Gao 2-26 Flashcards
cycloposphamide
alkylating agent- crosslinks DNA during replication
cisplatin
platinum drug- crosslinks Guanines in DNA during replication
5-FU
5-fluorouracil, prevents pyramide synthesis, interferes in RNA processing, causes bp substitutions, inhibits thymidylate synthase
paclitaxel
anti-mitotic, taxane class, promotes tulbulin growth, blocks dissasembly- stops cell at mid-mitosis
vincristine
anti-mitotic, vinca-alkyloid class, inhibits tubulin assembly, so mitosis is never reached
doxorubicin
anti-cancer antibiotic, topoisomerase inhibitor
Which cells are most affected by chemotherapy
stem cells: bone, hair, G.I.
What major side effect can be caused by vincristine, paclitaxel
nerve damage, because tubulin activity is affected, so neurotransmitters are not being transported for release
What hallmark of cancer would PARP inhibitors mitigate?
genome instability, mutation. These enzymes are overactive in cancer cell replication
What hallmark of cancer would VEGF inhibitors mitigate?
angiogenesis
What hallmark of cancer would B3 mimetics mitigate?
resistance to apoptosis
Drug ending in -mab
Monoclonal Ab
Drug ending in -ib
small molecule inhibitor
Oncogene Addiction theory
cancer cells become dependent on one survival pathways above any other; a limited number of oncogenes drive malignant phenotype
Describe Philadelphia Chromosome (Ph)
Fusion in hametopeotic cells of the BCR-ABL genes that make constitutively active tyrosine kinase, causing uncontrolled growth and apoptotic resistance leading to CML (Chronic Myeloid Leukemia)
Gleevec
A.K.A. Imatinib. Successful, but resistance-inducing, drug inhibiting specifically the BCR-ABL created tyrosine kinase (in CML)
Herceptin
A.K.A. Trastuzumab, a humanized AB for Estrogen receptor HER2 in breast cancer
P-glycoprotein
drug efflux channel protein
MDR1
multi drug resistance gene. Can affect chemotherapeutic results in patients.
New anti-cancer drugs are being developed to block the interaction between p53 and MDM2. Which group of patients are most likely to benefit from this type of drugs?
wt p53
After treating with p53/MDM2 interaction inhibting drugs, what is most likely to happen in cancer cells?
level of p53 upregulated
Application of EGF receptor inhibitors as anti-proliferation drugs in cancer therapy will mostly likely to arrest cell cycle at which checkpoint?
R-point in G1
