Neoplasia II Flashcards

1
Q

Name the 4 types of carcinogens

A

chemical, radiation-induced, viral, bacterial

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2
Q

What occurs during the initiation step of chemical carcinogens? Promotion step?

A

irreversible mutations in the genome; tumor induction in previously initiated cells

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3
Q

What is the #1 target of chemical carcinogens?

A

DNA - RAS, p53

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4
Q

ionizing radiation induces DNA mutations and increases risk of ____ and ____ carcinomas

A

leukemia; thyroid

note: less likely to cause cancers of lung and breast

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5
Q

In regards to viral carcinogens, name the RNA and DNA viruses

A

RNA viruses: HTLV, HCV

DNA viruses: HPV, EBV, HBV

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6
Q

True or false? nonlethal genetic damage is at the heart of carcinogenesis

A

true

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7
Q

There are four classes of normal regulatory genes that are principal targets of genetic damage. Name them

A
  1. growth promoting proto-oncogenes
  2. growth inhibiting tumor suppressor genes
  3. genes that regulate apoptosis
  4. genes involved in DNA repair
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8
Q

Describe the sustained proliferative signal

A

proliferate without external signals. Usually a consequence of oncogene activation

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9
Q

_____ promote autonomous cell growth; their un-mutated cellular counterparts are called ____-____ and participate in signaling pathways that drive proliferation

A

oncogenes; proto-oncogenes

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10
Q

_____ are encoded by oncogenes and are able to promote cell growth in the absence of normal growth-promoting signals

A

oncoproteins

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11
Q

Cancer cells don’t respond to molecules that inhibit growth of normal cells. This is usually due to inactivation of what type of genes?

A

tumor suppressor genes

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12
Q

Tumor cells switch to aerobic glycolysis, this enables what?

A

rapid growth

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13
Q

What is the prototypic anti-apoptotic protein that can be overexposed in tumor cells to extend survival?

A

bcl-2

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14
Q

True or false? DNA repair genes are directly oncogenic

A

false; but permit mutations to occur in other genes that induce carcinogenesis

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15
Q

A defect in this DNA repair pathway is evident in hereditary nonpolyposis colon cancer syndrome

A

mismatch repair

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16
Q

A defect in this DNA repair pathway is evident in xeroderma pigmentosum

A

nucleotide excision repair

17
Q

A defect in this DNA repair pathway is evident in bloom syndrome, fanconi anemia, hereditary breast cancer syndromes

A

recombination repair

18
Q

Which of the following are possible mechanisms of evasion of the host response?

a. selective outgrowth of antigen-negative variants
b. loss or reduced expression of MHC molecules
c. activation of immunoregulatory pathways
d. secretion of immunosuppressive factors by tumor cells
e. induction of regulatory T cells
f. all of the above

A

f. all of the above

19
Q

Tumor clones compete with one another for survival and the “winners” tend to be more ____ over time

A

aggressive

note: cancer becoming resistant can be explained by selection of fittest cells