Genetic Basis of Cancer Flashcards

Matise's Lecture

1
Q

C-Myc causes cancer problems by _____

A

Overproduction

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2
Q

Why does (Unilateral) Sporadic Retinoblastoma form later and more rarely compared to familial?

A

Because two copies of the genes are usually still intact with sporadic “Double Hit hypothesis”

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3
Q

p53 two main functions:

A
  1. Halt Cell division (Inhibit CDK)
  2. Initiate Apoptosis (Bax)
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4
Q

C-Ras mutations cause cancer through___

A

Inactivation prevention; GTP ends up staying bound

(Reduce GTPase)

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5
Q

MDM2 is an anti-apoptotic gene that does what to p53?

A

It ubiquinates p53 and makes sure that cells don’t get killed or arrested.

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6
Q

C-Able proto-oncogene causes cancer problems through _____

A

Genetic Self Activation through Philadelphia chromosome

(Constitutive Activity of Protein Kinase)
transloc(9;22) (q(34;q11)

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7
Q

p14ARG does what to p53?

A

Competes against MDM2 and phosphorylates p53 so that it can do the killing and arresting.

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8
Q

The tumor supressor gatekeeper gene _____ inhibits the G1/S transition by inhibiting E2F

A

Rb
“The Arby and the ChE2F”

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9
Q

Rb and p53 are two important examples of _____ genes

A

Gatekeeper (Tumor Suppressor)

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10
Q

Two types of Tumor-Suppressor Genes

A
  1. Care taker Genes (repair) 2. Gatekeeper genes (stop cell divi)
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11
Q

Oncogene vs Proto-Oncogene

A

The proto-oncogene needs to be altered/mutated to become an oncogene.
- The Oncogene simply needs to be activated to run the risk of developing cancer

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12
Q

MLH, ERCC1, and BRCA are examples of ______ genes

A

Care Taker (Tumor Suppressor)

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13
Q

The Proto-Oncogene, mTOR, promotes cell _____

A

Growth

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