Cancer MCQ’s W6 Flashcards
Which of the following statements is FALSE?
A)Most cancers are sporadic
B)Familial cancer is caused by a combination of genetic and
environmental factors with relatives showing the same type of cancer
C)Familial cancer shows no specific pattern of inheritance and is not
passed from parent to child
D)Retinoblastoma patients are an example of patients with familial cancer
E)Hereditary cancer is caused by an altered gene or gene change that is
passed from parent to child.
C
Which type of human cancer is NOT caused by viral infection?
A)Burkitts lymphoma
B)Kaposi’s sarcoma
C)Squamous cell carcinoma of the cervix
D)Hepatocellular carcinoma
E)Non small lung cell carcinoma
E
Which of the following is the most common type of cancer?
A)Carcinoma
B)Sarcoma
C)Lymphoma
D)Leukaemia
E)Benign tumours
A
Which of the following causes myeloid leukemia:
A ras
B raf
C Rb
D BCR-Abl
E EGFR
D
Which of the following statements about angiogenesis is
INCORRECT?
A)Tumour cells secrete platelet derived growth factor to induce
neoangiogenesis
B)Blood vessel endothelial cells secrete matrix metalloproteinases to
break down extracellular matrix in order to allow blood vessels to
grow towards the tumour
C)Tumour microvasculature has a more organised hierarchical
structure than that observed in normal tissue
D)Angiogenesis allows the tumour to grow to a large size and
increases the metastatic potential of tumour cells
E)The angiogenic switch results in an overexpression of pro-
angiogenic factors such as fibroblast growth factor from tumour
cells
C
Which of the following does NOT cause immunosuppression in the tumour
microenvironment:
A Antigenic loading onto HLA/MHC molecules on tumour cells
B IL-10 secretion from tumour cells
C TGF-b and IL-10 secretion from tumour cells
D upregulation of PDL-1 on tumour cells
E PD-L1 on tumour cells binding to PD-1 on T cells
A
Explain in detail how cancer cells have a limitless ability to replicate and do not undergo senescence or cell death and become immortal. (50%)
Key mechanisms that enable cancer cells to become immortal:
1. telomere maintenance
- they are protective caps at ends of chromosomes that shorten with every divide
- once they become critically short the cell enters senescence or apoptosis
- but in cancer cells the telomere maintenance is often altered, enabling limitless replication
- there is an activation of telomerase which adds repetitive nucleotide sequences at the ends of telomers preventing the shorteneing
- Avoidance of senescence
- is a state where cell stops dividing in response to DNA damage, oncogene activation or telomere shortening
- evade by inactivate tumor suppressor genes such as p53 and RB - Resist apoptosis
- overexpression of anti-apoptotic proteins - Oncogene activation
Define the terms proto-oncogene and oncogene (5%).
Using a named example of an oncogene, briefly describe how it affects cell growth. Indicate which part of the cell cycle an on cogene affects. (15%)
Proto-oncogene: A normal gene involved in regulation of normal cell proliferation
Oncogene: A mutated proto-oncogene or increased expression
Example: RAS oncogene
- Most well known
- is a GTPase acting as a molecular switch between active and inactive state
- when bound to GTP it activates a cascade of downstream signalling pathways which promote cell proliferation, survival and growth
- in its mutated form it remains active and so is always bound to GTP and continuously signals for cell division and leads to uncontrolled cell growth
- affected the G1 phase
- its activation drives thre cell to transition from G1 to S phase, promoting cell cycle progression
- by continuously activating cell cycle progression, the mutated RAS bypasses normal growth allowing cells to proliferate uncontrollably, contributing to tumorigenesis
Outline with the aid of a diagram the underlying mechanism of action of EGFR tyrosine kinase inhibitors used in non-small cell lung cancer treatment (25%).
Name one of these inhibitors. (5%)
Which of the six hallmarks of cancer does this relate to? (5%)
(EGFR) is a receptor tyrosine kinase that plays a crucial role in cell growth, survival, and differentiation. In non-small cell lung cancer (NSCLC), EGFR mutations can lead to overactivation of this receptor, driving uncontrolled cell proliferation.
When bound by its ligands (ie EGF) it undergoes dimerization and activated it intrinsic kinase activity
Activation leads to phosphorylation of tyrosine residues on the receptor
Erlotinib is one of the commonly used EGFR TKIs in the treatment of EGFR-mutant non-small cell lung cancer
Sustaining Proliferative Signaling
Explain how a mutation in the tumour suppressor gene p53 can lead to altered cell proliferation and apoptosis that causes cancer. Include a cell signalling diagram in your answer (50%)
often referred to as the “guardian of the genome” because of its role in maintaining genomic integrity. When the DNA is damaged, p53 activates processes that can either repair the damage or induce cell death if the damage is irreparable, thus preventing the propagation of mutated cells.
A mutation in p53 can lead to a loss of function of this tumor suppressor, which in turn can promote uncontrolled cell proliferation and avoidance of apoptosis, two key features of cancer development.
Mutations in p53 impair its ability to bind to DNA and activate the transcription of genes required for cell cycle arrest, such as p21 (a cyclin-dependent kinase inhibitor). Without this checkpoint, damaged cells may continue to proliferate, allowing genomic instability and cancer progression.
When p53 is mutated, this apoptosis pathway is disrupted, preventing the elimination of cells with damaged DNA. This allows cells with genomic mutations to survive,
Mutation of p53 can prevent this senescence response, allowing cells with damaged DNA to bypass this protective mechanism and continue to divide, contributing to tumor formation.
Activating invasion and metastasis is a Hallmark of Cancer. Describe the key steps in this process. Discuss the key molecules and cells involved in this process. (50%)
This involves a series of complex steps that allow cancer cells to leave their primary site, invade surrounding tissues, and establish secondary tumors in distant organs.
- Local invasion
- loss of adhesion between tumor cells so cnacer cells detach from primary tumor - Degradation of extracelular matrix
- for cancer cells to invade surrounding tissues they need to break down the ECM and degradation is facilitated by MMPs and serine proteasers which break down the collagen b so cancer cells can migrate through the tissues - Migration and invasion
- Intravasation into blood
- Survival in circulation
Name the six Hallmarks of Cancer and describe the key principles of each of these hallmarks (30%)
- Sustaining Proliferative Signaling: Cancer cells can continuously signal for their own growth.
- Evading Growth Suppressors: Cancer cells bypass signals that normally inhibit cell proliferation.
- Resisting Cell Death: Cancer cells avoid programmed cell death (apoptosis) even in the presence of significant stress.
- Enable Replicative Immortality: Cancer cells can avoid normal replicative limits, often through telomerase activation.
- Inducing Angiogenesis: Cancer cells stimulate the formation of new blood vessels to support their growth.
- Activating Invasion and Metastasis: Cancer cells gain the ability to invade surrounding tissues and spread to distant organs.
What is the difference between a tumour suppressor gene, a proto- oncogene and an oncogene? (15%)
Tumor Suppressor Gene: Inhibits cell growth and division. Mutations cause loss of function, contributing to cancer (e.g., p53, RB).
Proto-Oncogene: A normal gene that promotes cell growth. Mutations or overexpression can convert it into an oncogene, leading to uncontrolled cell proliferation (e.g., Ras, EGFR).
Oncogene: A mutated or overexpressed proto-oncogene that leads to cancer by promoting excessive cell growth and survival (e.g., HER2, Ras).
