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Cancer Biology > Bad Cancer > Flashcards

Bad Cancer Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What is the most common cancer in males and females?

A

Lung cancer

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2
Q

What is the second most common cancer in males?

A

CRC

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3
Q

What is the second most common cancer in females?

A

Breast

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4
Q

What is the third most common cancer in females?

A

CRC

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5
Q

What influences the development of CRC?

A

Diet

  • meat and increased dietary fat increases risk
  • fruit, veg, folate intake decrease risk
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6
Q

What are the therapies for CRC?

A

Surgery (almost all patients)
Chemotherapy - 5-FU
Radiotherapy

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7
Q

What is the common metastatic location for CRC?

A

The liver

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8
Q

Which lifestyles have a higher chance of developing CRC?

A

Western lifestyle

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9
Q

If you eat meat regularly, how much does your chances of developing CRC increase?

A

68%

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10
Q

If you red eat meat regularly, how much does your chances of developing CRC increase?

A

~130%

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11
Q

If you smoke regularly, how much does your chances of developing CRC increase?

A

~50%

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12
Q

What carcinogens are found at high levels in cooked meats?

A

Heterocyclic amine

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13
Q

What does marinading your meat cause?

A

A decrease in heterocyclic amine carcinogens

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14
Q

Give an example of a heterocyclic amine carcinogen

A

PhIP

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15
Q

How does PhIP induce cancer?

A

It is metabolised by the cytochrome P450, CYP1A2 -> addition of a hydroxyl group -> very reactive and reacts with DNA

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16
Q

How can you investigate the functioning of P450 enzymes?

A

Genotyping by ‘Tagman’
- take a finger print and do a PCR -> split them into groups, those with functioning enzyme, those with an inactive form and a heterozygous group which have reduced activity of enzyme

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17
Q

How does smoking cause cancer?

A

The inert protein is metabolised by the P450 enzymes continuously until it has lots of functional groups and causes DNA damage

18
Q

What protects us against smoking?

A

Enzyme such as glutathione-S-transferases which detect the protein with lots of functional groups and releases glutathione

19
Q

What is glutathione?

A

A cytoprotective compound

20
Q

What does glutathiones structure consist of?

A

Glycine
Cysteine
Glutamic acid

21
Q

Name 2 polymorphisms of glutathione-S-transferases

A

GSTM1

GSTT1

22
Q

Name two compounds which increases carcinogen activation

A

CYP1A1

CYP2C

23
Q

Name 2 compounds which reduce detoxification of carcinogens?

A

GSTM1

GSTM2

24
Q

Name 2 protective alleles

A

GSTT1

GSTP1

25
Q

When APC binds to beta-catenin, what does it induce?

A

Degradation of beta-catenin

26
Q

What happens if APC is not bound to beta-canenin?

A

beta-catenin accumulates and enters the nucleus and binds to T-cell factor -> transcription of genes and cell division

27
Q

Why is beta-catenin likely to be mutated?

A

Since it is a large protein

28
Q

Where are intestinal cells created?

A

At the bottom of the crypt where the stem cells are

29
Q

How do mutations in APC or beta-catenin form the polyp?

A

get a progenitor-like phenotype and accumulate

They are unable to continue outward migration

30
Q

How many CRC are APC mutant?

A

~70%

31
Q

What happens if you get a mutation in familial adenomateous polyposis (FAP)?

A

Get familial cancer syndrome

They form 100s/1000s of polyps in their colons and therefore have a large chance of developing cancer

32
Q

What commonly happens to FAP mutated patients as a preventative measure?

A

Have a large part of their bowel removed

33
Q

What cancer most commonly has p53 mutations?

A

Ovarian

34
Q

where do p53 mutations occur?

A

In hotspot regions

35
Q

What cancers typically have Ras mutations?

A

CRC
Pancreatic cancer
NSCLC

36
Q

What cancers typically have Raf mutations?

A

Melanomas
CRC
Esophageal
Ovarian

37
Q

What codon of Ras is highly mutated?

A

13

38
Q

Are APC, p53 and Kras mutations all needed in CRC?

A

No, any one of them or combinations of any of them can cause cancer

39
Q

When do Kras mutations commonly occur in CRC?

A

Later on in CRC development (Duke’s C)

40
Q

What is Kras mutations associated with?

A

Poor survival

41
Q

What monoclonal antibody targets EGFR?

A

Cetuximab

Cancer Biology (13 decks)

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