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DND Unit 2 > Epidemiologic and Environmental Aspects of Cancer > Flashcards

Epidemiologic and Environmental Aspects of Cancer Flashcards

1
Q

What percent of malignant neoplasms are caused by environment?

A

80%

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2
Q

T or F, migrants and their descendants adopt the relative risk of the country that they move to. What does this imply?

A

T.can’t attribute everything to genetics. Matters where you came from and where you go.

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3
Q

Identify the three most common types of cancer (other than skin cancer) among men (incidence).

A

Prostate- 26%
Lung- 14%
Colon/Rectum- 14%

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4
Q

Identify the three most common types of cancer (other than skin cancer) among women (incidence)

A

Breast- 29%
Lung-13%
Colon/Rectum- 8%

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5
Q

Identify the three most common types of cancer (other than skin cancer) among men (death).

A

Lung-28%
Prostate-9%
Colon/Rectum-8%

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6
Q

Identify the three most common types of cancer (other than skin cancer) among women (death).

A

Lung-26%
Breast-15%
Colon/Rectum-9%

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7
Q

An environmental chemical must be activated by what molecule to be considered carcinogenic?

A

P450

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8
Q

What are the four groups of chemical carcinogens?

A
  1. Polycyclic aromatic hydrocarbons (benzo(a)pyrene)
  2. Aromatic amines (anilines)
  3. Nitrosamines
  4. Aflatoxins
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9
Q

What are some examples of Polycyclic aromatic hydrocarbon carcinogens?

A

-benzo(a)pyrene-anything with a diol or epoxide group-at risk any time you burn stuff

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10
Q

What are some facts of Aromatic amine carcinogens?

A
  • aniline
  • requires N-hydroxylation and sulfation
  • industrial and consumer products
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11
Q

What are some facts of nitrosamine carcinogens?

A

-carbonium intermediate-in preservatives in food (cheetohs)-2 amines in food react with nitrous acid in stomach

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12
Q

Where do aflatoxins come from?

A
  • moldy grains, nuts, corn especially in tropics
  • produced by aspergillus flavus
  • microsomal epoxidation is required to be a carcinogen
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13
Q

If an epoxide is formed during a P450 reaction, _____

A

the product becomes cytotoxic and mutagenic.

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14
Q

Outline Miller’s theory of carcinogenesis

A
  • CYP450 turns chemicals into active forms
  • metabolites become strong electrophiles
  • electrophilic species can chemically modify proteins, RNA, DNA
  • The bases can be attacked and cause frameshifts and mispairings

P450 generates electrophiles which screw with RNA/DNA.

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15
Q

What is the Ames test?

A

A rapid and inexpensive test for mutagens. Tests ability to mutagenize Salmonella typhimurium.

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16
Q

Generally all carcinogens are mutagens but not all mutagens are carcinogens, T or F?

A

False:

Mutagens are carcinogens but not all carcinogens are mutagens.

17
Q

A positive Ames test says what about the chemical?

A

it is mutagenic. It is assumed that it is already proven to be carcinogenic.

18
Q

How does the Ames test work?

A

Media is lacking His and the is plated with lots of His negative bacteria. The bacteria needs His to grow. Apply carcinogen to central disk on agar; if some His+ bacteria start to grow it is assumed that the carcinogen did this and thus it is mutagenic.

19
Q

T or F. Effect of a carcinogen is non-dose dependent in causing cancer

A

F

20
Q

Is carcinogenesis a quick or lengthy process

A

lengthy, requires time

21
Q

Carcinogens are specific to one type of cancer T or F?

A

T

22
Q

Which tissues are at the most risk of carcinogenesis?

A

tissues that continually divide (epithelium, bone marrow)

23
Q

The cellular triggers of carcinogenesis are _______. what does this mean?

A

stably inherited. Tumors are proliferations of clones of a malignant cell

24
Q

T or F, only stem cells can become malignant.

A

T. Fully differentiated cells cannot become malignant

25
Q

What are the two steps through which cancers develop?

A
  1. initiation

2. promotion

26
Q

What is initiation?

A

the irreversible effect of the carcinogen

27
Q

What is promotion?

A

A reversible step that requires the repeated application of a promoter (i.e. something that causes inflammation)

28
Q

What is the difference between a carcinogen and a tumor promoter?

A

carcinogens cause mutations, tumor promoters drive proliferation without causing more mutations.

29
Q

What happens if you reverse the order of cancer initiation and promotion.

A

Nothing. Think about the definitions of each.

30
Q

Smoking is a carcinogen or promoter?

A

Promoter. it has phenols that cause inflammation?

31
Q

How much time can be between initiation and promotion?

A

A long time. Skin cancer sometimes takes years to proliferate after it has mutated.

32
Q

What are some common promoters?

A

urethan, phorbol esters, bile acids, saccharin, phenobarbitol, butylated hydroxytoluene phenols.

33
Q

How do bile salts supports the idea that tumor promotion plays a role in development of human cancer?

A

they promote cancer in benign colon polyps in rats

34
Q

What is evidence that tumor promotion plays a role in development of human cancers?

A

Former smokers lose increased risk of cancer after 14 yrs smoke free. if only apply carcinogen, don’t get proliferation of cancer.

35
Q

Why is cancer more common among the elderly?

A
  • 2 hit hypothesis (LoH)
  • Lose tumor suppressors or gain oncogenes over time
  • Cancers take time to develop
  • Most are epithelial cancers (being old doesn’t put you at higher risk of every kind of cancer)
36
Q

What is the difference between somatic and germline mutations?

A

S can’t be passed on while G mutations can be transmitted to offspring

37
Q

Define epigenetic mutations.

A

These are not coded for in the DNA but are modifications that are added to proteins or DNA (as in methylation) that repress genes. They

38
Q

How can epigenetic mutations cause cancer?

A
  • methylation inactivates
  • messes with reading
  • they can silence a tumor suppressor
  • loss of methylation can activate an oncogene.

DND Unit 2 (15 decks)

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