425 Flashcards

1
Q

Are mutations that cause cancer permanent?

A

Yes

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2
Q

What do mutations in oncogenes do/

A

Cause cell to reject normal functions one by one

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3
Q

Common solid tumors come from cell lines

A

That frequently divide

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4
Q

What types of cells can tumors arise from?

A

Any and all, including stem cells

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5
Q

Is cancer subject to natural selection? What type?

A

Yes, cells best for tumor growthP

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6
Q

Precancerous

A

Showing signs of cancer but not the full criteria

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7
Q

Tumor suppressor gene

A

encode proteins that restrain cell growth and prevent cells from becoming malignant

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8
Q

Oncogene

A

encode proteins that promote the loss of growth control and the conversion of a cell to a malignant state. Usually accelerate cell division.

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9
Q

proto-oncogenes,

A

with the potential to subvert the cell’s own activities and push the cell toward the malignant status

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10
Q

If genes are mutated or deleted

A

The protein can have an altered structure/function

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11
Q

If genes are duplicated

A

They can be synthesized to a greater degree

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12
Q

If genes are translocated

A

Proteins can be up or down regulated or combined with other proteins,

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13
Q

Mutations make proteins…

A

Less responsive to normal growth controls

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14
Q

Are oncogenes dominant or recessive?

A

Dominant

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15
Q

Cells won’t become cancerous if their _________ are intact

A

Tumor suppressor genes

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16
Q

How can someone have a mutated form of a tsg and not get the cancer?

A

Their other copy is intact

17
Q

What does pRB do?

A

Regulates passage from G1 to S phase

18
Q

Why is p53 so important?

A

Binds to a lot of proteins to prevent tumor growth

19
Q

What does p53 do?

A

Alters cell cycle regulation, apoptosis, and/or senescence in response to stress. altering the expression of a large number of genes involved in cell cycle regulation, apoptosis, and/or senescence. When levels get too high (because protein doesn’t degrade) cell stops reproducing, and can either lead to repair or apoptosis/necrosis

20
Q

How does p53 degrade?

21
Q

even if a “crucial” gene such as RB or TP53 is not mutated or deleted, the function of that gene

A

can be affected as the result of alterations in other genes whose products are part of the same pathway as the “crucial” gene.

22
Q

What makes cancer susceptible to chemo/radiation?

A

They don’t follow pathways that’d fix their damage or kill off cells that are too badly damaged to survive

23
Q

Why are cells with a mutant p53 so bad?

A

Won’t die when they’re damaged

24
Q

Senescence

A

Ability to stop growth (but may or may not be metabolixally active)

25
BRCA mechanism
1. DNA damage causes ds breaks 2. BRCA genes fix them, or not if they're mutated 3. p53 level rises uninhibited by MDM2 4. Gene activation of p21 (causing cell cycle arrest) or BAX (causing apoptosis)
26
Is cancer associated with more or fewer receptors? How does this work?
More, divide with less growth hormone
27
Raf
Controls growth, can very well be oncogene