3.8 Apoptosis/Cancer & 3.10 Cancer Flashcards

1
Q

Define apoptosis

A

Programmed cell death

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2
Q

Apoptosis is needed for

A

multicellular development

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3
Q

What are the 2 ways cells regulate cell death?

A

Intrinsic and extrinsic pathways

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4
Q

Intrinsic signals causing apoptosis

A
  • Deprivation of survival factors
  • DNA damage or senscence triggers cell death
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5
Q

Extrinsic signals that trigger apoptosis

A

Activation of death receptors by ligands from outside of cell

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6
Q

Purpose of apoptosis

A
  • To sculpt tissues during development (ex: neurons)
  • Allow for normal cell turnover (ex: epithelial, immune cells)
  • Remove damaged cells
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7
Q

What are characteristics of morphological changes due to apoptosis?

A
  • Cell shrinkage
  • Chromatin condensation
  • Membrane blebbing
  • Nuclear fragmentation
  • Formation of apoptotic bodies
  • No cell lysis

Susan Can’t Bake Nachos For Nick

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8
Q

Define caspase

A

the “hit man” of the cells

Chews everything up

Digests cellular proteins and causes death

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9
Q

How does caspase become active

A

Procaspase (inactive form of caspase) is activated by binding of cytoplasmic cytochrom C

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10
Q

Anti-apoptotic family members ___ cytochrome-C release

A

Inhibit

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11
Q

Pro-apoptotic family members ___ cytochrome-C release from mitochondria

A

Facilitate

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12
Q

What are the Bcl-2 family proteins and what are the types within those?

A

Anti-apoptotic (Bcl-2 and Bcl-XL)

Pro-apoptotic (Bax, Bad, Bim)

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13
Q

Steps for caspase activation by cytochrome C release

A
  1. cytochrome C binds to apoptotic protease activating factor 1 (Apaf1)
  2. Formation of CARD domain
  3. assembly of apoptosome triggered by release of dADP in exchange for dATP
  4. activation of procaspase-9
  5. caspase-9 cleaves and activates executioner procaspases
  6. caspase cascade leading to apoptosis
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14
Q

Steps for extrinsic apoptosis

A
  1. ligand on approaching cell binds to death receptors on the doomed cell
  2. death receptor gathers caspases with a death domain adaptor
  3. caspases become activated
  4. cell dies
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15
Q

How does a caspase know its supposed to be used for extrinsic apoptosis?

A

They have death domain adaptor sequences

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16
Q

Steps for intrinsic apoptosis

A
  1. apoptotic stimulus
  2. cytochrome C release
  3. Apaf1 binding
  4. caspase activation
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17
Q

Describe cancer cells

A
  • Proliferate without restraint
  • Ignore signals
  • Resistant to apoptotic signals
  • Degrade the restraining extracellular matrix
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18
Q

Define carcinoma

A

Cancers arising from epithelial cells

Most common

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19
Q

Define sarcomas

A

Come from CT or muscle cells

20
Q

Define leukemias and lymphomas

A

Cancers of WBC

21
Q

Cancer is a ___ cell disease from accumulated muations

22
Q

Each tumor is ___

23
Q

Define benign tumor

A

If it stays in its designated tissue

24
Q

Define malignant tumor

A

It can break out of its niche

25
Define metastatic tumor
It can colonize other tissues/sites Requires a lot of mutations
26
Types of cancer-associated genes
Proto-oncogenes Tumor suppressor genes
27
Define proto-oncogenes
Genes whose proteins promote cell growth or motility and promote tumorogenesis when hyperactivated
28
Define oncogenes
Mutated proto-oncogenes Can cause cancer
29
Define tumor suppressor genes
Protein products limit cell growth or survival and the cell's released from restraint when they're inactivated by mutation
30
Ways cancer genes can be mutated
Point mutation (GOF or LOF) Gene amplification Chromosomal translocation or deletion
31
For tumor cells to escape, they must adopt a more ___ phenotype
Mesenchymal
32
When tumor cells are mesenchymal, it allows them to be
more mobile and have more flexible cytoskeletons
33
What intermediate filaments do you have when changing from epithelial to mesenchymal phenotype?
Change from keratins to _vimentin_
34
What junctions do you have when changing from epithelial to mesenchymal phenotype?
Changing from desmosomes to _focal adhesions (integrins)_
35
Example of EMT
Cleft lip/cleft palate
36
Steps for mammalian palate fusion
1. Adhesion 2. Epithelial-mesenchymal transition (EMT) 3. Apoptosis and mesenchyme confluence
37
Example of growth factors and receptors in oncogenes and tumor suppressors
TGF-alpha EGFR
38
Example of intracellular messengers
RAS
39
Example of cell cycle regulators in oncogenes and tumor suppressors
Cyclin-D1
40
Example of tumor suppressors
P53
41
Example of apoptosis inhibitors
Bcl-2
42
Drugs to treat carcinomas that are DNA synthesis inhibitors
Methotrexate, fluorouracil, cisplatin
43
Drugs to treat carcinomas that are mitotic inhibitors
Taxol (stabilizes microtubules)
44
Specific pathway inhibitor drugs treat \_\_\_
carcinomas
45
Describe squamous cell carcinoma
* All red/red and white patches * Persistent hoarseness and oral ulceration * Unilateral nasal obstruction * Neck mass * Unexplained tooth mobility