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78 Cards in this Set
- Front
- Back
what happens if a cell doesn't adapt to injury
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they undergo necrosis
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neoplasia means
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'new form'
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what is the downside to cellular adaptation to injury
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can lead to growth disturbances which predispose to neoplastic disease
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point of loss of reversibility = ?
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the point where tissues no longer respond to normal signals
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non-neoplastic growth disturbances are responsive to _______________. (what about neoplastic?)
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normal controls for growth; in neoplastic growth disturbances, response to normal controls for growth is lost. They ignore the body's signals
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non-neoplastic growth disturbances occur _________________________. (what about neoplastic?)
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separately or in combination; neoplastic are usually multiple
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how do you reverse a non-neoplastic growth disturbance? neoplastic?
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remove the stimulus. neoplastic are irreversible
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how do you determine the point of loss of reversibility?
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you can't, you can only observe the consequences
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what type of growth disturbance is most significant in neoplasms
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dysplasia (or combinations with dysplasia)
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rank growth disturbances in terms of significance in causing neoplasms
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hypertrophy < atrophy < hyperplasia < prosoplasia < metaplasia < dysplasia < combos with dysplasia
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atrophy
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shrinkage of a tissue due to a reduction in number of cells
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hyperplasia
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increase in the size of tissue due to increase in number of cells
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hypertrophy
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increase in size of tissue due to increase in size of cells
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prosoplasia
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substitution of a more highly specialized tissue for a less specialized tissue
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metaplasia
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substitution of a less specialized tissue for a more highly specialized tissue
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dysplasia
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abnormal pattern of maturation
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examples of atrophy
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cancers of the prostate & stomach
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example of hyperplasia
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reaction to irritation or hormones
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examples of hypertrophy
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physical stresses or exercise of muscle
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examples of prosoplasia
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GERD, barrett's esophagus
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examples of metaplasia
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smoker's bronchi
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examples of dysplasia
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CIN, oral precancer
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one way in which neoplastic cells differ from normal cells
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they don't respond to normal controls for growth
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which neoplastic diseases are caused by hypertrophy
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hypertrophy is not known to lead to neoplastic disease
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various injuries to cells may damage ________
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DNA
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what types of injuries create the conditions favorable to the production of free radicals that attack DNA
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ischemia and ischemia-re-profusion injuries
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nutritional deficiencies can lead to ______________________________
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a lack of adequate levels of essential components for cell growth, maturation
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downregulation of PTEN stimulates _____________________________
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cell cycle progression
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in hyperplasia there is an increased chance for _______________________________
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spontaneous DNA errors or action of deleterious agents on replication DNA
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promotors
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increase the number of tumors that form
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initiators
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cause mutations
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example of epithelial hyperplasia of the oral cavity
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acanthosis with hyperkeratosis (leukoplakia)
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what must you do if you find leukoplakia
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- remove stimulus
- biopsy! 5% of leukoplakias are already malignant |
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what does it mean if a leukoplakia does not reverse after the stimulus is removed
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it is headed towards carcinoma
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what % of high-grade dysplastic barrett's esophagus become malignant
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10%
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what must happen in order for adenocarcinoma of the esophagus to occur
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a preceding change from stratified squamous epithelium to gastric-like mucosa (often followed by dysplasia)
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example of prosoplasia in the oral cavity
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erythroplakia
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what % of low-grade dysplastic barrett's esophagus become malignant
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1%
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cells present in premalignant barrett's esophagus
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normal cells and prosoplastic cells
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what happens ti TP53 in oral cancer
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mutated
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during immortilization, invasion and metastasis, there is upregulation of ________
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VEGFA
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metaplasia represents ________________________________
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adaptive substitution - cells sensitive to stress are substituted by cells better able to withstand it
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most common epithelial metaplasia
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ciliated columnar epithelium to simple squamous epithelium in the trachea and bronchi in response to chronic irritation
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vitamin A deficiency induces
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squamous metaplasia in the respiratory epithelium
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vitamin A excess suppresses
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keratinization
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what important function is lost in respiratory squamous metaplasia
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mucous secretion
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the most common form of cancer in the respirtatory tract is composed of _______________________
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squamous cells
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most cancer appear to arise from tissues that exhibit
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prior dysplasia
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microscopic characteristics of dysplatic cells are similar to (or very often indistinguishable from) _______________________________
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cytologic features of malignancy
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microscopic features of displasia
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- hyperkeratosis*
- acanthosis* - increased numbers and/or abnormal mitosis - keratin pearls - individual cell keratinization - loss of polarity and cellular orientation - large, prominent nucleoli - dyskarynosis - basilar hyperplasia - increased nuclear:cytoplasmic ratio - poikilocarynosis - hyperchromatism HA! I KILL'D BIPH! (i know it's lame) |
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what protein plays a pivotal roll in maintaining cell proliferation
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Ki-67
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Ki-67 is present in which phases of the cell cycle
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all non-G0 phases (G1 --> S --> G2 --> M)
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in which phase of the cell cycle does Ki-67 peak
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M
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what happen to Ki-67 after M phase
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it is rapidly catabolized
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Ki-67 labeling index = ?
Represents? |
the percentage of cells in a tissue staining for Ki-67; represents the growth fraction
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for dysplasia in barrett's esophagus Ki-67 LI is associated with
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progression
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in benign tumors, high LI is associated with
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high recurrence rate
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LI greater than 20% is seen in ___________
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high grade non-hodgkins lymphoma
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in low grade lymphomas, LI>______ have a worse prognosis than those with LI<______
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5%
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p27 protein encodes _______________________
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encodes a cell cycle inhibitor protein that binds to cyclin D and CDK4 and causes arrest in G1 phase
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p27 is activated by
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transforming growth factor beta
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mutation to p27 may lead to
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loss of control of cell cycle ---> uncontrolled cellular proliferation
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minichromosome maintenance proteins are essential for ____________________________
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initiation of DNA replication
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what proteins are relevant markers for prognosis in various types of tumors
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MCM proteins
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how can MCM2 be used?
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- assess tumor proliferation
- prognostic tool to predict the outcome in a variety of cancers |
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which is useful as a prognosticator in mucoepidermoid carcinoma of intraoral minor salivary glands, Ki-67 or p27?
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p27
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hallmark of many tumors:
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p53 gene is mutated and expressed at greatly elevated levels
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a normal p53 gene encodes
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a DNA binding transcription factor that is responsible for cell cycle checkpoints that are activated after exposure to DNA-damaging agents
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in a normal cell p53 is inactivated by
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mdm2
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what does p53 do once activated
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it causes cell cycle arrest to allow for cell repair or causes apoptosis of damaged cell to occur
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p53 gene is a ____________ gene. its function?
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tumor suppressor; stops the formation of tumors
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p53 has been mapped to what chromosome
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chromosome 17
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li-fraumeni syndrome
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inheritance of only one functional copy of p53 --> prediposes to cancer --> individuals develop several tumors in different tissues in early adulthood
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mutations to __________ are found in most tumor types
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p53
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in the normal cell p53 protein binds ________ which in turn stimulates another gene to form ____________
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DNA; protein p21
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what happens when p21 interacts with cdk2
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the cell cannot pass through to the next stage of cell division
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why is mutated p53 ineffective
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it cannot bind DNA in an effective way
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which gene is known as the 'guardian of the genome'
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p53
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