Cancer Flashcards
(26 cards)
The difficulties with associating environmental factors with cancer
The difficulties with associating environmental factors with cancer
- Variety of things that may increase or decrease risk
- Diet: People eat foods composed of different nutrients/ non-nutritive compounds. People may recall diet incorrectly. Some factors may increase as well as decrease risk
- Issues with research: length and time of studies. Gap between carcinogen exposure and cancer development can be long and make it hard to establish relationship.
- People are different and may respond to carcinogens differently
- Genetic susceptibility may affect reaction to environmental factors
- There may be interplay between factors
- Size of effect may be minuscule in comparison to other factors
- Biomarkers may help to reduce issues with research
- Tumour hetrogeneity: different subtypes might have different dietary associations
Dietary factors for predisposing to or protecting against cancer
Dietary factors for predisposing to or protecting against cancer
PROTECTIVE:
- Fibre
- Vitamins and minerals
- Plant anti-carcinogens
INCREASES RISK:
- Mutagens: Naturally occurring contaminants: Alfatoxins, Chemicals generated during food preservation: N-nitroso compounds, Chinese style salted fish
- Alcohol
- Energy balance
Define the mechanisms for dietary factors for predisposing to cancer: ALFATOXINS
PREDISPOSING TO:
- Alfatoxins: can cause liver cancer
- Alfatoxins: found on agricultural crops such as maize (corn), peanut
- Found in warm and humid regions of the world
- Alfatoxins accumulate in food crops> people consume the food contaminated with alfatoxins or animals that ate contaminated feed
> liver biotransformation to Alfatoxins-8,9-epoxide (AF-8,9) (toxic metabolite)> AF-8,9 binds to DNA to form adducts (alter DNA structure and cause a mutation)> Hepatocellular carcinoma (cancer is formed)
Define the mechanisms for dietary factors for predisposing to or protecting against cancer [ALFATOXINS]
PREDISPOSING TO:
- Alfatoxins are mutagens that can cause liver cancer
- Alfatoxins accumulate in food crops> people consume the food contaminated with alfatoxins
> liver biotransformation to Alfatoxins-8,9-epoxide (AF-8,9) (toxic metabolite)> AF-8,9 binds to DNA to form adducts (alter DNA structure and cause a mutation)> Hepatocellular carcinoma ( liver cancer is formed)
Discuss the association of dietary factors with the risk of most common cancer types
Discuss the association of dietary factors with the risk of most common cancer types
- PROSTATE CANCER: Probable evidence INCREASED RISK: Body fatness (increases advanced PC risk) and adult attained height increases risk (increases PC risk).
Suggestive evidence INCREASED RISK: dairy, high calcium diet, low plasma Vit E, low plasma selenium may increase risk.
- COLON/COLORECTAL CANCER: Convincing evidence INCREASED RISK: processed meat, alcoholic drinks, body fatness, adult attained height.
Convincing evidence DECREASED RISK: Physical activity
Probable evidence INCREASED RISK: Red meat
Probable evidence DECREASED risk: Wholegrains, foods containing dietary fibre, dairy products, calcium supplements
Limited suggestive INCREASED risk: low intakes of non-starchy veg, low intakes of fruits, foods containing haem iron.
Limited suggestive DECREASED risk: Foods containing Vitamin C, Fish, Vitamin D, multivitamin supplements.
Discuss the association of dietary factors with the risk of most common cancer types: PROSTATE CANCER
Discuss the association of dietary factors with the risk of most common cancer types
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PROSTATE CANCER: Probable evidence INCREASED RISK: Body fatness (increases advanced PC risk) and adult attained height increases risk (increases PC risk).
Suggestive evidence INCREASED RISK: dairy, high calcium diet, low plasma Vit E, low plasma selenium may increase risk.
Discuss the association of dietary factors with the risk of most common cancer types: COLORECTAL CANCER
- COLON/COLORECTAL CANCER: Convincing evidence INCREASED RISK: processed meat, alcoholic drinks, body fatness, adult attained height.
Convincing evidence DECREASED RISK: Physical activity
Probable evidence INCREASED RISK: Red meat
Probable evidence DECREASED risk: Wholegrains, foods containing dietary fibre, dairy products, calcium supplements
Limited suggestive INCREASED risk: low intakes of non-starchy veg, low intakes of fruits, foods containing haem iron.
Limited suggestive DECREASED risk: Foods containing Vitamin C, Fish, Vitamin D, multivitamin supplements.
Wholegrains and colon cancer mechanisms
Wholegrains and colon cancer mechanisms:
- Wholegrains are a source of dietary fibre: short-chain fatty acids production, reduced transit time or prevention of insulin resistance.
- Wholegrains are also a rich source of various bioactive compounds including vitamin E, selenium, copper, zinc, lignans, phytoestrogens and phenolic compounds.
- Several phenolic acids have been shown in experimental studies to stimulate anti-oxidative activity.
- Wholegrains may also protect against colorectal cancer by binding carcinogens and regulating glycaemic response.
High calcium and prostate cancer mechanisms
High calcium and prostate cancer mechanisms
High calcium Ca → Low 1,25 dihydroxy vitamin D3 formation from Vitamin D → High
cell proliferation in the prostate
•Rats treated with 1,25 dihydroxy vitamin D3 had significantly smaller prostate cancer tumors
• Higher intakes of milk and calcium may increase insulin-like growth factor-1 (IGF-1) (Gunnell et al, 2003), which may be associated with increased prostate cancer risk (Renehan et al, 2004).
Red and processed meat cancer mechanisms
Red and processed meat cancer mechanisms:
High-fat diets could promote carcinogenesis via insulin resistance
or faecal bile acids;
•Generation of carcinogenic N-nitroso compounds in meat and endogenously by nitrosation of amines and amides
•Production of heterocyclic amines and polycyclic aromatic hydrocarbons during cooking meat at high T
•Heme iron in red meat can promote carcinogenesis because it increases cell proliferation in the mucosa, through lipoperoxidation and/or cytotoxicity of fecal water
Folate dual role in cancer development mechanisms
Folate may have a dual role in cancer development depending on the stage of cell transformation
* In normal tissues, folate deficiency predisposes them to neoplastic transformation, while modest levels of folic acid supplementation suppress,
* supraphysiologic supplemental doses enhance, the development and progression of (pre)neoplastic lesions in the colorectum.
- In established (pre)neoplastic lesions folate deficiency has an inhibitory effect, whereas folic acid supplementation has a promoting effect on the progression of theses lesions
Vitamin C cancer inhibition
Vitamin c cancer inhibition:
- Anti-oxidant
-Anti-inflammatory
- Restoration of cell to cell communication so body can destroy tumours
- Vitamin C inhibits oxidative DNA damage (ROS involved in cancer initiation and promotion)
Define cancer
Cancer is uncontrolled cell division. Cancer develops via carcinogénesis.
How many times can differentiated cells divide in humans?
In humans, differentiated cells can divide 52 times before apoptosis
What does p53 do?
P53 is a transcription factor that promotes expression of genes that prevent mitosis
Fibre potential cancer inhibiting mechanisms
Fibre potential cancer inhibiting mechanisms
- Increased stool bulk, reduced transit time (i.e., amount of time harmful
substance in contact with lining (potential harm is removed)) and absorption e.g., carcinogens
• Increased dilution of gut contents and binding carcinogens for faecal
excretion
• Increase of short chain fatty acids e.g., butyrate (pH reduction, anti-
carcinogenic, anti-inflammatory properties)
• Regulation of blood glucose level (GI index, insulin can affect cancer development ) and sex hormones
Alcohol potential cancer forming mechanisms
Alcohol potential cancer forming mechanisms:
- Carcinogenic mechanisms of action
remain unclear • Ethanol may act as co-carcinogen
•Mechanisms?
•Acetaldehyde. formation – damages
DNA/inhibits repairing mechanisms
•Alcohol may enhance the role of other
carcinogens by facilitating their
absorption in the gut
•Impaired DNA repair – may interfere
with usual repair mechanisms
- Inflammation is the result that may lead to cancer cell development
Energy balance potential cancer mechanisms
Energy balance potential cancer mechanisms
Energy restriction: can reduce cancer incidence in animals
Reduction in circulating levels of growth factors, anabolic hormones, inflammatory cytokines and oxidative stress markers associated with various malignancies. Reduced inflammation lowers cancer development.
Obesity (causes low grade inflammation): increases risk for several cancers (breast, colorectum,
endometrium, kidney, oesophagus) • Endometrium cancer: increased risk due to increased inflammation,
hyperinsulinemia and estrogen hyperactivity
Breast and endometrium: high estrogen levels in obese stimulates the
growth and division of cancer cell
Insulin has ____ stimulating effects. Elevated levels may promote _______ growth
Insulin has cell stimulating effects. Elevated levels may promote cancer growth
Define the mechanisms for dietary factors for predisposing to cancer: ALCOHOL
Define the mechanisms for dietary factors for predisposing to cancer: ALCOHOL:
* Carcinogenic mechanisms are unclear
* May act as a co-carcinogen
* Mechanisms: Acetaldehyde formation:enhancing the role of other carcinogens by facilitating gut absorption
* May intefere with DNA repair mechanisms
Dietary factors for protecting against cancer: ENERGY RESTRICTION
Dietary factors for protecting against cancer: ENERGY RESTRICTION:
* Proven in animals not humans: In mice/rats, 25% reduction in energy led to reduced cancer incidence.
* Reduction in circulating levels of growth factors, anabolic hormones, inflammatory cytokines and oxidative stress markers associated with various malignancies
What do the high oestrogen levels linked to obesity do?
The high oestrogen levels linked to obesity stimulate the growth and division of cancer cells.
Define the mechanisms for dietary factors for predisposing to cancer: OBESITY
Define the mechanisms for dietary factors for predisposing to cancer: OBESITY
* Increased risk of: breast, endometrium, colorectum, kidney and oesphageal cancer
* Increased risk for endometrium cancer due to increased inflammation, hyperinsulinaemia, and oestrogen hyperactivity
* Increased risk for breast and endometrium due to high oestrogen levels that stimulate cancer growth and division.
Dietary fibre and colon cancer
Dietary fibre and colon cancer
* Enhances healthy gut microbiota
* Produces short chain fatty acids (acetate, propionate, butyrate)> provide energy, reduce food intake, maintain colon health, increase cancer call cycle arrest and apoptosis, reduce cancer cell migration and invasion, lowers chronic inflammation
* Reduces colon content transit time/exposure to carcinogens > healthy gut intestinal barrier
