Cancer Flashcards

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1
Q

what is cancer?

A

abnormal regulation of cell growth and division.
invasion of areas where they don’t belong
increased cell division/decreased apoptosis

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2
Q

what is the difference between a benign and malignant?

A

malignant can spread

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3
Q

what causes cancer?

A

accumulation of mutations, older more likely to contract it

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4
Q

what are cancer stem cells?

A

invoke a new cancer when transferred into a new animal

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5
Q

what is contact-inhibition?

A

normal cells stop growing when they touch, cancers just go all out man

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6
Q

what is metastasis?

A

spread of cancer cells, digest basal lamina and squeeze between them to travel in blood vessel. adheres to blood vessel wall to squeeze into a new space

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7
Q

what is angiogenesis?

A

formation of new blood vessels inside cancer ball of cells. vascular endothelial growth factor secreted

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8
Q

what is ames test of mutagenicity?

A

testing compounds to see how well they cause mutations (if highly mutagenic will likely cause cancer) (compound, histidine-dependent salmonella, and liver to see how its gonna be modified)

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9
Q

what are cancer-critical genes?

A

if u fuck up these genes ur gonna get cnacer

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10
Q

what are 2 classes of genetic mutations in cancer?

A
  1. proto-oncogenes- genes that have proteins associated with cell cycle regulation
  2. tumor-suppressor genes-inhibit cell cycle, needs mutation on both chromosome copies
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11
Q

how do proto-oncogenes get mutated?

A

deletion/point mutation in coding sequence, regulatory mutation (promoter sequence), gene amplification, chromosome rearrangement

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12
Q

how do tumor suppressor genes get mutated?

A

nondisjunction causes chromosome loss->duplication
mitotic recombination
gene conversion during mitotic recombination
suppressor gene is gone
point mutation, not expressed for working properly

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13
Q

what are epigenetic genes?

A

genes sequences not affected, it’s about how your genes are packaged into chromatin.
genes accidentally packed in heterochromatin and it never gets expressed->division
genes accidentally methylation

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14
Q

what is a driver mutation?

A

the cell that drives the cells around it towards cancer

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15
Q

what is a passenger mutation?

A

cells that get affected by a driver mutation

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16
Q

what are 3 signaling pathways that are commonly involved in tumors?

A

Rb, RTK/Ras/PI3K, P53

17
Q

how does HPV turn malignant?

A

virus integrates itself into the genes

18
Q

how does viral protein e7 affect Rb?

A

it binds to Rb and so the proliferation factor thats supposed to be inhibited isnt so its over active

19
Q

how does viral protein e6 affect p53?

A

e6 binds to p53 to inactivate it and so cell cycle does not stop

20
Q

what is RhoC?

A

small GTPase that regulates actin-based cell motility

can be linked to metastasis

21
Q

what is epithelial-to-mesenchymal transition?

A

loss of adhesiveness, loss of cadherins

22
Q

normal cells usually have ____ dna repair pathways.

A

2

23
Q

why do tumor cells lose a dna repair pathway?

A

genetic instability

24
Q

how do tumor cells use multidrug resistance?

A

they amplify Mdr1 to pump drugs out of a cell

25
Q

how doe tumor specific antibodies work?

A

they bind to tumor cells and natural killer cells kill it LOL

26
Q

how do tumor-specific antibodies conjugated to toxins work?

A

antibody binds to tumor cell and the toxin tagged on it gets absorbed

27
Q

how do tumor-specific antibodies conjugated to radioisotopes work?

A

antibody binds to tumor cell and the radiation kills the tumor cell and neighboring tumor cells

28
Q

how does CML occur?

A

Bcr and Abl gene mixed

29
Q

what does Gleevec do?

A

gleevec blocks mutated kinase from phosporylating target protein and stops over activity

30
Q

why should you treat cancer cells with multiple drugs?

A

no cell is resistant to both drugs so cancer is cured

if done one at a time then cells will keep mutating and becoming resistant

31
Q

what is immune therapy?

A

boost in immune system to better recognize cancer cells

32
Q

what is PD1 and how does it relate to cancer?

A

programmed cell death protein can get inhibited by tumor cells