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Cell Bio > Stem Cells & Cancer > Flashcards

Stem Cells & Cancer Flashcards

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Biology 101 flashcards
1
Q

what happens to a fertilized egg during development

A

it will repeatedly divide leading to the formation of a complex multicellular organism

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2
Q

what is totipotency

A

the ability of one cell to divide and produce all differentiated cell types in an organism

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3
Q

totipotency is orchestrated by what

A

the genome

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4
Q

what is an example of totipotency

A

a fertilized egg

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5
Q

what tissue is skin composed of

A
  • epithelial
  • connective
  • (each dermal tissue differs in compositions of cell type/ proteins etc)
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6
Q

what 3 factors contribute to stability of tissue renewal

A
  • cell communication
  • selective cell adhesion
  • cell memory
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7
Q

label which layers are which

A
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8
Q

after a cell becomes specialized, will their future divisions follow that specialization, or can it continue to specialize in different manners

A
  • future divisions will only produce cells of the same variety
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9
Q

a proliferating cell relies on what to maintain its idenitty

A

cell memory

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10
Q

how do proliferating cells maintain their identity

A

patterns of gene expression are passed onto daughter cells

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11
Q

how do cells facilitate memory

A
  • many ways, including:
  • activation of master transcription regulators (typically results in a positive feedback loop)
  • DNA methylation (methylation of C residues which attract proteins that inhibit transcription)
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12
Q

describe how master transcription regulators work

A
  • a protein will not be made because it is required for the transcription of its own gene
  • a transient signal turns on the expression of the gene
  • the gene will then continue to be transcribed in absence of the initial signal
  • (signal will produce a little bit of A which, which turns on gene A, producing lots of A, positive feedback loop producing more A)
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13
Q

can most specialized, differentiated cells that need replacement divide

A

most are unable to divide (terminally differentiated)

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14
Q

what are terminally differentiated cell examples

A
  • RBC
  • superficial epidermal cells
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15
Q

cells that replace terminally differentiated cells are generated by what

A

from a stock of proliferating precursor cells

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16
Q

where are precursor cells derived from

A

a smaller pool of stem cells that are not differentiated and can divide without limit

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17
Q

where are precursor and stem cells typically retained

A

typically retained in resident tissues along w their differentiated progeny

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18
Q

what allows differentiation in precursor and stem cells

A

transcription regulations

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19
Q

describe the pathway of stem cell to terminally differentiated cells

A
  • stem cell
  • precursor cell
  • proliferating precursor cells
  • terminally differentiated cells
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20
Q

describe the structure of the small intestine

A
  • comprised of absorptive and secretory cells arranged as simple epithelium
  • tissues includes crypts which descend into the underlying connective tissues
  • stem cells are near the bottom of the crypt
  • stem cells give rise to precursor cells which move upwards
  • precursor cells differentiate as they move upwards until they reach the tip, where they are shed into the gut lumen
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21
Q

describe the structure of of the epidermis

A
  • stratified epithelium
  • proliferating stem cells and precursor cells are confined to the basal layer, adhered to the basal lamina
  • differentiating cells travel outwards and the terminal ones shed from the surface
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22
Q

can a single type of stem cell give rise to several types of differentiated progeny

A

oftenly yes

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23
Q

what is hematopoiesis

A

blood formation

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24
Q

what is an example of stem cells giving rise to several types of differentiated progeny

A
  • hematopoiesis
  • all types of blood cells originate from hematopoietic stem cells found in the bone marrow
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25
Q

how are stem-cell systems controlled

A
  • extracellular signals exchanged between stem cells
  • stem cell progeny
  • other cell types as well as the intracellular signaling pathways they activate
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26
Q

how is intestinal stem cell system control mediated

A

Wnt proteins

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27
Q

what do Wnt proteins do (broadly)

A

promote the proliferation of stem cells and precursor cells at the base of each intestinal crypt

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28
Q

what produces signals to prevent the activation of the Wnt pathway outside the crypt

A

cells in the crypt

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29
Q

what kind of signals do cells in the crypt produce

A
  • signals to prevent the activation of the Wnt pathway outside the crypt
  • diversification signals to ensure some cells differentiate into secretory cells while others become absorptive cells
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30
Q

what does the Wnt pathway maintain

A

the proliferation of stem cells and precursor cells in intestinal crypts

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31
Q

what happens in the absence of Wnt signaling

A

the adenomatous polyposis coli (APC)- containing complex degrades the signal molecule beta-catenin

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32
Q

what happens in the presence of Wnt signaling

A

the APC containing complex is inactivated leading to the transcription of genes that promote the proliferation of stem cells and precursor cells

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33
Q

what enables continuous renewal and repair of their designated tissues

A

stem cells

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34
Q

why are stem cells developmentally restricted

A

to ensure progeny differentiate to the appropriate cell type

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35
Q

what do embryonic stem cells retain

A

nearly unrestricted developmental potential

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36
Q

what does pluripotent mean

A

can give rise to all cell types and tissues in an organism

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37
Q

what is an example of a pluripotent cell

A

embryonic stem

38
Q

what are iPS cells

A

induced pluripotent stem cells

39
Q

can you produce pluripotent stem cells without the use of embryos

A

yes

40
Q

can differentiated cells be taken from an adult

A

yes

41
Q

how can you produce pluripotent stem cells without embryos

A
  • differentiated cells taken from an adult
  • grown in culture
  • reprogrammed into an ES-like state
42
Q

which transcription regulators need to be modulated in expression when forming iPS cells

A
  • Oct4
  • Sox2
  • Klf4
43
Q

Differentiated cells can be taken from an adult, grown in culture, and reprogrammed into an ES-like state are called what

A

induced pluripotent stem cells

44
Q

which cell types are used to form organoids

A
  • ES (embyonic stem)
  • iPS (induced pluripotent stem)
45
Q

which cell type are often used to study and treat genetic diseases

A

iPS

46
Q

what is often used to study organ development and how it can be impacted by disease

A

organoids

47
Q

how are organoids formed

A

ES and iPS cells can be made to proliferate, differentiate, and assemble into organoids

48
Q

cancer cells are defined by which heritable properties

A
  • they and their progeny proliferate in defiance of normal constraints
  • they invade and colonize territories normally reserved for other cells
49
Q

when are benign tumors formed

A

when the cells proliferate in defiance of normal
constraints, but DONT invade and colonize territories normally reserved for other cells

50
Q

when do tumors become cancerous

A

when the cells invade and colonize territories normally reserved for other cells (becomes malignant)

51
Q

what happens when tumors become malignant

A

can spread, leading to secondary tumors or metastases

52
Q

what is the underlying cause of cancer

A
  • a genetic disease
  • somatic mutation
53
Q

most identified agents known to promote cancer development are what

A

mutagens

54
Q

how do mutagens promote cancer development

A

cause changes in the sequence of DNA

55
Q

what are passenger mutations

A

found in cancer but don’t cause the disease

56
Q

what are cancer-critical or driver mutations

A

actively promote cancer but do not act alone

57
Q

outside of environmental factors, why are we still prone to cancer

A

accumulating spontaneous mutations

58
Q

which spontaneous mutations make us prone to cancer

A
  • passenger mutations
  • cancer-critical or driver mutations
59
Q

what 3 main things work together to cause cancer

A
  • alterations in cell growth
  • alterations in cell proliferation
  • alterations in cell survival
60
Q

why do many cancer cells speed up the aquisition of mutations

A

because they’re genetically unstable

61
Q

what contributes to genetic instability

A
  • defects in DNA replication
  • defects in DNA repair
  • defects in cell-cycle checkpoint mechanisms
  • mistakes in mitosis
  • abnormal chromosome numbers
62
Q

malfunctions in mitosis leads to what

A
  • chromosomal damage
  • chromosome breaks, rearrangements, aneuploidy
63
Q

what is aneuploidy

A

gain or loss of whole chromosomes

64
Q

what is given to cells with accumulating mutations that lead to cancer

A

competitive advantage

65
Q

what happens as an initial population of cancer grows

A
  • new chance mutations occur
  • some are favoured by natural selection (enhance proliferation and survival)
66
Q

what may further the development of cancer by altering selection pressures in tissues

A

environmental and lifestyle factors (like obesity)

67
Q

how do environmental and lifestyle factors further favour the development of cancer

A

alters selection pressures in tissues

68
Q

what are general characteristics of cancer

A
  • can survive typically lethal stress and internal derangement
  • they can proliferate indefinitely
  • secrete signals that influence the behaviour of cells in surrounding tissue
  • can survive and proliferate in inappropriate locations
  • most are genetically unstable
  • abnormally avid for nutrients
  • abnormally invasive
  • reduced dependence on external signals for survival, growth, division
69
Q

what are the most dangerous mutations in many cancer-critical genes

A

render the encoded protein hyperactive

70
Q

what is a common atribute of the gain-of-function mutations in cancer-critical genes

A
  • have a dominant effect
  • only one copy of the gene needs to be mutated to promote cancer development
71
Q

genes susceptible to gain-of-function mutations are called what

A
  • proto-oncogenes
  • once they mutate, they are called oncogenes
72
Q

once proto-oncogenes have been mutated, what are they called

A

oncogenes

73
Q

what kind of gene are loss-of-function genes

A
  • recessive
  • require both copies of the gene to be eliminated or inactivated to contribute to cancer treatment
74
Q

what kind of mutations are those that destroy cancer activity

A

loss-of-function

75
Q

how can tumor suppressor genes be silenced

A
  • genetic alteration
  • epigenetic changes altering gene expression without changing genetic sequence
76
Q

where does colorectal cancer most commonly occur

A
  • older demographics
  • those who are genetically predisposed to earlier development
77
Q

the onset of colorectal cancer is foreshadowed how

A

by the development of many little tumors (called polyps)

78
Q

the development of polyps is due to what

A
  • the deletion or inactivation of a tumor suppressor gene (adenomatous polyposis coli APC)
  • inherited one mutated copy and one normal cop
79
Q

what is the class and effect of Ras gene mutation

A
  • proto-oncogene
  • activating mutations: render the Ras protein continuously active, promoting cell proliferation
80
Q

what is the class and effect of β-catenin gene mutation

A
  • proto-oncogene
  • activating mutations: make it resistant to degredation, promoting cell proliferation
81
Q

what is the class and effect of p53 gene mutation

A
  • tumor suppressor gene
  • inactivation: allow cancer cells to continue to survive and divide, even in the presence of damaged DNA
82
Q

what is the class and effect of APC gene mutation

A
  • tumor suppressor gene
  • inactivation: excessive proliferation in intestinal crypt
83
Q

what is the class and effect of Brca1 and Brca2 gene mutation

A
  • tumor suppressor gene
  • inactivation: allows cancer cells to continue to survive and divide in the presence of massively damaged DNA
84
Q

describe the pathway of cumulative mutation needed for metastasis

A
85
Q

what are some established methods of cancer treatment

A
  • surgery
  • radiation
  • chemotherapy
86
Q

what are some novel methods of cancer treatment

A
  • targeted drug treatment
  • immune activation
87
Q

what is targeted drug treatment and how does it treat cancer

A

raise genetic instability in cancerous cells while normal cells persist through repair mechanisms or block activity of specific oncogene products

88
Q

how does immune activation treat cancer

A

leads immune cells to protein structures unique to cancerous cells or neutralize inhibitory cell surface proteins to prevent inactivation of immune cells

89
Q

what are the 2 major classes of genes critical for cancer

A
  • oncogenes
  • tumor suppressors
90
Q
A

Cell Bio (11 decks)

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