Flashcards in Quiz 6 (oncology) Deck (62):
Geftinib drug target
Erlotinib drug target
Afarinib drug target
Crizotinib drug target
Receptor tyrosine kinase/ALK
Ceritinib drug target
Receptor tyrosine kinases/ALK
Cetuximab drug target
Panitumumab drug target
Which oncology meds are used for colorectal cancer?
Which oncology med is used for head and neck cancer?
What are the majority of oncology meds used for?
EGFR activation leads to cell ____
What are the 2 types of lung cancer classifications?
Non-Small Cell Lung Cancer
Small Cell Lung Cancer
Which type of lung cancer is more common?
Non-Small Cell Lung Cancer (NSCLC)
What is traditional first-line therapy for NSCLC?
Activation/inactivation of EGFR causes cancer?
HER1/ErbB1 mutations in EGFR predict _____ may be more effective.
If mutation not present in EGFR, then ____ is more effective.
What is the structure of EGFR?
Crosses cell membrane
Abs bind outside
Tyrosine kinase inhibitor intracellular
What do TKIs do?
Inhibit phosphorylation by tyrosine kinase
What factors of a tumor indicate poor prognosis (there are 5)?
EGFR Inhibits all of these
Angiogenesis (creating its own blood supply)
Which EGFR mutations indicate susceptibility to TKI?
in exons 18, 19, 21
Which EGFR mutations indicate resistance to TKIs?
in exon 20
What mutation in exon 19 causes susceptibilty to TKIs?
What mutation in exon 21 causes susceptibility to TKIs?
What are the EGFR tyrosine kinase inhibitors?
Erlotinib and afatinib are most effective with ___ EGFR expression
T/F: Gefitinib had a survival benefit in patients who had high levels of EGFR
False - fast-track approval has failed
When are erlotinib and afatinib first-line treatment?
exon 19 deletions
exon 21 (L858R) substitution mutations
What is the barrier to using genotype guided dosing with TKIs?
It's desired to begin therapy before genotype results are available
Which meds are antibodies against overexpressed EGFR?
___ mutations are associated with resistance to TKIs in patients with EGFR mutations
T/F: Activation of KRAS proteins would cause cancer development regardless of EGFR signaling
True - EGFR signaling is upstream of KRAS
Cetuximumab/Panitumumab are used in patients with ______ colon cancer and _______
EGFR-expressing colon cancer; KRAS mutant negative
ALK mutation is fusion of the ____ gene to ____
ALK to EML4 (which is constitutively promoted, so makes ALK always active)
What are the ALK inhibitors?
Which ALK inhibitor is first-line for ALK positive NSCLC patients?
Crizotinib increases he risk of ___ adverse effect over chemotherapy
hepatotoxicity (increased LFTs)
When is ceritinib used?
If crizotinib fails
What ADE with ceritinib?
What is the mechanism of mercaptopurine?
inhibits purine nucleotide synthesis
What gene is associated with mercaptopurine?
What gene is associated with irinotecan?
What is the MOA of irinotecan?
Inhibits topoisomerase I
___ TPMT activity increases the risk of _____ toxicity
Low; mercaptopurine toxicity
What is mercaptopurine toxicity?
Myelosuppression (reduced WBC, RBC, platelets)
When is irinotecan used?
Metastatic colorectal cancer
What is the active metabolite of irinotecan?
___ inactivates SN-38
Which UGT1A1 allele decreases function?
What does decreased UGT1A1 function increase the risk of with irinotecan?
Neutropenia and severe (deadly) diarrhea
How should you adjust irinotecan dosing for patients with UGT1A1*28?
Reduce by 1 dose level
Is genotyping for UGT1A1 normally done?
No - no clear dosing guidelines
Most familiar cancer syndromes are related to tumor suppressor genes or oncogenes?
Tumor suppressor genes
What is loss of heterozygosity?
Losing chromosomes - maybe 23, maybe just part of some of them - but only have 1 copy left of a gene
Heritable retinoblastama is autosomal dominant or recessive?
Herital retinoblastoma is normaly bilateral or unilateral?
Average age at diagnosis is younger for pts with nonheritable or heritable retinoblastoma?
T/F: Retinoblastoma follows the two-hit hypothesis model
The RB1 gene (involved in retinoblastoma) is involved in ______ when normally functioning
Cell cycle regulation
P53 prevents cell from completing cell cycle if what?
DNA or cell is damaged
How does p53 stop cell cycle if damage is minor?
Halts until it can be repaired