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Questions and Answers
What is primarily responsible for the excessive deposition of extracellular matrix (ECM) components during chronic inflammation?
What is primarily responsible for the excessive deposition of extracellular matrix (ECM) components during chronic inflammation?
- Fibroblasts (correct)
- Neutrophils
- Epithelial cells
- Macrophages
What role do Reactive Oxygen Species (ROS) play in cancer development?
What role do Reactive Oxygen Species (ROS) play in cancer development?
- They decrease inflammation.
- They inhibit cellular growth.
- They increase oxidative stress. (correct)
- They repair DNA damage.
Which condition is characterized by excessive scar tissue formation in the liver?
Which condition is characterized by excessive scar tissue formation in the liver?
- Renal fibrosis
- Cardiac fibrosis
- Liver fibrosis (correct)
- Pulmonary fibrosis
What is a common consequence of pulmonary fibrosis?
What is a common consequence of pulmonary fibrosis?
What type of DNA damage is specifically caused by ionizing radiation?
What type of DNA damage is specifically caused by ionizing radiation?
What is a consequence of inefficient DNA repair mechanisms?
What is a consequence of inefficient DNA repair mechanisms?
The inability to resolve inflammation properly can lead to which of the following outcomes?
The inability to resolve inflammation properly can lead to which of the following outcomes?
Which process involves two adjacent thymine bases becoming covalently bonded, disrupting DNA function?
Which process involves two adjacent thymine bases becoming covalently bonded, disrupting DNA function?
In cardiac fibrosis, what is primarily affected?
In cardiac fibrosis, what is primarily affected?
How does chronic oxidative stress contribute to cancer?
How does chronic oxidative stress contribute to cancer?
Which cell type's overproduction is primarily involved in excessive ECM deposition during chronic inflammation?
Which cell type's overproduction is primarily involved in excessive ECM deposition during chronic inflammation?
What effect does high-energy radiation exposure have in terms of cancer risk?
What effect does high-energy radiation exposure have in terms of cancer risk?
What is a significant factor contributing to liver fibrosis?
What is a significant factor contributing to liver fibrosis?
What effect does cardiac fibrosis have on health?
What effect does cardiac fibrosis have on health?
What happens to DNA when it undergoes persistent damage due to radiation?
What happens to DNA when it undergoes persistent damage due to radiation?
Which of the following repair mechanisms can fix double-strand breaks in DNA?
Which of the following repair mechanisms can fix double-strand breaks in DNA?
What are Reactive Oxygen Species (ROS)?
What are Reactive Oxygen Species (ROS)?
What DNA damage can UV radiation specifically cause?
What DNA damage can UV radiation specifically cause?
What role does acetaldehyde play in DNA damage?
What role does acetaldehyde play in DNA damage?
What kind of damage does ionizing radiation typically lead to?
What kind of damage does ionizing radiation typically lead to?
What can be a consequence of not repairing methylation errors in DNA?
What can be a consequence of not repairing methylation errors in DNA?
Which chemical agent is often associated with increased DNA adduct formation?
Which chemical agent is often associated with increased DNA adduct formation?
How do external chemical agents like those found in tobacco smoke affect DNA?
How do external chemical agents like those found in tobacco smoke affect DNA?
What is a common source of oxidative stress leading to DNA damage?
What is a common source of oxidative stress leading to DNA damage?
What role does the Golgi apparatus play in the secretion of matrix metalloproteinases (MMPs)?
What role does the Golgi apparatus play in the secretion of matrix metalloproteinases (MMPs)?
How does the Golgi apparatus influence the epithelial-mesenchymal transition (EMT)?
How does the Golgi apparatus influence the epithelial-mesenchymal transition (EMT)?
What is one consequence of altered Golgi function in cancer cells?
What is one consequence of altered Golgi function in cancer cells?
In what way does the Golgi apparatus support cancer cell proliferation?
In what way does the Golgi apparatus support cancer cell proliferation?
Which of the following describes Barrett's esophagus?
Which of the following describes Barrett's esophagus?
What is the significance of the Golgi apparatus in the context of cancer metastasis?
What is the significance of the Golgi apparatus in the context of cancer metastasis?
What occurs during the epithelial-mesenchymal transition (EMT) in cancer cells?
What occurs during the epithelial-mesenchymal transition (EMT) in cancer cells?
How can the Golgi apparatus be linked to increased cancer cell invasion?
How can the Golgi apparatus be linked to increased cancer cell invasion?
What is the role of tumor suppressor genes in relation to cancer?
What is the role of tumor suppressor genes in relation to cancer?
How do mutations in proto-oncogenes contribute to cancer development?
How do mutations in proto-oncogenes contribute to cancer development?
What is a consequence of the inhibition of DNA repair mechanisms by carcinogens?
What is a consequence of the inhibition of DNA repair mechanisms by carcinogens?
What mechanism allows cancer cells to survive despite significant DNA damage?
What mechanism allows cancer cells to survive despite significant DNA damage?
Which of the following best describes cell cycle deregulation in cancer?
Which of the following best describes cell cycle deregulation in cancer?
What effect do accumulated mutations have in the context of cancer development?
What effect do accumulated mutations have in the context of cancer development?
Which aspect of tumor suppressor genes is critical in preventing cancer?
Which aspect of tumor suppressor genes is critical in preventing cancer?
What role do carcinogens play in the context of cancer cell behavior?
What role do carcinogens play in the context of cancer cell behavior?
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Study Notes
DNA Damage and Repair
- Reactive Oxygen Species (ROS): Byproducts of normal cellular metabolism that can cause oxidative damage to DNA.
- Metabolic Byproducts: Substances like acetaldehyde from alcohol metabolism can bind to DNA and cause mutations.
- External Sources:
- UV Radiation: Causes thymine dimers, where two adjacent thymine bases in DNA bind together.
- Ionizing Radiation: Leads to various types of DNA damage including double-strand breaks.
- Chemical Agents: Found in tobacco smoke and industrial chemicals can directly damage DNA.
- Acetaldehyde: A toxic byproduct of alcohol metabolism, it binds to DNA (forms adducts) increasing the risk of cancer in the liver and digestive tract.
- Methylation: Another form of DNA adduct that can lead to mutations if not repaired.
- DNA Repair Pathways: Cells have mechanisms like homologous recombination and non-homologous end joining to repair double-strand breaks. Errors during repair can lead to mutations.
- Genomic Instability: Inefficient or faulty DNA repair results in genomic instability increased risk of cancer.
- Radiation-Induced Genomic Instability: Radiation can cause persistent DNA damage leading to genomic instability over time.
- Dose and Type of Radiation: The risk of cancer increases with the dose and type of radiation exposure. High-energy radiation is more damaging.
Cellular Changes Leading to Cancer
- Gene Mutations:
- Tumor Suppressor Genes: Mutations in genes like TP53 can prevent cells from undergoing apoptosis, allowing damaged cells to survive and proliferate.
- Proto-oncogenes: Mutations in genes like KRAS can lead to their activation, promoting uncontrolled cell growth.
- Inhibition of DNA Repair: Carcinogens can inhibit DNA repair mechanisms, leading to the accumulation of mutations.
- Promotion of Uncontrolled Cell Growth:
- Cell Cycle Deregulation: Carcinogens can disrupt cell cycle control leading to uncontrollable cell proliferation.
- Evasion of Apoptosis: Cancer cells often develop mechanisms to evade programmed cell death (apoptosis), allowing them to survive despite significant DNA damage.
Extracellular Matrix and Cancer
- Excessive ECM Deposition: Chronic inflammation leads to excessive production of extracellular matrix (ECM) components such as collagen by fibroblasts.
- Failure in Resolution: Inability to resolve inflammation properly results in continuous tissue remodeling and scarring.
- Examples of ECM-Related Disorders:
- Liver fibrosis: Excessive scar tissue in the liver, often due to chronic hepatitis or alcohol abuse.
- Pulmonary fibrosis: Thickening and scarring of lung tissue, reducing lung function.
- Cardiac fibrosis: Scarring of heart tissue, impairing heart function and potentially leading to heart failure.
- Matrix Degradation: The Golgi apparatus is involved in the secretion of matrix metalloproteinases (MMPs) and other proteases, which degrade the ECM and facilitate cancer cell invasion.
Golg Apparatus Function in Cancer
- Role in Epithelial-Mesenchymal Transition (EMT): The Golgi apparatus plays a key role in EMT, a process where cancer cells gain migratory and invasive properties. This transition is essential for metastasis.
- Protein Secretion and Migration: Changes in Golgi function can lead to increased secretion of proteins that promote cell migration and invasion, aiding in the spread of cancer cells.
- Impact on Cell Proliferation: The Golgi apparatus supports rapid proliferation of cancer cells by modifying and sorting proteins necessary for cell growth and division.
Metaplasia and Dysplasia
- Metaplasia: Normal tissue transformed into another type.
- Dysplasia: Abnormal cell growth and development.
Barret's Esophagus:
- Involves the transformation of the normal squamous epithelium lining the esophagus into columnar epithelium, which is more typical of the intestinal lining. This is a metaplasia change.
- Caused by: Chronic acid reflux, often related to gastroesophageal reflux disease (GERD). It is a risk factor for esophageal cancer.
Oxidative Stress and Cancer
- Reactive Oxygen Species (ROS): Chemical carcinogens can increase ROS levels leading to oxidative stress and damage to cellular components.
- Inflammation: Chronic oxidative stress causes inflammation which is a known cancer promoter.
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