Samenvatting Class notes - Oncology

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- Oncology
- Steenbergen
- 2020 - 2020
- Vrije Universiteit Amsterdam
- Biomedische Wetenschappen
188 Flashcards en notities
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Samenvatting - Class notes - Oncology

  • 1585692000 1. Chapter 1

  • From which tissue does a carcinoma arise?
    Epithelia
  • From which tissue does an adenocarcinoma arise?
    Glandular tissues
  • From which tissue does a sarcoma arise?
    Mesodermal tissues (e.g. Bone, muscle)
  • From which tissue does a lymphoma arise?
    (Progenitors of) white blood cells
  • What is the difference between a cytotoxic and cytostatic effect?
    Cytotoxic: prevention of cell division
    Cytostatic: killing of cells
  • What are the three phases of clinical trials?
    Phase I: assessment of safety of a limited number of patients. Also, assessment of pharmacokinetics and metabolism.
    Phase II: assessment of efficacy at a safe dose
    Phase III: extensive trials. Assessment of added value. Comparison with current standard treatment.
  • 1585864800 3. Chapter 2 (2)

  • What is ionizing radiation?
    Radiation which causes ionization of an atom, resulting in emission of an electron. The electron can damage the DNA of cells directly or indirectly via production of ROS.
  • What is the linear energy transfer (LET)?
    The average energy per unit distance deposited by a charged particle. The higher the LET, the more cell kill per Gy.
  • How is radiotherapy used in the clinic?
    As teletherapy (local external beam radiotherapy) or as brachytherapy (bring the radioation inside).
  • What is the radiation carcinogenic process?
    Initiation -> promotion -> progression
  • What is a secondary tumor?
    Radiation-induced tumors after being treated with chemotherapy.
  • What type of DNA damage does ionizing radiation cause? Which cell cycle phase is sensitive?
    • Single strand DNA breaks
    • Double strand DNA breaks
    • Base damage
    The G2/M phase is sensitive
  • What type of DNA damage does non-ionizing radiation cause? Which cell cycle is sensitive?
    Pyrimidine dimers that lead to point mutations.
    The S phase is sensitive.
  • How does UV cause cancer?
    A cytosine is recognized as a thymine, this leads to an A:T instead of a G:C.
  • What is the working mechanism of genotoxic carcinogens?
    Timing: DNA synthesis
    Mechanism: DNA adduct formation
    Effect: DNA adducts disturb the DNA structure and replication
    Result: if not repaired sufficiently there is a carcinogen specific mutation.
  • How can radiation resistance occur?
    • Location of cells in a tumor (for away from blood vessels (=hypoxic) are more likely to be resistant to radiation)
    • Tumor cell heterogeneity
    • 'Acquired' drug resistance
  • 1586124000 5. Chapter 4

  • What type of molecules are most transcription factors?
    Tyrosine kinases
  • Describe the signal transduction pathway of EGF.
    1. EGF binds to its receptor EGFR
    2. Dimerization
    3. Autophosphorylation
    4. The SH2 domain of GRB2 recognizes phosphorylated EGFR
    5. The SH3 domain of GRB2 interacts with the SH3 domain of SOS
    6. SOS activates RAS (GTP is bound)
    7. Raf activation by RAS
    8. Activated Raf phosphorylates mitogen-activated protein kinase kinase (MEK)
    9. MEK activates MAPK by phosphorylation
    10. MAPK targets the AP-1 transcription factor
  • What is v-sis?
    A growth factor that secretes PDGF (normally a component of wound response). It is an oncogene that can lead to unregulated growth when secreted in the wrong location or with the wrong timing.
  • What is v-erbB?
    A growth factor receptor that looks like EGFR. The extracellular domain is deleted and this causes cells to divide in the absence of EGF.
  • How can ras work as an oncogene?
    If ras cannot go back to the inactive RAS-GDP, there is constitutive activation of the RAS protein.
  • What is v-fos?
    V-fos can lead to an increase in AP-1 and thus AP-1 regulated genes.
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Laatst toegevoegde flashcards

What is panitmumab/cetuximab?
An anti-EGFR antibody. This results in the inhibition of tumor growth, metastatic potential, and angiogenic factors.
What is trastuzumab?
An anti-HER2/neu antibody. It inhibits HER-2 mediated signaling, activates antibody dependent cellular toxicity (ADCC), and it inhibits tumor cell proliferation.
What is the maximum tolerated dose (MTD)?
The highest dose at which 1 or 0 out of six patients experiences DLT.
What is the 3+3 design?
Treat 3 patients at dose K.
  • if 0 patients experience dose-limiting toxicity (DLT) escalate to dose K+1
  • if 2 or more patients experience DLT, de-escalate to dose K-1
  • if 1 patient experiences DLT, treat 3 more patients at dose level K
    • if 1 of 6 experiences DLT, escalate to dose K+1
    • if 2 or more of 6 experience DLT, de-escalate to K-1
What is vemurafenib?
Vemurafenib is able to inhibit the BRAF pathway that leads to promotion of cell proliferation.
Describe the different phases of clinical trials.
Phase 0: testing the drug for a short period
Phase 1: dose escalation, new combinations. Primary endpoint: safety, tolerability.
Phase 2: one dose in a specific cancer type. Primary endpoint: efficacy.
Phase 3: randomized study in specific cancer types. Endpoint: superiority or non-inferiority to standard treatment.
Phase 4: one dose in specific cancer type. Endpoint: safety in larger group of patients.
What is imatinib?
An inhibitor of the BCR-ABL tyrosine kinase. It is a selective treatment for CML.
What is E5?
It interferes with EGFR signaling (immune response)
What are E6 and E7?
Viral oncogenes. They inactivate p53 and pRB and activate telomerase.
HPV16 is mainly produced in differentiated cells. Why?
These cells are not dividing anymore so the activation of the replication machinery does no do any harm to these cells. The only thing that happens is that more virions are produced.