L10- Cancer Pharmacology Flashcards
*Oncogenes are mutated forms of what gene types?Which signaling pathways do oncogenes disrupt?
a. Tumor suppressor genes that regulate apoptotic signaling
b. Cell proliferation genes that regulate receptor tyrosine kinase (RTK) signaling
c. Tumor suppressor genes that regulate receptor tyrosine kinase (RTK) signaling
d. Cell proliferation genes that regulate apoptotic signaling
e. Cell proliferation genes that regulate angiogenesis signaling
b. Cell proliferation genes that regulate receptor tyrosine kinase (RTK) signaling
*Which receptor processes are important for up-regulating proto-oncogene/dominant gene expression?
a. Death receptor trimerization and cleaving cytosolic domain
b. RTK receptor trimerization and cleaving cytosolic domain
c. RTK receptor dimerization and phosphorylation of cytosolic tyrosine residues
d. Death receptor dimerization and phosphorylation of cytosolic serine residues
e. None of the above
c. RTK receptor dimerization and phosphorylation of cytosolic tyrosine residues
*Mutations in Recessive/Tumor Suppressor genes affect which general signaling pathway and in what way? (Choose one)
a. RTK Signaling: Mutations surpass cell proliferation
b. Apoptosis: Mutations enhance apoptotic signaling
c. RTK: Mutations enhance cell proliferation
d. Apoptosis: Mutations suppresses apoptotic signaling
e. None of the above
d. Apoptosis: Mutations suppresses apoptotic signaling
*Which of the following are hallmarks of cancer?
a. BRAF mutations, limitless replicative potential, evade apoptosis
b. Evading apoptosis, tissue invasion and metastasis, sustained angiogenesis
c. Evading apoptosis, respond to monoclonal antibodies, mutations of tumor suppressor genes
d. Benign growth, mutations of proto-oncogenes, mutations of p53
e. Activation of telomerase, neoplasm, resistance to radiotherapy
b. Evading apoptosis, tissue invasion and metastasis, sustained angiogenesis
Which best describes the mechanism of action of alkylating agents, such as cyclophosphamide - Select one.
A. Bind GDP-bound tubulin, thereby inhibiting depolymerization of microtubules
B. inhibit DNA polymerase by acting as nucleotide analogs
C. prevent unwinding of DNA by disrupting phosphodiester bonds
D. Cross-link DNA by covalently coupling DNA nucleotides
E. all of the above
D. Cross-link DNA by covalently coupling DNA nucleotides
Mutations to ______ genes are often _______
A. Tumor suppressor genes; dominant
B. Proto-oncogenes; recessive
C. Proto-oncogenes; neutral
D. Tumor suppressive genes; recessive
E. None of the above:
D. Tumor suppressive genes; recessive
Vemurafenib (PLX4032) inhibits which kinase?
A. MEK
B. RAS
C. BRAF V600E
D. K-Ras
E. Estrogen receptor
C. BRAF V600E
Vinca alkaloids are used for the treatment of cancer because they inhibit _______ which is needed for mitosis
A. microtubule breakdown
B. cell cycle re-entry
C. telomerase reactivation
D. tumor supressor gene inhibition
E. microtubule formation
E. microtubule formation
Cancer types are named based on the place of origin of the cancer
a. True
b. False
A. True
Why is p53 called the “guardian of the genome?”
a. Prevents cancer cells from performing DNA replication
b. Prevents proto-oncogenes from mutating
c. Prevents damaged DNA from proliferating
d. Prevents premature apoptosis
c. Prevents damaged DNA from proliferating
Which hallmark of cancer does bevacuzimab block?
a. Evading apoptosis
b. Self-sufficiency in growth signals
c. Insensitivity to anti-growth signals
d. Sustained angiogenesis
e. Tissue invasion and metastasis
d. Sustained angiogenesis
Mutation of tumor suppressor genes is normally what type of inheritance?
a. Dominant
b. Recessive
c. Codominant
d. X-linked
e. None of the above
b. Recessive
Which drug competitively binds to the ATP binding site of BCR-ABL kinase?
And What type of Cancer is this typically used to treat?
Drug: Imatinib
Cancer: Chronic myeloid leukemia
Which hallmark of cancer does bevacuzimab block?
Blocks Angiogenesis of tumors
Would you treat patient A with cetuximab if they had a KRAS mutation?
No
Cyclophosphamide
Chemotherapy Drug
Inhibit DNA synthesis by Cross-linking base pairs to prevent formation of replication fork
Methotrexate
Chemotherapy Drug
Inhibit DHFR enzyme, which makes FH4
(cofactor for dTMP, which is needed for DNA and purine synthesis)
Fluorouracil
Chemotherapy Drug
- Inhibit thymidylate synthase (DUMP -> DTMP) by depleting thyidine
- Converts to F-UMP and incorporates into RNA -> inhibits RNA processing
Vinca Alkaoids
(Vincristine)
Chemotherapy Drug
Prevent Tubulin from polymerizing to microtubules (which is needed for mitotic spindles)
Taxanes
(Taxol)
Chemotherapy Drug
Induces abnormal bundles in microtubule assembly
Tamoxifen
Hormone Therapy
Binds to estrogen receptors and prevent shape so co-activators cant bind (to alter gene expression)
Vemurafenib
Target Therapies
Binds mutated BRAF to inhibit it from activating MEK-ERK pathway
Gleevec
(imatinib)
Target therapy
Competitively binds to ATP binding site of BCR-ABL kinase to prevent stimulation of proliferation
(Chronic myeloid leukemia)
Ipilimumab
Immunotherapy
Antibody to CTLA-4 (normally down-regulate T-cell) to increase T-Cell activity
Nivolumab/Pembrolizumb
(Anti-PD1)
Immunotherapy
Anti-PD1 (PD1 normally inhibit T cells from killing tumor, along with PD-L1)
Avelumob
Immunotherapy
Anti-PD-L1 (normally inhibit T-cell from killing tumor cell)
Cetuximab
Immunotherapy
Prevent activation of RAF-MEK-ERK pathway (Targeted therapy)
*doesn’t work on mutations of KRAS
Bevacizumab
Immunotherapy
Binds to VEGF to block angiogenesis of tumors
