20.4 Molecular Approaches to Cancer Treatment Flashcards

1
Q

the most effective way to deal with cancer is to ()

A

prevent the development of the disease

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2
Q

second-best way to deal with cancer is ()

A

reliable early detection of premalignant stages that can be treated easily

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3
Q

many cancers can be cured by () before they metastasize

A

localized treatment

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4
Q

why is it important to take into consideration the selectivity of drugs targeted for oncogenes

A

oncogene blocking can also affect proto-oncogene activity needed for normal cell function

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5
Q

most oncogene-targeted drug therapies target ()

A

specific oncogene proteins

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6
Q

() of oncogene proteins (e.g. protein kinases) are also being developed as a means of dealing with cancer

A

small molecule inhibitors

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7
Q

() is an inhibitor of the bcr/abl tyrosine kinase → blocks proliferation of chronic myeloid leukemia cells

A

imatinib or Gleevec

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8
Q

resistance to imatinib most often results from mutations of the bcr/alb domain that ()

A

prevent imatinib binding

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9
Q

imatinib is also a potent inhibitor of the (1) and the (2) → effective therapy for cancers that resulted from the oncogenic activation of the genes encoding these proteins

A
  1. PDGF receptor
  2. Kit tyrosine kinase
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10
Q

() is activated as an oncogene by point mutations resulting in constitutive protein kinase activity in 90% of gastrointestinal stromal tumors

A

Kit

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11
Q

(1) and (2) are small-molecule inhibitors of the EGF receptor that have shown activity against a subset of lung cancers in which EGF receptor is activated as an oncogene by point mutations

A
  1. gefinitib
  2. erlotinib
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12
Q

sensitivity of tumors to inhibition of activated oncogene

A

oncogene addiction

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13
Q

how can oncogene addiction be exploited in cancer treatment

A
  • targeting the activity of the activated oncogene becomes much more important than focusing on the pathways that the cancer has affected
  • in normal cells, alternative signaling pathways can compensate in one pathway is blocked
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14
Q

effectiveness of many oncogene-targeted therapies is limited by the development of ()

A

resistance

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15
Q

resistance can result from mutations in the (1), (2), and (3)

A
  1. targeted kinase
  2. activation of other tyrosine kinases
  3. activation of downstream oncogenic pathways
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16
Q

booster the immune response against cancer

A

immunotherapy

17
Q

one of the main strategies of immunotherapy involves genetic engineering to ()

A

create an enhanced immune response against tumor cells (e.g. targeting cancer surface cell receptors)

18
Q

blocking () of T cells has become an effective therapeutic strategy against cancer cells

A

down-regulaton

19
Q

T cells are normally regulated to prevent them from destroying normal tissues → but this ()

A

can hinder immune response against cancer cells

20
Q

() is expressed on T cell surfaces to regulate T cells by inducing apoptosis

A

PD1 (programmed cell death protein 1)

21
Q

T cells are genetically engineered to respond against a protein expressed by cancer cells

A

Car-T cell therapy

22
Q

in Car-T cell therapy, () is introduced into a patient’s T cells by viral infection

A

chimeric antigen receptor (CAR)