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Questions and Answers
What is the primary result of hypermethylation of CpG islands in cells exposed to tobacco smoke?
What is the primary result of hypermethylation of CpG islands in cells exposed to tobacco smoke?
Which enzyme is primarily responsible for generating methylated residues in DNA?
Which enzyme is primarily responsible for generating methylated residues in DNA?
How does chronic tobacco smoke exposure modify the epigenome?
How does chronic tobacco smoke exposure modify the epigenome?
What type of modification is characteristic of epigenetic alterations due to tobacco smoke?
What type of modification is characteristic of epigenetic alterations due to tobacco smoke?
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What role does epigenetic modification play in tumorigenesis as a result of tobacco smoke exposure?
What role does epigenetic modification play in tumorigenesis as a result of tobacco smoke exposure?
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What type of environmental exposure is linked to significant epigenetic changes in lung tissue?
What type of environmental exposure is linked to significant epigenetic changes in lung tissue?
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Which of the following best describes epigenetic modifications?
Which of the following best describes epigenetic modifications?
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What cellular process is often disrupted by the epigenetic modifications induced by tobacco smoke?
What cellular process is often disrupted by the epigenetic modifications induced by tobacco smoke?
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What type of DNA damage is primarily associated with UVA radiation?
What type of DNA damage is primarily associated with UVA radiation?
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Which enzymes are primarily involved in the metabolism of carcinogenic chemicals?
Which enzymes are primarily involved in the metabolism of carcinogenic chemicals?
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What are the molecules that execute the damaging effects of certain chemical carcinogens called?
What are the molecules that execute the damaging effects of certain chemical carcinogens called?
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Which of the following is a characteristic of the primary action mechanism of chemical carcinogens?
Which of the following is a characteristic of the primary action mechanism of chemical carcinogens?
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Which of these groups is NOT classified as a carcinogen?
Which of these groups is NOT classified as a carcinogen?
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How do DNA adducts affect DNA replication?
How do DNA adducts affect DNA replication?
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Which of the following is a known source of high levels of polycyclic aromatic hydrocarbons (PAHs)?
Which of the following is a known source of high levels of polycyclic aromatic hydrocarbons (PAHs)?
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What type of compounds can convert inactive phenanthrene into an active carcinogen?
What type of compounds can convert inactive phenanthrene into an active carcinogen?
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Which of the following are classified as intrinsic risk factors for cancer development?
Which of the following are classified as intrinsic risk factors for cancer development?
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What role do reactive oxygen species (ROS) play in cancer development following ionizing radiation exposure?
What role do reactive oxygen species (ROS) play in cancer development following ionizing radiation exposure?
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Which of the following statements is true regarding the effects of ionizing radiation on DNA?
Which of the following statements is true regarding the effects of ionizing radiation on DNA?
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What is a common consequence of exposure to chemical carcinogens?
What is a common consequence of exposure to chemical carcinogens?
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Which risk factor is particularly modified by lifestyle changes to reduce cancer risk?
Which risk factor is particularly modified by lifestyle changes to reduce cancer risk?
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Which cancer type has a dose-dependent relationship with radiation exposure?
Which cancer type has a dose-dependent relationship with radiation exposure?
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What are the primary mechanisms through which ionizing radiation affects cellular structures?
What are the primary mechanisms through which ionizing radiation affects cellular structures?
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Which of the following factors is not considered a modifiable risk factor for cancer?
Which of the following factors is not considered a modifiable risk factor for cancer?
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Study Notes
Molecular Biology of Cancer
-
Risk Factors for Cancer Development:
-
Intrinsic risk factors (unmodifiable):
- Random errors in DNA replication
- Biologic aging
- Genetic susceptibility
- DNA repair machinery
- Hormones
- Growth factors
- Inflammation
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Non-intrinsic risk factors (partially modifiable):
- Endogenous factors as above
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Exogenous risk factors (modifiable):
- Radiation
- Chemical carcinogens
- Tumour causing viruses
- Bad lifestyles such as smoking, lack of exercise, and nutrient imbalance
- Other factors like obesity, tobacco, alcohol, sedentary lifestyle, poor diet, excessive UV exposure, carcinogens, age, and genetics
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Intrinsic risk factors (unmodifiable):
Common Risk Factors for Cancer
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FOR CANCER:
- Obesity
- Tobacco
- Alcohol
- Sedentary lifestyle
- Poor diet
- Excessive UV exposure
- Carcinogenic chemicals
- Age
- Genetics
- Radiation
Radiation as a Carcinogen
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Ionizing radiation increases the risk of:
- Leukemia
- Breast cancer
- Thyroid cancer
- Other solid tumors
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Immediate effects of radiation exposure on cells:
- Increase in reactive oxygen species (ROS)
- Generation of single-stranded DNA breaks (SSBs)
- Generation of double-stranded DNA breaks (DSBs)
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Ionizing radiation damages cellular structures
- Directly damaging DNA
- Forming free radical-containing reactive molecules
Downstream Molecules and Effects Following DNA Damage Due to Ionizing Radiation
- Ionizing radiation damages DNA both directly and indirectly
- Double-stranded breaks (DSBs) are a common form of damage
- A cascade of enzymatic processes is activated to allow for DNA repair or apoptosis
- Non-homologous end joining (NHEJ) and homologous recombination (HR) are two common pathways for DNA repair
- BRCA 1 and BRCA 2 enzymes are involved in homologous recombination
UV Radiation as a Carcinogen
- UVB radiation is most effective in causing carcinogenesis
- UVB radiation causes:
- Cyclobutane pyrimidine dimers
- Pyrimidine-pyrimidone photoproducts
- UVA radiation can damage DNA indirectly through free radical-mediated damage
- This damage is causing G→T transversions
Carcinogenic Chemicals
- Many chemicals are involved in carcinogenesis
- Carcinogens are electrophilic
- Some require metabolism to become active
- Ultimate carcinogens are the active form that executes damage
- The Cytochrome P450 enzymes (drug-metabolizing enzymes) are important in activating carcinogens
- Different people have varied responses to chemical carcinogens due to genetic factors
- 10 groups of carcinogens: polycyclic aromatic hydrocarbons, aromatic amines, azo dyes, nitrosamines and nitrosamides, hyrazo and azoxy compounds, carbamates, halogenated compounds, natural products, inorganic carcinogens, and miscellaneous compounds
Polycyclic Aromatic Hydrocarbons (PAHs)
- Coal tar is a source of PAHs that have been shown to induce skin cancer
- PAHs are present in cigarette smoke, vehicle exhaust, and charcoal-grilled foods
- Metabolic activation of BP resulting in highly reactive mutagenic BP diol epoxides
- Most commonly causes G→T transversions
Tobacco Smoking
- At least 60 known carcinogens are present in cigarette smoke
- Includes PAHs and nitrosamines
- Metabolism of chemicals in smoke often produces electrophilic moieties that react with DNA
- DNA mutations are frequent and lead to a mutational burden in cancers linked to smoking.
- Some adducts may be corrected but permanent procancerous mutations can remain
- Epigenetic modification frequently leads to reduced expression of tumor suppressor genes
Effects of Physical Activity, Excess Body Fat, and Sedentary Behavior to Cancer Risk
- Insulin, IGF-1, and their binding proteins are anabolic hormones
- Excess body fat is positively correlated with insulin resistance
- Insulin resistance causes elevated blood levels of IGF-I which can elevate the risk of several malignancies
- High levels of IGF-I may promote tumorigenesis
- Prolonged hyperinsulinemia may reduce SHBG, elevates free estrogens and androgens, increasing risk of cancers
Age
- Advancing age is the most important and prevalent risk factor for overall cancer.
- Cancer incidence rates climb steadily with age.
- Cancer rates tend to be lower in younger age groups before peaking in older age groups
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Description
Test your knowledge on the molecular biology of cancer. This quiz covers various intrinsic and extrinsic risk factors associated with cancer development. Understand the interplay of genetics, lifestyle choices, and environmental influences on cancer risks.
