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BIOL 103 > Lecture 7-8 (Quiz 4) > Flashcards

Lecture 7-8 (Quiz 4) Flashcards

1
Q

What are the two main abilities of stem cells (in context of cell fate)?

A

Self renewal or differentiation (make more of themselves, or become something else)

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1
Q

What are the two types of stem cells?

A

Embryonic stem cells and adult step cells (somatic and germ line)

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2
Q

Of embryonic and adult stem cells, which is totipotent?

A

Embryonic stem cells are totipotent,

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3
Q

When do stem cells stop lose their totipotency?

A

After the 8-cell stage (blastocyst)

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4
Q

What are trophoblast stem cells?

A

They give rise to extraembryonic tissue

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5
Q

How do synthetic embryos form?

A

Stem cells can divide and self organize into an embryo on their own in an incubator (using knowledge of early embryonic devo as guide)

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6
Q

What can cause teratomas?

A

teratomas can be formed by early embryonic cells when transplanted to certain adult tissues

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7
Q

What are two ways to convert differentiated cell into ESCs?

A

Therapeautic cloning (somatic nuclear transfer), and induced pluripotent stem (iPS) cells

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8
Q

What is transdifferentiation?

A

Bypassing stem cells by directly converting one cell type to another

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9
Q

What is the default state for ESC?

A

Self renewal is the ground state (inhibition of differentiation)

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10
Q

In what way do cells lose flexibility during development?

A

They become more and more specialized as development proceeds

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11
Q

Is differentiation reversible?

A

Yes. Somatic nuclear transfer, induced pluripotent stem cells

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12
Q

What is somatic nuclear transfer?

A

The process of taking an adult (somatic) nucleus and putting it into an egg cell. The embryo that forms will eventually develop into an organism with an identical genome to the donor organism.

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13
Q

What is cloning also known as?

A

Somatic Nuclear Transfer

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14
Q

What is the broader legacy of cloning research?

A

Cell differentiation is reversible, and nuclei can be reprogrammed

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15
Q

What are the goals of therapeutic cloning?

A

To establish embryonic stem cell lines (that can be manipulated and used for tissue repair or replacement), not to clone a human being

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16
Q

What is induced pluripotency?

A

Using a set of defined factors to directly reprogram a differentiated somatic cell back to the pluripotent state

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17
Q

What are some properties of adult stem cells?

A

Can generate a particular tissue or are derived from this tissue, they have some capacity of self renewal (multipotent), they can generate cells other than themselves, and self renewal capacity lasts a lifetime

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18
Q

What are some tissues with amazing regenerative capacity?

A

Bone marrow, liver hair, skin, blood, gut, muscle. female breast

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19
Q

Does tissue turnover necessarily need stem cells?

A

Maybe not. For example, differentiated cells in liver and pancreas can divide and replenish themselves

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20
Q

What are benign tumors?

A

Cells resemble their tissue of origin, grow slowly, and are localized to tissue of origin

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21
Q

What are malignant tumors?

A

Cells do not resemble tissue of origin, have irregular structure, and can invade surrounding tissues and spread to other organs (metastasis)

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22
Q

Where are carcinomas?

A

Epithelial tissues

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23
Q

Are cancer cells similar or different to the cells from which they originate?

A

They are very different. They lose control over cell division and can migrate to to other locations in the body (metastasis)

24
Q

Cancer development is a _______ process that takes a _____ _____

A

multistep; long time

25
Q

What do solid tumors need to fuel their growth?

A

Blood vessels.

26
Q

What are the two main ways that cancers can arise?

A

Emvironmental factors or genetics

27
Q

Many mutagens are ______ but not all _______ are mutagens

A

carcinogens; carcinogens

28
Q

What are the biggest contributors the cancer worldwide?

A

Smoking, drinking alcohol, and obesity

29
Q

What are oncogene proteins?

A

Positive regulators that stimulate cancer cells to divide more. They are mutated to be overly active or are present in excess. They are components of signal transduction pathways

30
Q

What are tumor suppressors?

A

Negative regulators in both cancer and normal cells. They become inactive in cancer cells.

31
Q

What are somatic mutations

A

Mutations that occur in cells of the body

32
Q

What are germ line mutations?

A

Mutations that occur in the germ cells (inherited from parents / transmit to next gen)

33
Q

Can cancers be caused by viruses?

A

Yes

34
Q

How does RSV cause cancer?

A

The v-src gene in RSV is required for cancer formation. c-src is a gene encoding a normal cellular protein and shares strong homology with v-src, but v-src lacks the inhibitory phosphorylation site near the c-terminus and is constitutively active

35
Q

What is RSV

A

A retrovirus (uses DNA as genetic material)

36
Q

What are protooncogenes?

A

A normal gene that gets mutated to become cancerous

37
Q

What is src?

A

Family of kinases. V-src specifically is involved in cancer proliferation

38
Q

How does v-src play a role in cancer?

A

It is a gene in RSV that is required for the formation of cancer. It is an oncogene

39
Q

How does c-src play a role in cancer?

A

It is a gene that encodes a normal cellular protein that share sequence homology with v-src. Normal c-src is only activated when required. It is a proto oncogene.

40
Q

What are some main differences between c src and v src

A

v src is an oncogene while c src is a proto oncogene. The v-src protein slacks the inhibitory phosphorylation site near C terminus and is constitutively active.

41
Q

How do viruses cause cancer?

A

They incorporate a proto oncogene into its viral genome. They insert next to proto oncogene in host DNA.

42
Q

How do carcinogens cause cancer?

A

They cause chromosomal translocation, and mutate DNA by making deletions or changing nucleotides.

43
Q

Can oncogenes imitate tumorigenesis?

A

Yes.

44
Q

How do cancers arive (tumor suppressors)

A

Activation of one oncogene allele is sufficient. Disruption of both tumor suppressor alleles is needed.

45
Q

Why do only a small percent of cells become cancerous?

A

Because there are checkpoints to prevent inappropriate proliferation

46
Q

Losing one copy of a tumor suppressor gene ______ cancer susceptibility

A

increases

47
Q

What are some well known tumor suppressors?

A

Rb, PTEN, BRCA2, TP53

48
Q

What encodes the p53 protein? What does p53 do?

A

TP53. p53 is a tumor suppressor that responds to DNA damage. Upon sensing DNA damage, p53 is activated, resulting in G1 cell cycle arrest or apoptosis

49
Q

How to target cancer cells?

A

Removing them physically, inhibiting proliferation, or utilization of immune system. Examples: Prevention, pallative care, surgical removal, radiation, chemotherapy, and immunotherapy

50
Q

What is oncogenomics?

A

A way of understanding cancer risks and signaling pathways for individualized treatment. It involves whole genome analyses of cancers in different people. This is done because cancers in different people may hijack different pathways to fuel growth.

51
Q

What is the difference between oncogenes and protooncogenes?

A

Mutated protooncogenes become oncogenes. Protooncogenes are naturally occurring genes involved in cell proliferation, and when it mutates, causes celll division to keep going. Becomes an oncogene upon mutation.

52
Q

How are all mutagens carcinogenic, but not all carcinogens are mutagens?

A

Carcinogens are things that can cause cancer, while mutagens cause mutations. While there are carcinogens that are also mutagens (uv radiation for example), not all carcinogenic things cause cancer via mutation (alcohol, asbestos).

53
Q

Describe how src was discovered and how it is linked to rsv?

A

Originally found in a virus, but looked like chicken gene. Viral protein slightly shorter than chicken protein. This extra part at c terminus contains regulatory domain that stops protein from functioning. Lack of this domain in viral protein means the kinase cant be turned off. As such, when the virus replicates, it will keep making this protein, leading to tumorogenesis.

54
Q

How does adult neurogenesis work?

A

Stem cells and lineage determined progenitor cells are in the SVZ of the lateral ventricle. Neuronal precursor cells migrate through RMS like a chain to become certain types of neurons.

55
Q

What is the niche hyporthesis?

A

Adult stem cells exist in niches, which are specialized regions of a tissue (which determine cell fate)

56
Q

Can organs be generated outside the body?

A

Yes. Scientists have grown self-organizing mini organs from single stem cells (from specific niches)

57
Q

What are iPSs?

A

induced pluripotent cells. The process of taking adult cells and expressing certain transcription factors (only found in ESCs) to induce pluripotency.

58
Q

Is a single mutation enough to cause cancer?

A

No! A single oncogenic event is not enough for carcinogenesis

BIOL 103 (6 decks)

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