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29 Cards in this Set
- Front
- Back
- 3rd side (hint)
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What stage of wound healing do we see PDGF and TGF-ß1 (transforming growth factor)?
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Epithelialization
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Which stage of wound healing do we see VEGF ?
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angiogenesis
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Which stage of wound healing do we see Fibrinogen --> fibrinogen?
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Break in skin (clot formation)
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Which stage of wound healing to we see MMP and reorganization of the ECM?
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Wound closure
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Which cells produce TGFß1, TGF-∂ PDGF-AB, PDGF-BB, FGF and VEGF?
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Platelets: TGFß1, and PDGF-AB… 2) Macrophages: VEGF, TGF-ß1/∂, PDGF-BB, and FGF… 3) Endothelial cells: VEGF and FGF
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None
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What is Avastin approved use in Rx? What does it also work on?
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CRC… Macular degeneration
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What is avastin mechanism of action?
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Anti-VEGF mAB
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None
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What is the difference between Avastin (Bevacizumab) and Lucentis?
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Lucentis is second generation Avastin… both are mAb against VEGF, but Lucentis is humanized (thus produces less inflammatory reponse), and is affinity maturized
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Which, Avastin (Bevacizumab) and Lucentis, has the Fc region?
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Avastin
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what is the pathway for GF (mitogen) to activate Myc genes?
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Mitogen binds (TKR) --> RAS --> MAP kinase --> Myc gene transcription
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Name the 3 different ways, Myc can activate E2F.
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1. Increased Cyclin-D activity --> G1/S-Cdk activation --> Rb phosphorylation --> increased E2F activity…
2. Increased p27 degradation --> G1/S-Cdk activation --> Rb phosphorylation --> increased E2F activity… 3. Increased E2F synthesis --> inceased E2F activity |
None
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What is p27?
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A Cdk inhibitor
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What does E2F activity lead to?
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entry of cells from G1 into S-phase
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Is Myc a tumor suppressor or pro-oncogene?
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pro-oncogene
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What is the mechanism of action of Becaplermin (Regranex gel)?
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since the PDGF-BB TKR crossphosphorylate by dimerization, Becaplermin is two ligands covalently bound and thus causes dimerization
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What does Becaplermin effective in binding and what is it used for?
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PDGF-BB.. Used for diabetic ulcer care
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What is the best practice for diabetic ulcer?
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debridement and Becaplermin (@ higher dose: 100 ug/g)
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what are the theoretical side effects of engineered growth factors used in wound healing?
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malignancy and hypertrophic scars
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What is an isozyme of an enzyme?
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polymorphisms for metabolizing drugs in different people.
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What two isozymes are of therapeutic value?
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1. The enzyme the converts the prodrug into an active drug… 2. The enzyme that converts an active drug into an inactive metabolic derivative.
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In CPT-11 (Irinotecan) which is a prodrug, certain patients have less activity in the enzyme that converts the active drug into an inactive metabolite, However, the metabolite (SN-38) is toxic at high dose and causes diarrhea and leukopenia. What do you do for those patients?
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Reduce the dosage
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Platinum compounds damage DNA. What mechanism repairs this damage?
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Nucleotide excision repair
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Which DNA repair mechanism is used to fix Xeroderma pigmentosum? (UV damage, oxidative damage and cross-links)
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Nucleotide excision repair
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What polymorphism do people with group D protein XPD (Xeroderma pigmentosum-D) have?
What does this polymorphism cause? What is the faulty repair mechanism associated with XP? |
1. polymorphism at 312 and 715…
2. Decreased response to 5-FU/oxaliplatin 3. Nucleotide Exclusion repair |
Arrested for 5-FU discount by the XPD
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What are the 4 stated steps of wound healing physiology, starting from and including a break in the skin?
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1. Break in the skin (clot formation) … 2. Epithelialization… 3. Neoangiogenesis… 4. Wound closure
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Which step of wound healing includes metabolic signals (need for oxygen and nutrients) VEGF?
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Angiogenesis
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Which step of wound healing includes degradation of ECM, Proliferation of epidermal cells, and PDGF and TGF-ß1?
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Epithelialization
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What step of wound healing includes fibrinogen --> fibrin (fibrin clot), inflammation, and platelet infiltration?
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Break in skin barrier (clot formation)
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What step of wound healing includes Reorganization of the ECM, MMPs secreted by macrophages, endothelial cells, fibroblasts, and epithelial cells in the context of signal transduction?
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Wound closure
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