31 - CANCER GENETICS 1 Flashcards

1
Q

what are the hallmarks of cancer

A
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2
Q

what does the src oncogene do

A

transforms normal cells to become insensitive to contact inhibition

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3
Q

what are some common inherited cancers for which genetic testing is available

A
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4
Q

what are oncogenes

A

positive regulators driving tumorigenesis

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5
Q

what are tumor suppressor genes

A

negative regulators that are inactivated in cancer

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6
Q

what are DNA repair genes

A

prevent mutations and maintain DNA integrity

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6
Q

what are proto-oncogenes

A

required for normal cellular function but when mutated become oncogenes and promote cancer formation

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7
Q

how was the tumor virus discovered

A

the first oncogene v-Src was isolated from Rous sarcoma virus

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8
Q

how do viruses cause cancer?

A
  • a retrovirus inserts its RNA into the cell
  • undergoes reverse transcription and inserts into host chromosome next to a proto-oncogene
  • when the virus reproduces, the proto-oncogene is incorporated into the virus
  • in repeated rounds of viral infection and reproduction, the proto-oncogene becomes rearranged, mutated or both
  • it produces an oncogene that is inserted back into the host chromosome
  • this leads to cancer formation when in normal cells
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9
Q

what is an alternative way that viruses can cause cancer

A
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10
Q

what are ways other than viral infections in which proto-oncogenes can be activated

A
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11
Q

what are receptor tyrosine kinases (RTKs)

A
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12
Q

how are RTKs coupled to Ras

A
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13
Q

what is the cascade after Ras has been activated

A
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14
Q

how is Ras activity controlled in normal cells

A
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15
Q

what happens when there has been oncogenic activation of Ras

A

glycine turns into valine

16
Q

what type of genes are proto-oncogenes

A

produce factors that stimulate cell division

17
Q

how are oncogenes expressed

A

tend to be dominant
one copy is enough to induce excessive cell proliferation

18
Q

what is an example of a reciprocal translocation associated with a cancer

19
Q

how does the translocation happen in Burkitt lymphoma

20
Q

how can reciprocal translocation cause chronic myelogenous leukemia (CML)

A

philadelphia chromosome: fusion between chromosome 9 and 22 is observed in 95% of people with CML
c-Abl is a protein kinase involved in many cellular processes (proto-oncogene)