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Clinical Nutrition 1 > Nutrition and Cancer > Flashcards

Nutrition and Cancer Flashcards

1
Q

What is the leading cause of death in developed countries?

A

Cancer

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2
Q

What suggests that cancer is largely environmental, and not genetic?

A

Differences in cancer prevalence worldwide, and changes in populations that migrate to western countries

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3
Q

Why does cancer develop? (3)

A

Due to interactions between genetic background, endogenous milieu and exogenous exposures

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4
Q

Why is a very important risk factor for cancer?

A

AGE - as cancer takes awhile to develop

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5
Q

Most prevalent type of cancer in men? Women?

A

Prostate, breast

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6
Q

What is the deadliest type of cancer in men? Women?

A

Lung

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7
Q

Define cancer

A

Uncontrolled growth abnormal cells in the body

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8
Q

Name some characteristics of cancerous cells

A
  • Escape normal growth signals
  • Can avoid programmed cell death
  • Avoid immune surveillance,
  • Can invade other tissues
  • Develop angiogenesis
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9
Q

Synonyms of cancer?

A

Malignant tumors, neoplasms, carcinoma

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10
Q

(T/F) Benign tumors are cancerous

A

False -as the do not invade and mestastasize

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11
Q

What is carcinogenesis?

A

The process of cancer development (ONCE the cancer has developed)

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12
Q

What is the 3-step classical view of carcinogenesis?

A
  • Initiation
  • Promotion
  • Progression
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13
Q

_____ will promote cell-growth and division

A

Proto-oncogenes

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14
Q

_____ will inhibit cell-growth and survival

A

Tumor suppressing genes

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15
Q

Explain the 3-step classical carcinogenesis

A

Begins with initiation, where there is a single cell with DNA damage, becoming a cancerous cell which will undergo proliferation and eventually form a mass –> Tumor

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16
Q

Is DNA damage normal?

A

Yes, but we have tumor suppressing genes which will inhibit cell-growth and survival

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17
Q

Explain the multi-stage modern view of carcinogenesis

A

The DNA damaged cell may mutate and proliferate, inactivating a DNA repair gene and change proto-oncogenes into oncogenes which will promote cell-growth and division –> ultimately by inhibiting tumor-suppressing genes, eventually leading to the formation of a cancerous mass.

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18
Q

In multi-stage carcinogenesis, what may there be defects in? What does it contribute to?

A
  • Terminal differentiation
  • Growth control
  • Resistance to cytoxicity
  • Programmed cell death
  • -> Selective clonal expansion
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19
Q

In multi-stage carcinogenesis, what is activated? Inactivated? What does this contribute to?

A
  • Activation of protooncogenes
  • Inactivation of tumor-suppressor genes
  • Inactivation of genomic stability genes
  • –> Selective colonal expansion
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20
Q

Initiated cell —> Preneoplastic lesion is progressed by what?

A

Selective colonal expansion

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21
Q

Preneoplasti lesion —> Malignant tumor is progressed by what?

A

Genetic change

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22
Q

Malignant tumor –> Clinical cancer is progressed by what?

A

Genetic change

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23
Q

Clinical cancer –> ______

A

Cancer metastasis, through genetic change

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24
Q

There are strategies at ____ to prevent cancer

A

every step of the way

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25
Q

Anti-initiation strategies?

A

Limit the development of the first, altered cell.

Limit genetic and epigenetic alteration

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26
Q

Anti-initiation strategy mechanism? (4)

A
  • Alter carcinogen metabolism
  • Enhance carcinogen detoxification
  • Scavenge electrophiles/ROS
  • Enhance DNA repair
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27
Q

Anti-promotion/progression strategies?

A

Limit the initiated, DNA damaged cell to developing into the preneoplastic stage.
Limit and increases in cell proliferation, additional genetic and epigenetic alterations.

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28
Q

Anti-promotion/progression strategy mechanisms?

A
  • Scavenge ROS
  • Decrease inflammation
  • Suppress proliferation
  • Enhance apoptosis
  • Enhance immunity
  • Discourage angiogenesis
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29
Q

How can the expression of one gene (i.e. phenotype) be increased?

A
  • Higher penetrance

- Epigenetic’s (environment, including nutrition)

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30
Q

the higher the penetrance, the ____ likelihood of the gene expressing it’s phenotype

A

greater

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31
Q

Define gene mutation

A

Structural change in the base pair sequence of DNA, may be inherited or due to exogenous factors

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32
Q

Which gene mutation is notable for increasing risk of beast and ovarian cancer? Why?

A

BRCA1 gene, high penetrance

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33
Q

Define polymorphisms

A

Structure of the gene varies amongst individuals, may or may not show phenotypes

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34
Q

(T/F) Polymorphisms are less common than gene mutations

A

FALSE - PM are more common

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35
Q

(T/F) Polymorphisms are more common than GM, but display LESS penetrance than GM

A

True

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36
Q

Example of polymorphisms?

A

SNP

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37
Q

What are SNPs?

A

Will affect response of genes to certain exposures, do NOT affect the reading of the gene

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38
Q

If an SNP is never exposed to _____ it may remain dormant

A

the right exposure

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39
Q

Define epigenetic changes

A

Affect gene structure, function and expression

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40
Q

Most common epigenetic changes?

A

DNA methrylation

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41
Q

What could cause the silencing of tumor suppressing genes, leading to increased cell growth and division?

A

DNA hypermethylation

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42
Q

What is a known epigenetic effect that could cause cancer cells to grow and proliferate?

A

DNA hypermethylation of tumor-suppressing genes

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43
Q

Define nutritional genomics and proteomics

A

The interaction between diet, genes and their products

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44
Q

(T/F) the greatest impact of bioactive food components is their direct effect on DNA

A

False, will impact more the epigenomic

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45
Q

What is the epigenomic?

A

Expression of mRNA and post-translational modifications of the protein

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46
Q

Knowing diet-gene interactions primarily impact the epigenome, how are proteins affected?

A

Structure of proteins, transport, enzymes and signalling by phosphorylation, glycosylation

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47
Q

How may bioactive food components directly impact DNA?

A

Oxidative damage to DNA from carcinogenic food products

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48
Q

What are the main possible causes of cancer?

A

-Tobacco, diet, obesity

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49
Q

What % does UV rays, pollution and professional exposure play in development of cancer?

A

Only 2-5% each, small

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50
Q

What do all the possible causes of cancer play on?

A

The individuals genetic variability

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51
Q

Dietary sources of carcinogens that may cause oxidative damage ?

A
  • Oxidized PUFA, free iron, nitrosamines

- Glycophosphates from pesticides

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52
Q

Dietary components that may reduce oxidative damage?

A

Antioxidant nutrients (Vit C, E, A) or cofactors in antioxidant enzymes (selenium, copper)

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53
Q

What may regulate cell proliferation and differentiation?

A

Vitamins A and D, interact with promoter regions of many genes

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54
Q

Which nuclear receptors are activated by oxidized fats?

A

PPAR-alpha

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55
Q

What can affect gene expression in cell culture?

A

Catechins (green tea, apples, chocolate)

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56
Q

What should be considered about in-vitro studies?

A

When any cell is exposed to something new in-vitro, there will be an effect and should be replicate in animal models..

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57
Q

Examples of roles of bioactive food components on carcinogenesis?

A
  • DNA repair
  • Cell differentiation
  • Hormone regulations
  • Carcinogen metabolism
  • Inflammatory response
  • Apoptosis
  • Cell growth cycle
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58
Q

Define incidence

A

New cases diagnosed

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59
Q

Define prevalence

A

All cases present at time of evaluation

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60
Q

Define mortality (cancer)

A

Number of cancer deaths, and related to each cancer.

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61
Q

Why are breast and prostate cancers more prevalent despite lunch and bronchus cancer being the highest cause of mortality?

A

Diagnosis and breast and prostate cancer is much easier, and can be made at an earlier stage.

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62
Q

Explain the diagnosis of prostate cancer

A

PCA protein measured through a simple, annual blood test and can be treated immediately

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63
Q

Explain the diagnosis of breast cancer

A

Self-breast examinations, and every 2 year mammographs for women over 50.

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64
Q

Diagnosis of lung cancer?

A

Much more harder to diagnose, as it is an internal organ and may not present symptoms, and typically picked up in a routine x-ray

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65
Q

Issue with lung cancer?

A

Even if diagnosed early, aggressive. Diagnoses are typically later

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66
Q

Describe our current population and how this relates to cancer incidence

A

Larger and agin population. Since we know the greatest risk factor for cancer is AGE, naturally we will have a higher incidence of cancer.

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67
Q

When adjusted for age and population growth, have incidences of cancer increased since 1987?

A

No

68
Q

When adjusted for age, has incidence of cancer increased in men? Women?

A

Women remains the same, while men slightly declines

69
Q

Trends in cancer mortality?

A

NUMBER of cancer has increased over time, and cancer remains the leading cause of mortality, however cancer mortality has DECREASED overall.

70
Q

What may explain the decrease in cancer mortality from men?

A

Less smoking

71
Q

Why has cancer mortality from smoking decreased?

A

Public health messages on smokin cessation

72
Q

Why has lung cancer mortality increased for women after 1987?

A

In general, women started smoking after men

73
Q

What is much more aggressive in pre-menopausal women?

A

Breast cancer (responsiveness to estrogens, which are mitogens)

74
Q

Cancer mortalities 0-14?

A
  • Brain/CNS
  • Leukema
  • Connective tissue
  • Bone
  • Kidney
75
Q

Cancer mortalities 15-29?

A
  • Brain/CNS
  • Leukemia
  • Bone
  • CT
  • Non-hodgkins lymphoma
  • Colorectal
  • Melanoma
76
Q

Cancer mortalities 30-49?

A
  • Breast
  • Lung/bronchus
  • Colorectal
  • Brain/CNS
  • Pancreas
77
Q

Cancer mortality 50-69?

A
  • Lung/bronchus
  • Colorectal
  • Breast
  • Pancreas
  • Prostate
78
Q

Cancer mortality 70+?

A
  • Lung/bronchus
  • Colerectal
  • Prostate
  • Breast
  • Pancreas
79
Q

Countries w/ highest cancer incidence?

A

-Canada, US, Australia, UK, Western Europe, Uruguay

80
Q

Cancers more prevalent in developed countries?

A

Lung, breast and prostate cancer

81
Q

Cancers more prevalent in developing countries?

A

Liver (Hep C infections)

-Overall cancer incidence is lower in developing countries

82
Q

What could explain differences in types and incidences of cancers amongst countries?

A

Different exposures and risk factors

83
Q

Describe the nature of the dose-response relationship between diet and cancer

A

We must know the quantity of the nutrient or component of the food that must be consumed to seen effects on cancer - is this amount realistic/seen in normal diets?

84
Q

Explain the temporal relationship between diet and cancer

A

If we are exposed to a certain diet or carcinogen throughout our life-time, how long will it take to develop cancer? Do we need continuous exposure?

85
Q 
List the type of studies addressing diet and cancer in increasing strength of association:
Prospective co-hort
Descriptive
Interventional
Case-control
A

Descriptive
Case-control
Prospective co-hort
Interventional

86
Q

Descriptive studies?

A

Study cancer in populations having different diets, and compared them to countries (i.e. Chine and Canada), linking diet to cancer

87
Q

Limitations to descriptive?

A
  • Many variables in each country than just diet

- nutrient intake data difficult to collect in large groups

88
Q

Case-control?

A
  • Will use matched controls (people similar sex, age and social-economic status) to link and trends in developing cancer, asking about their long-term diet Hx
  • Earlier diets reported by pts with cancer are compared with matched controls w/o cancer
89
Q

Case-control limitations?

A
  • May use proxy respondent
  • Possible recall and selection bias
  • Retrospective, memory reliant
90
Q

Prospective co-hort?

A

Will follow huge co-hort foe long period of time, and periodically assessing diet and development of cancer

91
Q

Limitations of prospective co-horts?

A
  • Need thousands of people to be enrolled, as only small amount of people will develop cancer
  • Difficult for rare types of CA
  • Very costly
92
Q

Interventional?

A

Two groups of randomized people on controlled, certain diets, will be followed over time to see who will develop cancer or not

93
Q

Limitations of interventional?

A
  • Adherence to dietary changes is difficult
  • Blinding often not possible
  • Optimal dosages need to be ascertained
  • Duration is unknown, may be long
94
Q

What kind of studies are the ONLY way that we can have a causal relationship? How?

A
  • Interventional studies

- Primarily be done with markers of cancer, should not wait until cancer completely developed

95
Q

How should epidemiological studies be viewed?

A

Complementary to metabolic, animal and in-vitro mechanistic studies

96
Q

How does energy restriction reduce the development of cancer?

A

Since the rate of cell division is influenced by energy balance and growth rate.

97
Q

In humans, growth rates and body size are indicators of _____

A

energy balance

98
Q

What does adult height reflect?Adult weight?

A

Height reflects pre-adult nutrition, and weight reflects positive energy balance later in life

99
Q

Is adult height associated with some kinds of cancers?

A

Maybe, but is NOT a cause - is more of an indication of pre-adult nutrition environment.

100
Q

What may rapid growth rates before puberty be related to?

A

Future risk of breast and other cancers

101
Q

What is adult obesity related to in terms of cancer?

A

Colon, kidney, pancreas, esophagus, endometrium, gall blader and liver

102
Q

When does obesity increase risk of breast cancer?

A

Greater risk only AFTER menopause

103
Q

Excess weight could account for ____ of cancers known to be influenced by nutrition

A

1/3

104
Q

What are the main associations made between dietary fat and cancer?

A

Mostly to do with colon and breast cancer

105
Q

What study in China determine about dietary fat intake?

A

NO association between dietary fat and cancer mortality

106
Q

Do low fat diet reduce the development of cancer?

A

No - one study even showed higher risk

107
Q

Is colon cancer relate to excess dietary fat?

A

No, more likely related to excess weight and low PA

108
Q

What types of foods are associated with colorectal cancer?

A

ed meat and processed meats

109
Q

Discuss the increased risk of processed meat and colorectal cancer

A

Increase of 49% probably risk in colorectal cancer with a 25-g increment increase of processed meat daily

110
Q

Discuss the increases risk of red meat an colorectal cancer

A

Increase of 12-17% possible risk in colon cancer with 100 g increment increase in red meat daily

111
Q

Is a 50% increase is risk that significant?

A

Depends on what the initial risk is, if we have a 1% initial risk, then it will only increase to 1.5%

112
Q

The effect of ____ is very evident, while the level of evidence for ____ is probably (not as strong)

A

Processed meats

red meats

113
Q

Explain the potential mechanisms of red and processed meats and the development of cancers

A

Nitrosamines are carcinogenic, where meats tend to contain a higher amount of nitrates and amino acids (protein).
-Nitrosamines formed in the stomach, and heme may encourage formation of these compounds

114
Q

Besides the formation of nitrosamines, how does preparation of meats produce carcinogens?

A

High heat preparation (frying, broiling, grilling) may form polycyclic aromatic hydrocarbons and heterocyclic amines

115
Q

(T/F) We can attribute increased risk of cancer and grilled meats

A

Fasle

116
Q

Practical recommendation regarding meats and cancer?

A
  • Choose leans, non-processed meats
  • Replace with plant proteins
  • Avoid burning meats, touching meat to flame
117
Q

Diary products and cancer?

A

May decrease colon cancer, same effect may be observed in calcium supplements

118
Q

Fruits and vegetables and cancer?

A

-Contain phytochemicals with potential anti-carcinogenic properties, associated with lower risk of CA

119
Q

Recent studies are showing weaker links between F&V and overall cancer reduction rate, why?

A

-Limitations of categories of foods in FFQ (i.e. french fires and baked potatoes in same category)

120
Q

Lycopene?

A

Decr prostate CA

121
Q

Cruciferous veg?

A

Decrease several CA

122
Q

Allium veg?

A

Stomach CA

123
Q

Folate-rich F&V a?

A

Decr colon CA

124
Q

Citrus F&V?

A

Decr lung CA

125
Q

Proposed mechanisms between dietary fibres and reduced cancer risk?

A

Fibres may dilute or bind to carcinogens, limit the contact of the carcinogen with the mucose (increasing transit), alter colonic flora, reduce pH

126
Q

How does dietary fibre alter colonic flora?

A

May serve as a substrate to produce SCFA, such as butyrate which has anti-proliferative effects against cancer

127
Q

Recommendation on fibres?

A

Good level of evidence, increase intake of high-fibre foods

128
Q

What is a VERY well-known cause of cancer?

A

Alcohol

129
Q

Cancers and alcohol?

A

Upper GI –> oral cavity, larynk, esophagus, andliver

130
Q

What increases risk of cancer when combined with high alcohol intake?

A

Cigarette smoking

131
Q

Proposed mechanism of alcohol and cancer?

A

Direct contact of the alcohol within the mucosal lining of the GI tracts, an then toxicity int he liver

132
Q

What may increase risk of breast and colon cancer?

A

> 2 drinks/day

133
Q

Why is alcohol associate with increased risk of breast and colon cancer?

A

May be due to “anti-folate” effect of diet of alcohol, mimicking the effects of a diet low in methionine and folate

134
Q

High intake of ___ reduces the risk of breast cancer associated with ____

A

folate

alcohol

135
Q

Mechanism for calcium and cancer?

A

Calcium may (1) bind to the toxic, secondary bile acids and the ionized FA to form soaps within the lumen and (2) educe proliferation and inducing apoptosis.

136
Q

Threshold of calcium to see beneficial effects?

A

700-800 mg/day

137
Q

Recommendation for calcium and cancer?

A

Reach calcium RDA through foods, then supplement if needed

138
Q

Population with greater sun exposure (Vit D) experience lower rates of what ?

A

Breast, colon and prostate cancers

139
Q

25 (OH) D can cancer?

A

Circulating levels of 25(OH)D are generally inversely proportional to colorectal cancer

140
Q

Vit,C, E and cancer?

A

Potential roles in reducing cancer risks through antioxidant species and ROS

141
Q

Are antioxidants strongly recommended for prevention of cancer?

A

NO, and epi and intervention trials have no consistently supported a role in cancer risk

142
Q

How does selenium act against oxidative stress?

A

Selenoproteins are incorporated into glutathione peroxidases

143
Q

Low folate intake and cancer?

A

Higher risk of colorectal, breast, cervical

144
Q

Are folate supplements recommended?

A

NO, although some studies suggest reduced risk of colorectal cancers, some increases recurrence of adenomas

145
Q

Explain the controversy surrounding B-carotene supplementation and lung cancer?

A

We observed that increased lung Ca was associated with low Vit A intake, however 4 major trails of B-carotene supplementation resulted in null or adverse effects (in smokers, especially when combined with alcohol)

146
Q

Bottom line on b-carotene supplements?

A

Increase risks of lung cancer, especially in smokers and increased alcohol intake

147
Q

CONVINCING evidence surrounding decreasing cancer risk?

A

PA in colon cancer

148
Q

CONVINCING evidence surrounding increasing cancer risk?

A
  • Overweight/obese
  • Alcohol
  • Processed meet
  • High dose b-carotene (lung)
  • Alfatoxins (liver)
149
Q

PROBABLE evidence surrounding decreased cancer risks?

A
  • PA (breast)
  • Calcium (colon)
  • Whole grains, fibre (colon)
  • Coffee (liver, uterus)
150
Q

PROBABLE evidence surrounding increased cancer risk?

A
  • Red meat (colorectal)

- Salt-preserved foods (stomach)

151
Q

Limited/suggestive evidence surrounding decreased cancer risk?

A
  • Carotenoids, vit C, veg

- Fish, vitD

152
Q

Limited/suggestive evidence surrounding increased cancer risk?

A
  • Grilled/BBQ meat (heterocyclic amines, polycyclic aromatics)
  • Nitrosamines from hem
153
Q

Limited / no conclusion surrounding increased cancer risk?

A

-Omega -3, carotenoids, B vitamins, folate, vit C, D,E, non-nutritive plants, garlic, soy, sugar, tea

154
Q

What probable evidence decreases risk of premenopausal breast CA?

A

-Vigorous PA, body fatness, lactation

155
Q

What probable evidence increases risk premenopausal breast CA?

A

Alcoholic drinks, greater BW

156
Q

What is convincing evidence that increases risk of premenopausal breast CA?

A

Adult attained height

157
Q

What probable evidence decreases risk of post-menopausal breast CA?

A

PA, body fatness in young adulthood, lactation

158
Q

What convincing evidence increases risk of post-menopausal breast CA?

A

Alcoholic drinks, body fatness, adult weight gain, adult attained height

159
Q

Discuss the risk of adult attained height and cancer

A

Is unlikely to influence the risk of cancer, however is a marker for genetic, hormonal, environmental and nutritional factors affecting growth

160
Q

Convincing evidence deceasing risk of colorectalCA?

A

PA

161
Q

Probably evidence deceasing risk of colorectal CA?

A

-Whole-grains, food containing dietary fibre, dairy products, calcium supplements

162
Q

Limited/suggestive evidence deceasing risk of colorectalCA?

A

Vit C, Vit D, fish, multivitamin supplements

163
Q

Convincing evidence increasing risk of colorectalCA?

A
  • Processed meat
  • Alcoholic rinks
  • Body fatness
  • Adult attained height
164
Q

Probable evidence increasing risk of colorectalCA?

A

Red meat

165
Q

Limited/suggestive evidence increasing risk of colorectalCA?

A
  • Low intake of non-starchy veg, fruits

- Foods containing heme iron

166
Q

Convincing evidence increasing lung cancer risk?

A

Arsenic in drinking water

High-dose beta-carotene

Clinical Nutrition 1 (30 decks)

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