3: 10 Hallmarks Of Cancer Flashcards
Treatment for HER2/neu mutation in breast carcinoma
Herceptin (Trastuzamab)
Treatment for ABL-BCR hybrid gene in CML
Tyrosine kinase inhibitors like Gleevec (Imatinib)
Oncogene addiction
Tumor genesis is extremely dependent, “addicted to” Abl kinase
Germline vs somatic mutation
Germline mutation: mutation to egg/sperm -> heritable
Somatic mutation: mutation to the individual -> not heritable
Four classes of genes in oncogenesis how to make them cancerous
- Proto-oncogenes: gain of function
- Tumor suppressor genes: loss of function
- Apoptosis-regulating genes: suppress apoptosis
- DNA repair genes: loss of function
Driver vs passenger mutations
Driver mutations: causal; directly confers growth advantage on tumor cells
Passenger: contribution to cancer growth isn’t fully established - many are seen in a cancer
Oncoprotein
Protein created by an oncogene
Most common extracranial solid tumor in children
Neuroblastoma
Knudson’s hypothesis
Two mutations are required in a tumor suppressor gene to make it cancerous; in germline mutations, only one hit is needed
Cancer stem cells
Can self-renew and give rise to heterogenous populations of daughter cells and proliferate extensively
Bevacizumab
Downregulates VEGF so tumors cannot undergo angiogenesis as easily
Principle immune defense against tumors
CD* cytotoxic T cells
Three types of triggers that activate T cells
- Mutated self proteins
- Over-expressed or aberrantly expressed self protein
- Oncogenic virus
PD-1 ligand in tumor cells
Inhibits T cells so they dont become activated
Common cancer marker in GI cancers
CA 19-9
