7 questions on the written exam

1. Explain the t(9,22) and t(15,17) and how can you treat them + what is the difference in treatment?
2. What is synthetic lethality? Explain with an example that we have seen in the course.
3. What is the role of chromatin 3D structures and how does the dysregulation contribute to cancer?
4. The graph about all the pathways was given in black and white → show with colors what are the oncogenes and what are the tumor suppressor genes? Which important tumor suppressor genes/oncogenes are missing? Is in the missing genes the cell of origin and background important? What therapies are available?
5. Give the evolution ways that tumor heterogeneity can occur (linear, branched, neutral, punctuated).
6. Give ways that you have mutational signatures and 4 examples.
7. Graph with all the little circles about T-cell leukemia was given: show using this example that you understand the complexity of aberrations in cancer.

Oral exam on 4 points

1. EGFR — what is it? How can it be contributing to cancer? How does the drug work on it? How can a patient develop relapse? Explain the graph with the therapeutic window and maximal therapy dose — this graph wasn't given but this is what you had to explain to answer the question.
2. About the CDK13 melanoma paper: how does the CDK13 mutation mechanism work in cancer?

OPEN BOEK

Meerkeuze (herleid naar 10 van de 20 punten, waren in totaal 20 vragen, geen gis of verhoogde cesuur, 40 minuten tijd):

• Mutational signature van APOBEC2 aflezen
• Which gene is not a proto-oncogene?
  • APC
  • CDK4
  • miR-17-92
  • ERBB2
• Link the following histone variants to their function: A) H3.3, B) yH2AX, C) macroH2A, D) DNA damage, E) Active transcription, F) X chromosome inactivation
  • A-E, B-D, C-F
• Andere opties (in totaal 4 opties)
• Which statement for PROTAC is not correct?
  • Clinical trials are ongoing
  • ...
• What is not true about lncRNAs?
• Which miRNA is no tumor suppressor?
  • miR-15a
  • let 7
  • miR-21
  • miR-34
• iets over PML/RARA
• iets over NHEJ
• onderzoek naar een codriver
  • MDM2
• iets over RTK's
• iets over CIMP
• which is not correct about hallmarks
  • loss of function in TSG does not contribute to the hallmarks
  • was implementated by hannahahahh and weinberg in cell
  • … was an additional hallmark
  • nog iets
• iets over MYC
• iets over oncogene amplification
• iets over philadelphia chromosome
• iets over synthetic lethality
• iets met CTCF en TAD
• wat zorgt niet voor enhanced cell cycle progression
  • deletion in cdc25
  • p16
  • ccdn1
  • cdk4

Mondeling (staat op 6 van de 20, 15 min voorbereiding en 15 min mondeling):

1. You are the new head of the precision oncology lab and you need to make sure that patients get the right treatment. Which important information do you need to obtain from the cancer of the patient?

2. Make up your own cancer cell by (in)activating three genes of the following pathway. Explain how this (in)activation would take place and what the effects on the cell would be. For the mutations that you chose, what is the role of 'cell of origin' and the 'context'?