Multiple Choice Questions – Wattle Quiz (30 chosen randomly)
1) The Rous Sarcoma Virus (RSV) genome contains:
a) v-ras
b) v-Myc
c) v-src
d) v-erbB
2) Chromosomal translocations in Burkitt’s lymphoma result in activation of:
a) MYC
b) RAS
c) SRC
d) TP53
3) Lymphoma patients likely to have the worst outcome if the tumours are:
a) Myc overexpressing
b) Bcl-2 loss-of-function
c) Myc overexpressing + Bcl-2 overexpressing
d) Bcl-2 loss-of-function and Myc overexpressing
4) Myc activates transcription when in complex with:
a) Mxd
b) Max
c) CycD
d) Mdm2
5) Segments of chromosomes that have broken loose and replicated as:
extrachromosomal elements are called:
a) Homogeneously staining regions
b) Chromosome fusions
c) Chromosome deletions
d) Double minutes
6) Which developmental pathway is frequently activated in medulloblastoma?
a) Bcl2
b) PTEN
c) p16
d) Shh
7) Single nucleotide polymorphisms (SNPs) are more common in:
a) Telomeres
b) Coding regions
c) Intergenic regions
d) Splice junctions
8) miRNA can:
a) Activate mRNA translation
b) Block receptor-ligand binding
c) Promote mRNA stability
d) Prevent mRNA translation
9) Benign neoplasms are:
a) Poorly differentiated
b) Metastatic
c) Able to move through the basement membrane
d) Well differentiated
10) Patient X was diagnosed with breast cancer. What antibody stain would you use to aid
diagnosis and direct treatment?
a) HER2 antibody
b) Ras antibody
c) Myc antibody
d) P21 antibody
11) What cellular changes cause cancer cells to stain more strongly for hematoxylin?
a) Increased cytoplasmic content
b) Increased DNA
c) Disruption to the cell membrane
d) Cellular senescence
12) Which is the most likely epigenetic modification of tumour suppressors in cancer?
a) DNA hypermethylation
b) DNA acetylation
c) Histone methylation
d) Histone acetylation
13) Which modification leads to open chromatin and DNA accessibility?
a) Acetylation
b) Methylation
c) Phosphorylation
d) Ubiquitination
14) Which are the first messengers in growth signalling?
a) Growth factors
b) Transcription factors
c) Ubiquitin ligases
d) Diacylglycerol
15) Oncogenic RAS mutations result in:
a) Decreased MYC transcription
b) Increased MAPK activity
c) RAF ubiquitination
d) RAF downregulation
16) MDM2 is a:
a) Protein kinase
b) CDK inhibitor
c) Ubiquitin ligase
d) Phosphatase
17) Oncogenic stress activates TP53 via:
a) Cyclin B
b) ATM
c) ATR
d) ARF
18) The spindle checkpoint is active in:
a) G1 phase
b) S phase
c) Pro-metaphase
d) Anaphase
19) Predict the breast cancer patient with the worst prognosis based on these
characteristics:
a) Progesterone Receptor Positive, TP53 Mutant
b) Progesterone Receptor Negative, TP53 WT
c) Progesterone Receptor Negative, TP53 mutant
d) Progesterone Receptor Positive, TP53 WT
20) Myc can drive progression past the G1 phase restriction point by:
a) Stabilising CycD protein
b) Phosphorylating pRb
c) Activating CycD transcription
d) Degrading pRb
21) Pocket proteins inhibit transcription by complexing with:
a) Histone deacetylases
b) Histone acetylases
c) DNA methylases
d) DNA acetylases
22) EGFR is frequently activated in glioma as a result of extracellular domain:
a) Deletion
b) Fusion
c) Phosphorylation
d) Duplication
23) P21, p27, p57 are:
a) Cyclin Dependent Kinases
b) Cyclin Dependent Kinase Inhibitors
c) Pocket proteins
d) RNA Polymerases
24) Apoptosis via the apoptosome requires mitochondrial release of:
a) TP53
b) Bcl-2
c) Cytochrome C
d) FasL
25) The essential change in the genome for cellular immortality is:
a) Telomere shortening
b) Histone phosphorylation
c) DNA methylation
d) Telomere lengthening
26) The Cancer Stem Cell Hypothesis is strongly supported by studies in:
a) Breast cancer
b) Brain cancer
c) Melanoma
d) Squamous cell carcinoma
27) Transit amplifying cells are at risk of mutation due to:
a) Low mitotic activity
b) Exposure to the environment
c) High mitotic activity
d) Ability to differentiate
28) The stem cell marker in the intestinal crypt is:
a) Lgr5
b) APC
c) Notch
d) Wnt
29) The process of haematopoiesis results in:
a) Formation of new blood vessels
b) Formation of new endothelial and smooth muscle cells
c) Production of stem cells
d) Production of blood cells
30) Tissue Inhibitors of Metalloproteinase (TIMPs):
a) Require zinc to coordinate their catalytic site
b) Inhibit the movement of fibroblasts
c) Suppress angiogenesis
d) Inhibit Cyclin Kinases
31) Which of the following events is essential for metastasis:
a) Checkpoint activation
b) Cell Migration
c) Epithelial-to-mesenchymal transition
d) Mitosis
32) Which of the following is NOT a standard treatment for metastatic cancer?
a) Immunotherapy
b) Chemotherapy
c) Radiotherapy
d) Dietary restriction
33) Which of the following statements does NOT support the idea that the immune system
monitors and eliminates cancer cells?
a) Immunocompromised patients experience a higher incidence of cancers
b) Patients whose tumours have high levels of tumour-infiltrating lymphocytes survive
longer than those whose tumours have low levels of tumour-infiltrating lymphocytes
c) Mice lacking perforin have an elevated incidence of spontaneous tumours
compared to control mice expressing perforin
d) Mice injected with live tumour cells develop tumours whereas mice injected with
dead tumour cells do not develop tumours
34) Which of the following statements is NOT correct?
a) MHC Class II on dendritic cells is presented to T helper cells
b) MHC Class I on dendritic cells is presented to precursor Cytotoxic T cells
c) MHC Class II is presented on cancer cells
d) MHC Class I is presented on cancer cells
35) Which of the following statements is correct:
a) Immunotherapy is used as frequently as chemotherapy
b) Immunotherapy is affordable for all cancer patients
c) Immunotherapies can induce innate and adaptive immune responses
d) CAR-T cell therapy targets immune checkpoint proteins
36) Melanoma drug Zelboraf (Vemurafenib) targets a mutant (V600E) version of:
a) A-Raf
b) B-Raf
c) Ras
d) MEK
37) The following statement is correct:
a) Single agent drugs are more effective than combination therapies in preventing drug
resistance
b) Treatment with combination therapies minimises the risk of developing drug
resistance
c) Combination therapies are more effective at preventing resistance when given
sequentially
d) Chemotherapy has less side effects than combination therapy
38) Mechanisms relating to drug half-life are called:
a) Pharmacokinetics
b) Pharmacodynamics
c) Pharmacoexcretion
d) Conjugation
39) What statement is true of the Philadelphia Chromosome?
a) It is a translocation between Myc and IgG promoter
b) Cells carrying this chromosome are unable to activate the PI3K pathway
c) It constitutively activates the p210 transcription factor
d) Tyrosine kinase inhibitors can be used for effective treatment
40) A possible mechanism of resistance to B-RAF inhibitors is:
a) Downregulation of Wnt5a
b) ERK hypermethylation
c) Loss of PTEN
d) P53 tetramerisation
Short Answer Questions – answer ALL questions
(35% of total mark)
Question
1. Describe
the
molecular
events
thatdue
promote
Burkitt’s
children
in equatorial
Africa
are more and
pronecellular
to this type
of cancer
to their location
nearlymphoma.
the equator this is due to the pr
mosquito thatAfrica?
is known to carry the virus.
Why might this cancer be common in children in equatorial
Chromsoomal translocation occur in BL where there is fusion from one chromosome with a second unrelated chromosome
8.. These translocation separate MYC gene from normal promotor ans place the coding region under the control if three
promotoes and as a consequence mYC transcription is highly activated and drives proliferative cell growl in BL whic dr
lymphocytes,lymph galds and lymphoma.
Question 2. Discuss how dysregulation of the non-coding genome can promote tumour
initiation and progression. Could this information be used to develop new cancer therapies?
Question 3. The genes activated by this pathway promote cell
migration. If protein B was mutated and could no longer bind
protein A what would happen to the cell? Discuss two ways
drugs could be designed to target this pathway in cancer cells.
A
B
Ub
C
Ub
D
D
Question 4. Platelets play a complex role in cancer progression. Discuss with the support of
examples. Could this knowledge be used to improve patient outcomes?
Question 5. Why might drugs that target one signalling pathway have limited efficacy in
treating metastatic cancer?
Question 6. What is immunoevasion? Provide examples supporting the concept of
immunoevasion. What are the implications for tumour progression?
Long Answer Questions – answer TWO questions
(50% of total mark)
Question 1. Tumour formation is a complex, multi-step process. Outline the molecular
changes required for initiation and progression of colorectal cancer. How could these
molecular changes be exploited to assist with diagnosis and treatment?
Question 2. Discuss the cellular process of local invasion by tumour cells, outlining the major
steps and including the key molecular events. Evaluate the evidence for and against EMT
being required for invasion.
Question 3. Anti-PD-L1 and anti-PD-1 monotherapy response rates have been reported to
be between 13% and 38%. This means a substantial proportion of patients are not
responsive to this immunotherapy. Apply your knowledge of the Cancer-Immunity cycle to
evaluate why this occurs. What are some alternative immunotherapies that might be more
effective and why?
Question 4. You aim to identify novel melanoma treatments which target the nucleolar stress
response. You have a library of human cell lines and pre-clinical animal models of melanoma.
Describe your drug discovery approach. How would you validate efficacy of lead candidates
and progress to clinic?
Question 5. Discuss the challenges of drug resistance to cancer treatment. Evaluate current
and future strategies for overcoming drug resistance.