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50 Cards in this Set
- Front
- Back
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Afatinib: use |
Metastatic NSCLC |
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Afatinib: mechanism
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Tyrosine kinase inhibitor
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Afatinib: genetics
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Positive for EGFR exon 19 del or exon 21 sub mutations.
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Capecitabine: uses
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Multiple metastatic cancers
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Capecitabine: mechanism
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A prodrug; gets converted to 5-fluorouracil.
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Capecitabine: genetics
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DPD deficiency; DPD metabolizes 80-90% of 5-FU to inactive metabolites; thus, homoz. mutants inevitably die from treatment.
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Cetuximab: use
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Colorectal cancers
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Cetuximab: mechanism
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A mAb against CD47, often overexpressed in tumors; this protein prevents macrophages and dendritic cells from destroying the tumor.
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Cetuximab: genetics
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Negative for codon 12 and 13 KRAS mutations.
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Cetuximab: other tests
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EGFR protein expression-positive.
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Cisplatin: uses
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Testicular cancer (very effective); often first-line in childhood cancers, where it has an 85% cure rate of all solid tumors.
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Cisplatin: mechanism
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Contains platinum; crosslinks DNA and terminates replication.
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Cisplatin: genetics
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Must identify intermediate or poor TPMT metabolizers in childrern, due to risk of ototoxicity.
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Crizotinib: use
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NSCLC
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Crizotinib: mechanism
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Acts as an ALK (anaplastic lymphoma kinase) and ROS1 (c-ros oncogene 1) inhibitor; competitively binds within the ATP-binding pocket of target kinases. |
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Crizotinib: genetics
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Candidates: positive for a chromosomal rearrangement that generates a fusion gene between EML4 and ALK results in constitutive kinase activity.
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Dabrafenib: use
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Used in combination with trametinib in patients with metastatic melanoma.
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Dabrafenib: mechanism
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Inhibits B-Raf protein, which plays a role in cell growth.
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Dabrafenib: genetics
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Positive for B-RAF V600E mutation.
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Erlotinib: uses
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NSCLC, pancreatic cancer, etc. |
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Erlotinib: mechanism
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Tyrosine kinase inhibitor that acts on EGFR.
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Erlotinib: genetics
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Positive for EGFR exon 19 del. or exon 19 sub. mutations.
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Erlotinib: other tests
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EGFR protein expression-positive.
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Fluorouracil: uses
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Treats colon, rectum, breast, stomach, and pancreas cancers.
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Fluorouracil: mechanism
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A pyrimidine analog; blocks actions of thymidylate synthase --> scarcity in dTMPs.
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Fluorouracil: genetics
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DPD deficiency; DPD metabolizes 80-90% of 5-FU to inactive metabolites; thus, homoz. mutants inevitably die from treatment.
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Irinotecan: use
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Mainly colon cancer
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Irinotecan: mechanism
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Inhibits topoismerase 1, and thus prevents DNA from unwinding; drug is then inactivated by UGT1A1.
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Irinotecan: genetics
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Carriers of the UGT1A1*28 allele, which metabolizes the drug poorly.
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Mercaptopurine: uses
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Acute lymphoblastic leukemia and other blood cancers, as well as IBD.
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Mercaptopurine: mechanism
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Inhibits purine nucleotide synthesis.
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Mercaptopurine: genetics
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6-MP is inactivated by 1 of 2 pathways: to 6-TG (toxic) and 6-MMP (non-toxic; catalyzed by TPMT). Interm. and poor metabolizers risk toxicity.
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Nilotinib: use
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Treats imatinib-resistant chronic myelogenous leukemia.
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Nilotinib: mechanism
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Tyrosine kinase inhibitor; inhibits BCR-ABL, KIT, DDR1, DDR2, and several other kinases.
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Nilotinib: genetics
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Carriers of the UGT1A1*28 allele may experience a reversible, benign elevation of bilirubin.
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Panitumumab: use
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Colorectal cancer
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Panitumumab: mechanism
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A fully human monoclonal antibody specific to the epidermal growth factor receptor; binds to the extracellular domain, preventing its activation.
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Panitumumab: genetics
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Negative for KRAS codon 12 and 13 mutations.
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Pazopanib: uses
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Approved for renal cell carcinoma and soft tissue sarcoma.
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Pazopanib: mechanism
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A tyrosine kinase inhibitor that works on multiple targets.
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Pazopanib: genetics
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Carriers of UGT1A1*28/*28 show a statistically significant increase in the incidence of hyperbilirubinemia.
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Tamoxifen: uses
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A prodrug used in the treatment of both early and advanced ER+ (estrogen receptor positive) breast cancer in pre- and post-menopausal women.
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Tamoxifen: mechanism
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An antagonist of the estrogen receptor in breast tissue via its active metabolite, 4-hydroxytamoxifen.
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Tamoxifen: genetics
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Screen for Factor II and Factor V mutations; increased risk of a thromboembolic event (TE).
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Trametinib: uses
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Metastatic melanoma
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Trametinib: mechanism
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Inhibits the mitogen-activated protein kinase kinase enzymes MEK1 and MEK2.
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Trametinib: genetics
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Positive for the BRAF V600E, which causes this kinase to be constituitively active.
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Vemurafenib: uses
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Late-stage melanoma
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Vemurafenib: mechanism
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Interrupts the B-Raf/MEK step on the B-Raf/MEK/ERK pathway, causing apoptosis to occur.
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Vemurafenib: genetics
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Only works when BRAF is mutated (V600E; 60% of melanomas); may actually encourage tumor growth in tumors without this mutation. |
