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Oncology > Chapter 11 > Flashcards

Chapter 11 Flashcards

1
Q

Does diet play a role in carcinogenesis?

A

Yes, diet plays both a preventive and causative role in carcinogenesis.

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2
Q

what are the basic food groups?

A

Carbohydrates, fats, and proteins.

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3
Q

What are the four major groups of dietary antioxidants?

A
  1. Vitamin C
  2. Isoprenoids (Vitamin E)
  3. Flavonoids
  4. Organosulfur compounds
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4
Q

Do nutrients have an effect on gene expression?

A

Yes, micronutrients and combinations of nutrients can have an effect on gene expression. Some may even work in a preventive manner while others may induce cancer.

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5
Q

What three main aspects can ve considered as causative in our diets?

A
  1. Food can carry carcinogenic substances
  2. Lack of certain nutrients can increase the risk of cancer
  3. Worldwide issues, like CVD, obesity, and alcohol can increase the risk of cancer.
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6
Q

How does healthy food like salmon increase the risk of cancer?

A

Salmon can accumulate pollutants from the water during their lifetime, and those pollutants may end up in our diet.

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7
Q

What other factors can influence the cancer-causing properties of food?

A

The way food is prepared and the way it is stored.

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8
Q

Deficiency in what nutrient can increase the risk of colorectal cancer? What kind of nutrient is it?

A

Deficiency in folate. Folate is part of the B vitamins.

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9
Q

What does folate affect?

A

Folate is a co-enzyme in nucleotide synthesis and DNA methylation. Disruption of DNA synthesis can lead to unstable DNA.

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10
Q

What DNA aberrations are visible in those with a deficiency in folate?

A
  1. Strand breaks, due to unstable DNA and failure to repair.
  2. Uracil misincorporated into the DNA.
  3. Hypomethylation
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11
Q

What example of the mechanisms of action does obesity have as a tumor promoter?

A
  1. altered sex hormone metabolism
  2. Generating more fat cell hormones called adipokines
  3. Increased insulin signaling pathways
  4. Alterations in gut microbiota
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12
Q

How does altered cholesterol production in obese people lead to cancer?

A

Adipose tissue can use its contents to create steroid hormones like estrogen and cholesterol. A metabolite of cholesterol and estrogen (27HC) can activate some receptors at high concentrations and put carcinogenic pathways in motion.

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13
Q

How does the inflammatory mechanism of fat cells promote cancer?

A

Fat can induce an inflammatory response after releasing adipokines. The inflammatory response contains tumor-promoting cytokines.

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14
Q

How does an altered hut bacteria configuration promote cancer?

A

The metabolite called “deoxycholic acid” is produced by a certain kind of bacteria in the gut. It is derived from bile contents that are released while eating fat. Deoxycholic acid is taken up to the liver where it can cause DNA damage.

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15
Q

How does alcohol lead to a higher risk of cancer?

A

Alcohol is metabolized into an aldehyde by Alcohol Dehydrogenase. The aldehyde binds to DNA and causes DNA adducts. This poses a greater risk for cancer development.

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16
Q

Do fruits and vegetables lead to a lower risk of cancer?

A

Yes, fruits and vegetables are proven to have an inverse association with the risk of cancer.

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17
Q

How do fruits and vegetables prevent DNA damage?

A
  1. some micronutrients found in fruits and vegetables are free radical scavengers, which prevent DNA damage from ROS.
  2. Fruits and vegetables induce the gene transcription of Phase I and Phase II enzymes, which aid in the metabolism of xenobiotics.
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18
Q

How are Phase I reactions related to cancer?

A

Phase I reactions can convert pro-carcinogens to ultimate carcinogens and it usually generates highly electrophilic molecules.

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19
Q

How do Vitamin C and Vitamin E help against free radicals?

A

They both donate an electron to ROS. They lose an electron in the process and eventually get degraded. This is why those vitamins must be replenished daily.

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20
Q

What is meant by nutrigenomics?

A

The study of how certain nutrients can alter gene expression.

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21
Q

What crucial link is there between micronutrients and preventing DNA damage?

A

Some micronutrients can lead to the expression of genes coding for antioxidant molecules. The genes are expressed after activation by an Antioxidant Response Element (ARE).

22
Q

How is gene transcription activated through ARE?

A

They are mediated by the transcription factor Nrf2 and Maf complex.

23
Q

Describe the pathway of gene activation through ARE.

A

KEAP1 is a repressor of Nrf2. When KEAP1 is bound to Nrf2, it flags it for degradation. When ROS is present in the cell, it reacts with cysteines on the KEAP1 molecule, preventing it from degrading Nrf2. Nrf2 and Maf then form a complex and bind to DNA, inducing gene transcription of Phase II enzymes.

24
Q

Can Nrf2 protect cancer cells as well?

A

Yes, Nrf2 is also highly expressed in cancer cells. This helps cancer cells in metabolizing drugs and eliminating them through a Phase II reaction, hereby giving cancer cells drug resistance.

25
Q

Except the prevention of DNA damage through antioxidants, what other two methods do fruits and vegetables have to protect against cancer?

A
  1. Regulation of cell proliferation
  2. Regulation of apoptosis

*Garlic has all the three mechanisms.

26
Q

Through what mechanism can the chemical compound of green tea (EGCG) help against cancer?

A
  1. It binds to the cysteines of KEAP1, preventing it from binding to Nrf2.
  2. EGCG binds to DNA methyltransferase and can potentially prevent the methylation of tumor-suppressor genes.
27
Q

What is the Warburg effect?

A

The Warburg effect is a condition in which cancer cells convert glucose to lactate in the presence of oxygen.

28
Q

How does too much Acetyl CoA affect gene transcription?

A

Acetyl CoA is used as a substrate for the acetylation of histones. Too much ACoA can be used by cancer cells to acetylate histones and express genes.

29
Q

What two mechanisms lead to altered metabolism in cancer cells?

A
  1. Genetic alterations

2. Response to Hypoxia via HIF-alpha 1

30
Q

What is the role of AMPK in a cell?

A

AMPK senses a low energy state by binding to increased levels of AMP and decreased levels of ATP. AMPK then gets activated by LKB1. Active AMPK then increases ATP production and decreases consumption.

31
Q

What is the link between AMPK and p53?

A

AMPK activates p53 in a low-energy state of the cell. p53 then activates cell arrest until energy is restored.

32
Q

Can differences in metabolism among individuals affect the risk of cancer?

A

Yes, some individuals can gain the ability to process some metabolites faster. It can prevent one type of cancer to arise but makes then susceptible to another one. This can be seen in combination with a poor/wrong diet.

33
Q

Why do albinos have a higher chance of skin cancer?

A

Their skin cannot produce melanin and is more susceptible to sunlight. DNA damage is more likely to occur and accumulate in the skin of an albino.

34
Q

What is the link between vitamin D and cancer risk?

A

Deficiency in Vitamin D seems to make individuals more prone to developing cancer.

35
Q

How can Vitamin D inhibit cell growth and differentiation?

A
  1. Vitamin D is a dominant-negative ligand for EGFR that binds to the receptor instead of EGF, preventing growth signal transduction.
  2. Vitamin D can indirectly activate the transcription of tumor-suppressor genes BRCA1 and p21.
  3. Vitamin promotes apoptosis through mitochondrial signaling, independent of caspase activation. It enables Bak/Bax to form holes in the mitochondria.
36
Q

What hormone plays an important role in the formation of breast cancer?

A

Estrogens (Estradiol and estrone)

37
Q

Why are early menarches and late menopauses an indication that women may be at risk of developing cancer initiated by hormones?

A

Early menarche and late menopause mean an extended time in which the ovaries produce estrogens.

38
Q

How does obesity increase the risk of breast cancer?

A

Adipose tissue becomes the main producer of estrogens in the post-menopausal period.

39
Q

What are the two models to explain how estrogens cause breast cancer?

A
  1. Estrogens can promote cell proliferation and gives the cell less time to correct DNA damage as it progresses through the cell cycle.
  2. Estrogen and its metabolites are genotoxic. It can form adducts to DNA and inflict DNA damage.
40
Q

What is chemoprevention?

A

Foods and nutrients that can prevent, inhibit, and reverse the effects of carcinogenesis.

41
Q

What therapeutic strategies are made to counter cancer in terms of nutrients and metabolism?

A
  1. Chemoprevention with adequate diets
  2. Drugs that inhibit metabolic pathways
  3. Drugs that target estrogen
42
Q

What is the role of aromatase?

A

Aromatase converts androgens to estrogens.

43
Q

What are the four mechanisms through which obesity can increase the risk of cancer?

A
  1. Sex hormone metabolism (fat cells and estrogen)
  2. Increased adipocyte hormone adipokine (causes inflammation that promotes tumor growth)
  3. Increased insulin signaling pathways (free fatty acids that increase insulin levels - tumorigenic effect)
  4. Alterations to gut microbiota (modified bile acids to deoxycholic acid, which damages liver DNA)
44
Q

What is controversial about Beta-Carotene?

A

While thought to decrease the risk of cancer in people, it increased the risk even more in smokers while healthy people were untouched.

45
Q

What are examples of causative factors?

A
  1. Carcinogenic contaminants
  2. Deficiencies of a certain nutrients
  3. Obesity
  4. Alcohol consumption
46
Q

Where can PAHs be found?

A
  • smoke, industry, car exhaust
  • Burned organic material (BBQ)
  • smoked food
  • burned fat
47
Q

What are some examples of the functions of folate?

A
  • Co-factor in DNA methylation by MTHFR

- Folate aids in dTMP production (dTMP is made into T base in DNA)

48
Q

How do bacteria in the mouth increase the risk of mouth cancer?

A

Bacteria transform alcohol into acetaldehyde, which is an intercalating factor that forms adducts and damages DNA.

49
Q

What three important compounds does garlic contain and what do they do?

A
  1. Organosulfur: scavenger and Phase II enzyme.
  2. Ajoene: apoptosis
  3. Allicin: Inhibits proliferation
50
Q

What does Reversatrol in wine do?

A

Reversatrol inhibits the Warburg effect of cancer cells.

51
Q

What are some examples of polymorphism in cancer metabolism?

A
  1. MTHFR: cancer risk increase with lack of folate
  2. N-acetyltransferase: risk increases when compounds of cooked red meat come into play
  3. Tyrosinase deficiency: No melanin production (albinism) - making the person more susceptible to UV damage
  4. Fymaryl enzyme: makes more untimate carcinogen from pro-carcinogens in a shorter period of time

Oncology (8 decks)

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