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Biology 201 > Topic I > Flashcards

Topic I Flashcards

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1
Q

cell necrosis

A

injured cells rupture and damage neighbouring cells (to be avoided)

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2
Q

apoptosis

A

cells that 1) are no longer required or 2) are a threat are dismantled and provide nutrients for other cells (preferred way)

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3
Q

examples of cells that perform apoptosis

A
  • cells holding leaves to branches
  • tails of tadpoles
  • human cells that are cancerous or infected with viruses
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4
Q

preparation for apoptosis

A
  • procaspases are present - Bcl2 protects mitochondria
  • DNases are inactive
  • phosphatidylserines are hidden
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5
Q

(Apoptosis) step 1: the trigger

A
  • damage to mitochondria
  • damage to DNA
    (severe DNA damage has p53 turn on PUMA gene)
  • absence of survival signals (eg cell death of overproduced neurons to match # of neurons to # of target cells)
  • death signal from a T cell (uses its Fas Ligand memb. proteins to trigger apoptosis)
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6
Q

The T cell using its Fas Ligand memb. proteins is ____ signalling

A

contact dependent

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7
Q

(Apoptosis) Step 2: Activation of procaspases

A
  • procaspases when brought together are activated by proteolysis
  • damage to mitochondria releases Cyt c and procaspases are brought together
  • damage to DNA -> p53 -> PUMA -> Bcl2 inhibited -> Cyt c release
  • no survival signals -> no Bcl2 -> Cyt c release
  • death signal from a T-cell (Fas ligand -> Fas receptors -> procaspases brought together)
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8
Q

(Apoptosis) Step 3: Caspase cascade

A

caspases activate other procaspases = caspase cascade

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9
Q

caspases also ____ target proteins

A

cleave

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10
Q

(Apoptosis) Step 4: Cell Destruction

A
  • chromosomes destroyed (caspases indirectly activate DNases)
  • nuclear envelope dismantled (caspases directly destroy nuclear lamins)
  • cells round up and become apoptopic bodies
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11
Q

what technique labels apoptotic cells?

A

TUNEL technique

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12
Q

(Apoptosis) Step 5: Phagocytosis

A

apoptotic bodies consumed by neighbour cells (non-professional phagocytes) or macrophages (professional phagocytes)

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13
Q

why does phagocytosis happen

A

apoptotic bodies display phosphatidylserine phospholipids (“eat me” signal)

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14
Q

why chop up DNA?

A

to make apoptosis irreversible and to make apoptotic bodies safe to eat (destroy virus/cancer genes)

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15
Q

how many cell types are in the human body (mammals)

A

200

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16
Q

when do cells become specialized

A

when transcription cells turn on/off specific genes

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17
Q

when does cell differentiation begin in mammals

A

early in development

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18
Q

stem cells

A

cells that both reproduce & differentiate

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19
Q

are embryonic stem cells multipotent or pluripotent?

A

pluripotent - can become any cell type

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20
Q

where are stem cells found?

A

in tissues and organs where cell reproduction occurs

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21
Q

types of stem cells

A
  • blood (hematopoietic)
  • skin (epidermis)
  • gut (small intestine)
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22
Q

blood stem cells

A

produced in the blood marrow, adult stem cells are multipotent (can become one or more related cells)

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23
Q

skin stem cells

A

can reproduce (make another stem cell) or become differentiated (mature skin cell)

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24
Q

gut stem cells at the base of villi can become what?

A

absorptive and goblet cells

25
Q

what can embryonic stem cells be used for?

A
  • research (eg. adding heart TFs)

- scams (stem cell therapy)

26
Q

what can skin stem cells be used for?

A

to treat burns and wounds using autograph transplantation (person A -> person A)

27
Q

what can bone marrow stem cells be used for?

A

treat blood and bone marrow diseases using allograft transplantation (person A -> person B), donor = a family member or related stranger

28
Q

where are the bone marrow stem cells harvested from a donor?

A

the pelvis which has the most blood stem cells

29
Q

what can umbilical cord blood stem cells be used for?

A
  • research
  • allograft for another child
  • scams (private cord blood banks that promote autographs which won’t work)
30
Q

what can induced pluripotent stem (iPS) cells be used for?

A
  • research

- potential treatment (eg. to replace damaged neurons)

31
Q

cancer

A

cancer cells reproduce and spread inappropriately, risk of cancer goes up with age

32
Q

benign cells

A

reproduce when they are not supposed to

33
Q

malignant/cancer cells

A

reproduce when they are not supposed to and go where they are not supposed to

34
Q

what cancer is the most common cause of cancer deaths in mem and women?

A

lung cancer

35
Q

stages of cancer

A
  • initiation
  • progression
  • spread (metastasis)
36
Q

initiation

A

one mutation in one cell causes it and its offspring, to divide inappropriately.

37
Q

progression

A

more random mutations that increase reproduction, survival and spreading of the cancer

38
Q

spread (metastasis)

A

cells leave the primary tumour and establish secondary tumours

39
Q

are cancer cells ‘trying’ to get worse?

A

no, this is a misconception. Mutations are random and are detrimental or have no effect

40
Q

do cancer cells reproduce quickly?

A

no, a misconception. Cancer cells are defective and reproduce ~100 days per cell cycle (vs ~25 days for a healthy cell)

41
Q

are cancer cells in a tumour identical?

A

no, a misconception. Cells have different properties and vulnerabilities

42
Q

are cells in a tumour cancer cells?

A

most cells in a tumour are not cancer cells, cancer cells recruit normal cells for support

43
Q

what are three main reasons why cells become cancerous?

A
  • cancer critical genes
  • new (somatic) mutations
  • inherited (germline) mutations
  • ## viral infection
44
Q

cancer critical genes

A

encode proteins involved in the cell cycle. Tumor suppressor genes that inhibit cell cycle and proto-oncogenes that promote cell cycle can have mutations occurring

45
Q

new (somatic) mutation

A

mutation happens within the person

46
Q

inherited (germline) mutations

A

mutation is inherited from a parent

47
Q

viral infection

A

some viruses deliberately cause cancer to facilitate their own reproduction. Viral proteins inhibit or activate the proteins made by critical cancer genes

48
Q

(initiation) unregulated cell reproduction due to loss of tumour supressor genes

A

normal function: inhibit cell proliferation

cause cancer when non-functional (eg. RB1 gene, without Rb proteins, cells can’t pause at the G1 checkpoint)

49
Q

(initiation) unregulated cell reproduction due to proto-oncogene -> oncogene

A

normal function: stimulate cell cycle

cause cancer when the normal proto-oncogene becomes an over active oncogene (eg. HER2 gene)

50
Q

(progression) genetic instability

A

cancer cells acquire new mutations at more than the spontaneous rate (eg. mutations in the TP53 tumor suppressor gene)

51
Q

(progression) no apoptosis

A

some cancer cells do not perform apoptosis because genes such as TP53, PUMA, BCL2 have mutations

52
Q

PUMA is a _____ because too ___ PUMA proteins is dangerous

A

tumour suppressor gene… few

53
Q

BCL2 is a ___ because too __ BCL2 proteins is dangerous

A

proto-oncogene… many

54
Q

what proportion of human cancers have mutations in TP53?

A

> 50%

55
Q

(spread) induce angiogenesis

A

tumours cannot grow beyond 1-2mm in diameter without recruiting blood vessels

56
Q

(spread) invade neighbouring tissue

A

cancer cells spread if some of them dismantle the extracellular matrix (as if they were fibroblasts)

57
Q

(spread) metastasis to new cites

A

0.1% of cells survive to reach new sites to make a secondary tumour

58
Q

what proportion of human cancers are due to viral infection?

A

> 10%

Biology 201 (8 decks)

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