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601 - Exam 2 > 3.8 Apoptosis/Cancer & 3.10 Cancer > Flashcards

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

A

Stem

22
Q

Each tumor is ___

A

clonal

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
Q

Define metastatic tumor

A

It can colonize other tissues/sites

Requires a lot of mutations

26
Q

Types of cancer-associated genes

A

Proto-oncogenes

Tumor suppressor genes

27
Q

Define proto-oncogenes

A

Genes whose proteins promote cell growth or motility and promote tumorogenesis when hyperactivated

28
Q

Define oncogenes

A

Mutated proto-oncogenes

Can cause cancer

29
Q

Define tumor suppressor genes

A

Protein products limit cell growth or survival and the cell’s released from restraint when they’re inactivated by mutation

30
Q

Ways cancer genes can be mutated

A

Point mutation (GOF or LOF)

Gene amplification

Chromosomal translocation or deletion

31
Q

For tumor cells to escape, they must adopt a more ___ phenotype

A

Mesenchymal

32
Q

When tumor cells are mesenchymal, it allows them to be

A

more mobile and have more flexible cytoskeletons

33
Q

What intermediate filaments do you have when changing from epithelial to mesenchymal phenotype?

A

Change from keratins to vimentin

34
Q

What junctions do you have when changing from epithelial to mesenchymal phenotype?

A

Changing from desmosomes to focal adhesions (integrins)

35
Q

Example of EMT

A

Cleft lip/cleft palate

36
Q

Steps for mammalian palate fusion

A
  1. Adhesion
  2. Epithelial-mesenchymal transition (EMT)
  3. Apoptosis and mesenchyme confluence
37
Q

Example of growth factors and receptors in oncogenes and tumor suppressors

A

TGF-alpha

EGFR

38
Q

Example of intracellular messengers

A

RAS

39
Q

Example of cell cycle regulators in oncogenes and tumor suppressors

A

Cyclin-D1

40
Q

Example of tumor suppressors

A

P53

41
Q

Example of apoptosis inhibitors

A

Bcl-2

42
Q

Drugs to treat carcinomas that are DNA synthesis inhibitors

A

Methotrexate, fluorouracil, cisplatin

43
Q

Drugs to treat carcinomas that are mitotic inhibitors

A

Taxol (stabilizes microtubules)

44
Q

Specific pathway inhibitor drugs treat ___

A

carcinomas

45
Q

Describe squamous cell carcinoma

A
  • All red/red and white patches
  • Persistent hoarseness and oral ulceration
  • Unilateral nasal obstruction
  • Neck mass
  • Unexplained tooth mobility

601 - Exam 2 (11 decks)

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