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37 Cards in this Set
- Front
- Back
Complete the chart |
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What are the three main types of skin cancer? They are cured if what...? |
Basal cell, squamous cell, melanoma
Cured if found and treated early |
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What are two topical treatments for localized superficial basal cell carcinoma?
What drug is used for advanced or metastatic disease basal cell carcinoma? (acts on SMO and competes with SHH) |
Flourouracil or imiquimod
Vismodegib |
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What is a drug that acts as an immunostimulant by activating TLR 7 or 8 (induces Th1 immune response), involves the adenosine receptor blockade, and activates NFkB to up regulate cytokines like TNFalpha and interleukins?
How is it applied? What does it increase (also think about sensitivities)? |
Imiquimod
Topically
Photosensitivities (compromise condom and diaphragm integrity), parabens or benzyl alcohol allergies
USED TO TREAT HPV => CONTRACEPTIVE FAILURE |
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What is an alternative of imiquimod (IMQ) action? |
Repressing HH signaling independent of TLR activity by modulating GLI (glioma-associated oncogene) activity in BCC. |
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What are some consequences of aberrant signaling of HH?
Is the pathway lingand independent? |
Upregulation of anti-apoptotic Bcl-2, induction of VEGF and angiopoietins => regulation of angiogenesis
Yes, blocking HH binding to PTCH1 inneffective |
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What are thee major toxicities of vismodegib (think baby)? |
Intrauterine fetal death Male-mediated teratogenicity Pregnancy
Need to practice contraception and DON'T GIVE BLOOD for 7 months! |
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What is the initial treatment for squamous cell carcinoma (are ANY drugs involved)?
What drug appears to be the most effective for metastatic of advanced SSC disease? |
Cut it out and/or radiation = initial (NO DRUGS!)
Metastatic or advanced = Cisplatin therapy
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What three melanoma drugs provide are classified as immunotherapy:
Aldesleukin; IL2, Interferon-a-2B, Sorafenib, Trametinib, Vemurafenib, Ipilimumab, Dacarbazine, Lomustine, Carmustine, Plantinums, Vincas, Taxanes |
Aldesleukin (IL-2) Interfereon-a-2B Ipilimumab |
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What are three "signal transduction inhibitors" for melanoma?
Aldesleukin; IL2, Interferon-a-2B, Sorafenib, Trametinib, Vemurafenib, Ipilimumab, Dacarbazine, Lomustine, Carmustine, Plantinums, Vincas, Taxanes |
Sorafenib Trametinib Vemurafenib |
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What is the BEST chemotherapy combo (but is short-lived)?
Aldesleukin; IL2, Interferon-a-2B, Sorafenib, Trametinib, Vemurafenib, Ipilimumab, Dacarbazine, Lomustine, Carmustine, Plantinums, Vincas, Taxanes |
Dabarbazine Lomustine Carmustine |
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What does Adlesleukin bind to? What does it induce proliferation of?
In what patients is it contraindicated?
How does it cause renal failure? |
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IL-2 sitmulates cytotoxic T cells to expand and activate anti tumor lymphocyte populations; however, it also stimulates TReg cells which does what?
What causes the wide range of adverse effects? |
Dimishes the beneficial effects of stimulating tumor or virus-specific T cell responses
Indiscriminate stimulation |
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Which three conditions should you avoid using Interferon-alpha 2b in (think general effects)? |
Autoimmune disease Cardiac disease Depression Also infection |
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What is the general mechanism of Interferon alpha-2b? |
Interferon binding to cell surface receptor => activation of tyrosine kinases => production of several IFN-stimulated enzymes |
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What is Ipilimumab?
What is its effect on the immune system? |
Cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4)
Bolsters anti-tumor response of immune system |
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What are two major adverse effects of Ipilimumab? |
Seere and fatal immune-mediated adverse reactions
Dermatitis (toxic epidermal necrolysis) |
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Numerous BBWs for Ipilimumab |
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What is the mechanism of ipilimumab? |
Binds to CTLA-4, blocks interaction of CTLA-4 with its ligands CD80/CD86. => augments T cells activation and proliferation |
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Sorafenib:
What kinases does it inhibit?
Major adverse effects?
Is a rash produced? |
Liver, HFM, rash, anemia, teratogen |
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What two types of signaling does sorafenib block? |
Proliferative signaliing and aniogenic signaling |
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Which drug is an oral reversible MEK inhibitor? It is used for melanoma patients with which mutations?
What are some adverse effects? |
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Where in the pathway does vemurafenib act and where does trametinib act? |
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What drug is an oral inhibitor of BRAF? What does it require just like Trametinib? How can resistance occur? What are patients at a significant risk of? Give four AEs (think liver, heart, skin and eyes) |
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BRAF-MEK inhibitors require ________ genotyping.
All three drugs are associated with _________, possibly severe.
BRAK/MEF inhibitors seem to have common toxicities: Name 4 general ones |
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What is the pregnancy status of each (C or D)? |
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How are fluorouracil and imiquimod applied with actinic keratosis?
Which drug is an inhibitor of anti-inflammatory mediators including PGE2 (rash, redness, dry skin, peeling are AEs).
Which drug is a chemical peel that rapidly penetrates and cauterizes skin, keratin, and other tissue (AEs = burning, inflammation, and tenderness)
TRICHLOROACETIC ACID AND DICLOFENAC |
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The drugs that act on HH signaling are all what? Why? |
Teratogens:
HH key player in organogenesis |
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Which two drugs require routine X-rays? |
Interferon-alpha-2b and adelsleukin
Check for damage to pulmonary tissue
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True or false: The kinase inhibitors are teratogenic. |
TRUE! |
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Which two drugs require BRAF mutation genotyping? |
Vemurafenib and Trametinib |
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3 ways to develop resistance to MAPK pathway targeted drugs: |
Downstream mutation Parallel pathways Binding site mutation |
