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BIOL 2030 > Ch. 21 Tissues and Cancer > Flashcards

Ch. 21 Tissues and Cancer Flashcards

1
Q

define tissues

A

organized mixtures of specialized cell types that are reflective of that particular tissues needs

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2
Q

what do tissues require

A
  • mechanical strength and support
  • innervation
  • defense (immune response)
  • metabolic support: nutrient uptake, oxygen, waste disposal
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3
Q

how do tissues receive mechanical strength and support

A

most often through fibroblasts interacting with extracellular matrix (connective tissue)

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4
Q

why do tissues require innervation

A

in order to respond to signals sent to them

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5
Q

what are the layers of the skin

A
  • epidermis w keratinocytes
  • dermis: loose connective tissue then dense connective tissue
    hypodermis: fatty connective tissue
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6
Q

what is the density of dermis connective tissue referring to

A

collagen fibres, fibroblasts, capillaries

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7
Q

what is the purpose of the hypodermis

A

supply of nutrients and removal of waste products

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8
Q

what are the key factors of structural stability in tissues

A
  • cell communication
  • selective cell-cell adhesion
  • cell memory
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9
Q

describe the main molecule present in selective cell-cell adhesion

A
  • cadherins
  • make adherin junctions
  • allow for specific attachment between cells
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10
Q

what is the importance of attachments to ECM in selective cell-cell adhesion

A

controls organization of tissues and set patterns of cell adherence

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11
Q

what do we mean by cell memory

A

patterns of gene expression turned on during embryonic development remain maintained thruout life of cell (Ex when fibroblast cells divide, more fibroblast cells are made)

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12
Q

what is the importance of tissue rate renewal variability amongst cells

A

reflects the sensitivity and roles of those cells

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13
Q

what are the cells involved in replacing the matrix and cells in bone

A

osteoclasts and osteoblasts

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14
Q

what is the role of osteoclasts

A

destroy and eat old bone matrix

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15
Q

what is the role of osteoblasts

A

deposit new matrix

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16
Q

how does red blood cell turnover occur

A
  • aged red blood cells have markers on surface
  • markers recognized by macrophages and phagocytose the cells
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17
Q

if terminally differentiated cells cannot divide in tissues, where do the replacement cells come from

A
  • stem cells
  • proliferating precursor cells
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18
Q

when stem cells divide, what pathway(s) could it take

A
  • remaining as stem cells (continuing self-renewing cycle)
  • differentiation into proliferating precursor cells which divide set number of times to make the terminally differentiated cells we see in tissues
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19
Q

what is the role of stem cells in tissues

A

to provide continuous cell supply for each tissue type

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20
Q

how is it ensured that stem cell progeny will be of a certain cell type

A

expression of specific gene regulatory proteins

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21
Q

why are stem cells difficult to study

A
  • present in tissues in very low numbers
  • don’t have unique markers because they are not terminally differentiated - hard to identify
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22
Q

draw out a cross section of a crypt

A

main points: differentiated nondividing terminally differentiated cells at top; rapidly dividing precursor cells in middle; slowly dividing stem cells lower; nondividing terminally differentiated cells at most bottom

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23
Q

what are paneth cells

A

secretory cells in the crypts of gut

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24
Q

draw a diagram of the gut lumen

A

includes: villus, crypt, loose connective tissue, epithelial cells, epithelial cell migration from bottom of crypt to top of villus

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25
what is a very good example of a tissue that goes through cell renewal
gut epithelium
26
explain cell replacement in the dermis
- multiple layers to skin - starts at basal lamina layer with dividing basal cells (stem) - move upward to epidermis whilst differentiating - surface layer has dead flattened cells packed w keratin where cells are continually shed
27
how are dead cells on the surface of skin connected
thru keratin IFs and desmosomes
28
draw a flowchart of how hemopoietic stem cells produce the different cell types in circulation and immune system
- hemopoietic stem cells make T and B lymphocytes, eosinophils, basophils, rbcs, megakaryocytes - neutrophils and monocytes stem from same branch - monocytes lead to osteoclast and macrophages - megakaryocytes make platelets
29
in intestinal epithelium, what are some cells are made thru stem cells
absorptive, goblet
30
describe embryonic stem cells
- isolated from embryos at about five to seven days in age - source is inner cell mass (inside trophoblast cell layer) - pluripotent
31
what is the source of maturation for the placenta
trophoblast
32
what are the non-embryonic stem cells
- umbilical cord blood - placental - adult (present at birth)
33
what is unique about the embryonic stem cells
- can keep dividing in culture - can also differentiate in culture if given appropriate hormones and growth factors, making them mature into distinct cell types - when returned to embryonic environment it will still give rise to all tissues and cell types in body (pluripotent)
34
what are the challenges to using embryonic stem cells for research
- hard to grow and establish culture - hard to maintain culture - controlling direction of differentiation (inconsistency) - unstable gene expression (unpredictable differentiation patterns) → tumour potential - transplant rejection
35
why is transplant rejection a problem; how could it be prevented
- immune system is very good at rejecting foreign tissue unless it is coming from same person or from extremely good match; - requires immunosuppressive drugs
36
why is there a shift towards research using adult stem cells
- adult stem cells are available in all tissues - some adult stem cells (ex bone marrow, brain) are able to produce very different cell types - rapid and long term division can occur
37
cancer cells and their progeny often violate the basic rules of
social cell behaviour (do opposite of what they should)
38
describe primary tumours
tumour located at its origin (the starting tumour)
39
describe secondary tumours
- aka metastases - colonies of cancer cells due to migration away from primary tumour (tumours that spread away from origin)
40
secondary tumours can exist if primary tumours have
properties that allow them to travel out from tissues to lymph/blood, and set up a new site
41
what are the heritable properties of cancer cells
1. ability to proliferate in defiance of normal constraints 2. invade and colonize locations meant for other cells
42
define benign tumours
tumours that form from cancer cells that only proliferate in defiance of normal constraints
43
why are benign tumours not as dangerous
- unable to invade and colonize other areas - removal by surgery
44
define malignant tumours
tumours that form from both heritable properties of cancer cells (i.e. can uncontrollably divide when not supposed to in one spot, and invade and migrate to other tissues)
45
why are malignant tumours able to invade surrounding tissue
- may produce enzymes that make it do so - may lack normal properties required for cell-cell communication and adhesion
46
define metastasize
tumours spreading to other sites in body
47
how do cancers develop
accumulation of mutations (usually somatic) by mutagens or spontaneous mutation (errors)
48
what are somatic mutations
non-germ (egg or sperm) cell that mutates
49
define mutagens
- agents able to cause mutations in DNA - ionizing radiation - chemical carcinogens
50
why are cancer cells genetically unstable
- mutations that interfere with accurate replication - mutations that decrease DNA repair efficiency - mutations that increase occurrence of chromosomal breaks and rearrangements these overall give enhanced mutation rates
51
why type of advantage do cancer cells receive with mutations
competitive
52
what types of cells does natural selection favour
cells with mutations that enhance cell proliferation and survival
53
define angiogenesis
formation of new blood vessels
54
why may cancer cells cause angiogenesis
blood supply is required to feed all the cells of the tumour that are internal
55
what does invasion mean in the context of cancer
ability to digest and take over underlying tissue
56
define metastasis
ability to enter and exit blood or lymph, and colonize new regions of the body
57
what are some key attributes of cancer cells
1. reduced independence on signals from other cells due to mutations 2. less prone to apoptosis 3. immortality 4. genetically unstable 5. abnormally invasive 6. ability to survive and grow well in other tissues
58
how do Ras gene mutations support cancer cells
- unable to "turn off" due to mutation in GTPase activity - leads to uncontrolled proliferation
59
how do p53 mutations support cancer cells
- unable to trigger apoptosis for cells with damaged DNA in the checkpoint stage - leads to uncontrolled proliferation
60
what does it mean when we say cancer cells are immortal
able to divide over and over again
61
how does telomerase activity support cancer cells
telomerase expression occurs which maintains telomere length (not normally expressed in mature cells)
62
why are cancer cells considered abnormally invasive
- due to enzymes that make it this way - often lacking or have down-regulated cell-adhesion molecules (like cadherins)
63
define oncogenes
- genes involved in triggering cancerous characteristics in cells (permanently turned on) - generally mutants of normal genes involved in control of cell growth or division
64
define proto-oncogenes
genes that normally help cells grow and divide to make new cells (ex Ras)
65
describe dominant mutations
when only one mutant copy is required to have a significant impact on a cell
66
what genes are critical for cancer cells
oncogenes, tumour suppressor genes
67
describe tumour suppressor genes
genes that normally inhibit progress through cell cycle
68
why are tumour suppressor gene mutations considered recessive
both copies of the gene must be lost before effect on cell is seen
69
define overactivity mutations
gaining of function
70
define underactivity mutations
loss of function (p53, Rb)
71
draw out a flowchart of overactivity mutations
...
72
draw out a flowchart of underactivity mutations
....
73
how does chronic myeloid leukemia occur
mutation in Abl gene (which encodes tyrosine kinase) leads to a hyperactive kinase, causing repeated signaling for cell division
74
describe oncogenic kinase activity; what does it result in
- substrate protein and active oncogenic kinase are bound with ATP - ATP hydrolysis occurs and the phosphate keeps the substrate protein activated - leads to signal for cell proliferation and survival; - leukemia
75
how can oncogenic kinase activity be prevented
- Gleevec drug binds to ATP binding site of the kinase - prevents signals from being received - no leukemia (effective in leukemia treatment)

BIOL 2030 (16 decks)

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