Skip to main content
United States
Jump To
Support
Register or Log In
Support
Register or Log In
Instructors
Browse Products
Getting Started
Students
Browse Products
Getting Started
Return to Cancer Biology and Treatment Student Resources
Chapter 4 Multiple choice questions
Quiz Content
*
not completed
.
Which of the following are involved in the stimulation of proliferation in cancer cells?
Epidermal growth factor and its receptor
correct
incorrect
RAS
correct
incorrect
MAPK
correct
incorrect
CDKN2A
correct
incorrect
Hormones such as oestrogen
correct
incorrect
*
not completed
.
Which of the following processes are directly involved in cancer cell death?
Apoptosis
correct
incorrect
Necrosis
correct
incorrect
Autophagy
correct
incorrect
Angiogenesis
correct
incorrect
DNA repair
correct
incorrect
*
not completed
.
Which of the following processes are regulated by the tumour suppressor and stress response functions of p53?
Cellular senescence
correct
incorrect
Cellular proliferation
correct
incorrect
Cellular necrosis
correct
incorrect
DNA repair
correct
incorrect
None of the above
correct
incorrect
*
not completed
.
How are telomeres maintained in cancer cells?
Activation of telomerase
correct
incorrect
Activation of DNA polymerase
correct
incorrect
TERT promoter mutation
correct
incorrect
Activation of a recombinational-based process called ALT
correct
incorrect
*
not completed
.
How does a mutation of codon 132 in the enzyme IDH1 affect tumourigenesis?
Loss of mitochondrial isocitrate dehydrogenase enzyme activity
correct
incorrect
Formation of oncometabolite 2HG
correct
incorrect
Deregulation of histone methylation
correct
incorrect
Deregulation of DNA methylation
correct
incorrect
*
not completed
.
Hypoxia stimulates which of the following cellular processes?
EMT
correct
incorrect
Angiogenesis
correct
incorrect
Autophagy
correct
incorrect
DNA repair pathways
correct
incorrect
*
not completed
.
Which of the following steps are involved in the elimination of cancer cells by the immune system?
Binding of tumour antigens by Antigen Presenting Cells
correct
incorrect
Activation of naïve T cells and differentiation into cytotoxic T cells in the lymph nodes
correct
incorrect
Binding of cytotoxic T cells to tumour cells via the major histocompatibility class II receptors
correct
incorrect
Tumour cell death can be triggered through interactions between death receptor ligands on T cells and associated receptors on the surface of tumour cells.
correct
incorrect
*
not completed
.
Which of the following are mechanisms used by cancer cells to evade immune destruction?
Increased expression of major histocompatibility class I proteins on the surface of tumour cells
correct
incorrect
Overexpression of CTLA-4
correct
incorrect
Inappropriate expression of PDL-1 on tumour cells and
correct
incorrect
Increased production of IL-10
correct
incorrect
*
not completed
.
Which of the following statements about the epidermal growth factor receptor (EGFR) are true?
EGFR is a member of the ErbB family of receptors which includes HER 2.
correct
incorrect
EGFR can be overexpressed in tumours either through somatic mutations and/or amplification of the EGFR gene.
correct
incorrect
Only the ligand EGF can bind to the EGFR at its ligand binding domain located at the extracellular side of the cell membrane.
correct
incorrect
EGFR signalling can only be initiated through EGFR homodimerization.
correct
incorrect
*
not completed
.
Which of the following statements relating to non-coding RNAs and cancer are true?
Overexpression of the long non-coding RNA ANRIL is related to cancer progression and poor tumour prognosis.
correct
incorrect
Exosomes can carry long non-coding RNAs and mediate drug resistance.
correct
incorrect
Non-coding RNAs only function as oncogenes in cancers.
correct
incorrect
Overexpression of miR-21 can contribute to invasion and metastasis in some cancers.
correct
incorrect
Previous Question
Submit Quiz
Next Question
Reset
Exit Quiz
Review all Questions
Submit Quiz
Are you sure?
You have some unanswered questions. Do you really want to submit?
Back to top
Printed from , all rights reserved. © Oxford University Press, 2024
Select your Country