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36 Cards in this Set
- Front
- Back
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T/F:
Hypertrophy is known to predispose to neoplastic disease. |
False.
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Atrophy:
What can create conditions that are favorable to free radical production? What do the free radicals attack? What can prevent normal growth/maturation of cells? |
Ischemia and ischemia-reprofusion injury.
Free radicals attack DNA. Nutritional deficiencies. |
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Hyperplasia:
What type of replication? What causes increase likelihood of cancer? What type of mouth cancer? |
Intrinsic/extrinsic stimulated cell replication.
Enlarged pool of cells duplicating DNA--higher chance for error. Oral squamous cell carcinoma. |
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Prosoplasia:
What is it? Best example? |
Substitution of a more highly specialized tissue for a less specialized tissue.
Barrett esophagus. |
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Prosoplasia:
What % progress to malignancy? |
10%
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What is Barrett's Esophagus?
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An inflammatory disorder where gastric or intestinal columnar epithelium replaces normal squamous epithelium in response to chronic reflux.
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Which type of growth disturbance is the most likely to precede cancer?
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Dysplasia or a combination with dysplasia.
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This is a shrinkage in size of a tissue (organ) due to a reduction in the number of cells.
Cancer risk? |
Atrophy.
Low cancer risk. Often occurs in stomach and prostate cancers. |
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This is an increase in the size of a tissue due to an increase in the number of cells.
Cancer risk? Caused by? |
Hyperplasia.
Low cancer risk. Caused by reaction to irritation or hormones. |
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This is an increase in the size of a tissue due to an increase in the size of cells?
Cancer risk? Cause? |
Hypertrophy.
No cancer risk. Caused by physical stress, exercising muscle. |
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This is the substitution of a more highly specialized tissue for a less specialized tissue.
Cancer risk? Example? |
Prosoplasia.
Low cancer risk. GERD--Barrett's Esophagus. |
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This is the substitution of a less specialized tissue for a more highly specialized tissue.
Cancer risk? Example? |
Metaplasia.
Moderate cancer risk. Smoker's bronchi. |
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This is an abnormal pattern of maturation.
Cancer risk? Example? |
Dysplasia.
High cancer risk. CIN. Oral precancer. |
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How do neoplastic cells differ from normal cells?
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1. Lack of responsiveness to normal growth controls.
2. Typically detrimental--serving no useful function or purpose. |
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Prostate Cancer:
What growth disturbance is it associated with? What is the first step in carcinogenesis? This leads to? |
Atrophy.
Proliferative inflammatory atrophy (PIA). Prostatic interepithelial neoplasia...which leads to cancer. |
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Hyperplasia:
Intrinsic vs. Extrinsic stimulated cell replication. |
If extrinsic, cell will go back to normal.
If intrinsic, cell may go back to normal, but neoplasia doesn't remove signals. |
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Hyperplasia:
What is the most vunerable time for mutation of the DNA? |
Replication.
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Hyperplasia:
In the carcinogenesis model, _________ increase the number of tumors that form, ______________ cause the mutations. |
promoters
initiators |
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Hyperplasia:
What leads to the increased chance for DNA errors? |
An enlarged pool of cells duplicating DNA.
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What type of cancer is typically associated with hyperplasia?
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Oral squamous cell carcinoma.
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What makes adenocarcinoma of the esophagus possible?
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There must be a preceding change from stratified squamous epithelium to gastric-like mucosa. This is often followed by dysplasia...then adenocarcinoma.
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What is a higher risk for cancer:
Erythroplakia or Leukoplakia? |
Erythroplakia.
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Carcinogenesis in Barrett's esophagus:
What is the primary transforming growth factor? |
Cyclin D1.
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Barrett's esophagus is associated with which type of growth disturbance?
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Prosoplasia.
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What does TP53 do in cells?
What happens when it is deficient. |
It checks DNA and promotes apoptosis if it finds it to be damaged.
Most oral cancers & Barrett's esophagus are due to loss of TP53 function. |
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What is VEGFA?
Where is it often upregulated? |
Vascular edothelial growth factor alpha--it promotes vessel growth for nourishment to neoplastic tissue.
Barrett's esophagus. |
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What is the most typical type of metaplasia (what cell type to what other cell type)?
Where? |
Columnar to squamous.
In the respiratory tract in response to smoking usually. Also in a Vitamin A deficiency--squamous metaplasia in respiratory epithelium. |
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What occurs with a Vitamin A deficiency?
Excess? |
Squamous metaplasia in respiratory epithelium.
Excess suppresses keratinization. |
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Why is metaplasia to squamous cells in the respiratory tract harmful?
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More capable of surviving harsh conditions, but they lose their ability to secrete mucus.
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Epithelial Dysplasia:
What are some of its features? |
1. Hyperkaratosis (not a dysplastic feature by itself)
2. Acanthosis (not a dysplastic feature by itself) 3. Increased numbers and/or abnormal mitoses 4. Keratin pearls (keratin in midst of epithelium instead of on surface) 5. Individual cell keratinization 6. Increased nuclear/cytoplasmic ratio 7. Loss of polarity and cellular orientation (loss of stratification) 8. Hyperchromatism 9. Large, prominent nucleoli, increased protein synthesis 10. Dyskarynosis 11. Poikilocarynosis (variation in size and shapes of nuclei) 12. Basilar hyperplasia (more than one layer of dividing cells) |
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What is the KI-67 protein?
Where is it present in the cell cycle? What is the Labeling index? |
A cellular marker for proliferation.
It's present every cell phase except Gzero. The % of cells that stain for KI-67, indicating the growth fraction. |
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KI-67:
Associated with? Can correlate with? |
Associated with dysplasia in Barrett's esophagus.
Can correlate with the tumor grade in many neoplasms and the mitotic count in soft tissue sarcoplasms. |
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What does the p27 protein do?
What activates it? |
It suppresses cell division. Arrest of G1 phase. Without p27 cell can proliferate uncontrollably.
Transforming Growth Factor beta activates it. |
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Mcm2 protein:
What is it used to determine? Mcm stands for what? Essential for? |
Used to determine if a tumor is aggressive or not.
Minichromosome maintenance. Essential for the initiation of DNA replication. |
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Which is useful in estimating prognosis of patients with mucoepidermoid carcinoma of intraoral minor salivary glands: KI-67 or p27?
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p27.
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p53 protein:
What is its function? |
It encodes a DNA-binding transcription factor responsible for cell-cycle checkpoints.
It either arrests growth to allow for repair or signals for apoptosis. With it mutated, we lose control of cell cycle and cell proliferation. |
