor gene (APC) leads to excessive proliferation of mutant cells
  2. One copy of proto-oncogene (Ras) activated leads to a small tumor
  3. Subsequent inactivation of both copies of another tumor suppressor gene leads to a large tumor
  4. Subsequent inactivation of both copies of a third tumor suppressor gene (p53) leads to an invasive cancer
  5. Rapid accumulation of other driver mutations results in metastasis
41
Q

Passenger vs. Driver mutations:

A

Passenger mutations are non cancer-causing, but are present in cancerous cells.

Driver mutations actively promote cancer progression (usually takes ~3 driver mutations)

42
Q

With Wnt signal:

A

The signal activates the Wnt receptor and releases another signaling protein that inactivates the APC-containing complex. This releases stable beta-catenin, which activates the TCF complex.

This results in the transcription of Wnt-responsive genes, leading to proliferation of gut stem cells and precursor cells.

43
Q

Without Wnt Signal

A

The Wnt receptor is inactive, so the APC-containing complex remains active and does not release the beta-catenin, which degrades. The Wnt-Responsive genes are off.

44
Q

What drives proliferation of colorectal cancer?

A

Wnt and APC mutations and loss

45
Q

What promotes proliferation of gut cells even in the absence of Wnt?

A

APC mutations

46
Q

How does APC loss drive cancer?

A

Uncontrolled cell proliferation

47
Q

What are RNA viruses?

A

viruses that have an RNA genome that must first be copied to DNA

48
Q

Are viruses alive?

A

No, they have no metabolism of their own

49
Q

How do DNA viruses use host cells?

A

To replicate DNA, transcribe RNA, and translate more virus proteins

50
Q

What is zoonosis?

A

Cross-species viruses

51
Q

Which receptor does SARS-CoV2 use to enter cells?

A

The ACE2 receptor, which is involved in angiotensin signaling

52
Q

How do you make an mRNA vaccine?

A
  1. Design an mRNA that codes for the spike protein
  2. Generate a lot of mRNA
  3. Package mRNA into lipid nanoparticles (this protects it as bare would be degraded too quickly)
  4. Inject into muscle
53
Q

APC is a…

A

tumor suppressor gene

54
Q

What does APC encode?

A

The restriction of activation of Wnt stimulation pathway (cell proliferation)

Cell Bio 2020 (8 decks)

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