Lecture 1 Flashcards

1
Q

Number of divisions in mitosis vs meiosis

A
  • mitosis: 1 division

- meiosis: 2 divisions

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2
Q

Location of mitosis vs meiosis

A
  • mitosis: all tissues (somatic)

- meiosis: germ-line tissue (testis and ovary)

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3
Q

Passenger vs driver mutations

A
  • passenger mutations: no effect on cancer cell phenotype, doesn’t driver cancer initiation
  • driver mutations: causes clonal expansion
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4
Q

What can relapse after chemotherapy be associated with?

A

can be associated with resistance mutations (may predate treatment)

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5
Q

How is cancer development analogous to Darwinian evolution?

A

based on two constituent processes:

  • continuous acquisition of heritable genetic variation in individual cells by more-or-less random mutation
  • natural selection acting on the resultant phenotypic change
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6
Q

What do mutations that are acquired while the cell lineage is phenotypically normal reflect?

A
  • intrinsic mutations acquired during normal cell division

- effects of exogenous mutagens

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7
Q

How does having an older father affect cancer development?

A

leads to more de-novo mutations with increasing age of father

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8
Q

Example of a familial disease (germline disease) and precision therapeutics

A
  • cystic fibrosis caused by G551D (glycine to aspartate at codon 551) mutation
  • responds extremely well to kalydeco/ivacaftor (only works to improve CFTR protein gating)
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9
Q

Describe CFTR

A
  • CFTR: cystic fibrosis transmembrane conductance regulator (2 membrane spanning domains (MSD) that forms a channel)
  • cAMP-activated chloride ion (Cl-) channel
  • expressed in apical membrane of epithelial cells in lungs, liver, pancreas, intestines, reproductive tract, submucosal glands
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10
Q

Different mutations in CFTR

A
  • Class I and II: little to no functional CFTR (quantity at cell surface affected)
  • Class V and VI: some functional CFTR (quantity at cell surface)
  • Class III and IV: function of CFTR at cell surface affected
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11
Q

Trastuzumab

A

monoclonal antibody for breast cancer patients with HER2 over expression (blocks ligand binding)

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