1What is mitosis?
A normal cell division where one parent cell gives rise to two genetically identical daughter cells
2What is the cell cycle?
An ordered series of events involving cell growth, DNA replication, and division producing two identical cells
3What are the two major phases of the cell cycle?
Interphase and the mitotic (M) phase
4What happens during interphase?
Cell growth and DNA replication/preparation for division
5Which phases make up interphase?
G0, G1, S, and G2
6What happens during the mitotic (M) phase?
Separation of replicated DNA and cytoplasmic division (mitosis + cytokinesis)
7What are the four stages of mitosis?
Prophase, metaphase, anaphase, and telophase
8What occurs in G1 phase?
Cell growth and preparation for DNA replication
9What occurs in S phase?
DNA synthesis (replication)
10What occurs in G2 phase?
Further growth and checking & repairing DNA before mitosis
11What is the G0 phase?
A resting/non-dividing phase where cells exit the cell cycle
12What are DNA damage checkpoints?
Control points that monitor DNA integrity and proper replication
13What can happen if DNA damage is detected at a checkpoint?
DNA repair, cell cycle arrest, or apoptosis
14What do spindle assembly checkpoints monitor?
Proper attachment and alignment of chromosomes on the mitotic spindle
15What controls progression of the cell cycle?
Cyclins and cyclin-dependent kinases (CDKs)
16What are cyclins?
Regulatory proteins whose levels rise and fall to control the cell cycle
17What are cyclin-dependent kinases (CDKs)?
Protein kinases activated by cyclins to drive cell-cycle transitions
18What is required for cyclins to function?
Binding to a specific CDK
19Which cyclins regulate G1 progression?
Cyclin D and cyclin E
20Which cyclin controls the G1/S transition?
Cyclin E
21Which cyclin controls DNA synthesis (S phase)?
Cyclin A
22Which cyclin-CDK complex controls entry into mitosis?
Cyclin B with CDK1
23What do cyclin-CDK complexes do?
Phosphorylate target proteins to control cell cycle progression
24Who discovered cyclin-dependent kinases (CDKs)?
Sir Paul Nurse
25What major recognition did Sir Paul Nurse receive?
The Nobel Prize
26Why is cancer described as a disease of the cell cycle?
Because it involves loss of normal control of cell division
27What is a mutation?
A change in a DNA sequence
28How can accumulation of mutations affect cells?
It can disrupt cell-cycle control and contribute to cancer
29What are proto-oncogenes?
Genes that normally stimulate/activate cell division
30What happens when proto-oncogenes are mutated?
They can become oncogenes
31What is an oncogene?
An overactive mutant of a proto-oncogene that promotes cell proliferation
32What are oncoproteins?
Proteins encoded by oncogenes
33Give an example of a proto-oncogene
Ras
34How does Ras promote cancer when mutated?
By continuously activating growth signalling and cyclins
35What are tumour suppressor genes?
Genes that normally inhibit cell division or promote genome protection
36What happens when tumour suppressor genes are switched off?
Uncontrolled cell division
37Give examples of tumour suppressor genes
p53 and Rb
38Why is p53 called the guardian of the genome?
It prevents division of cells with damaged DNA and can trigger apoptosis
39What does p53 do when DNA damage is repairable?
Activates genes that repair DNA and pauses the cell cycle
40What does p53 do when DNA damage is irreparable?
Stops cell division and triggers apoptosis
41Where is the p53 protein located?
In the nucleus
42What types of damage can activate p53?
DNA damage from toxic chemicals, radiation, and UV light
43What is Peto’s paradox?
Large animals do not have higher cancer rates despite having more cells
44How do African elephants resolve Peto’s paradox?
They have multiple copies of p53 retrogenes (increased genome protection)
45What is Li-Fraumeni syndrome?
Inherited cancer predisposition caused by mutations in p53
46How is Li-Fraumeni syndrome inherited?
Autosomal dominant
47What cancers are associated with Li-Fraumeni syndrome?
Breast cancer, brain tumours, leukaemia, sarcoma, and others
48What gene is mutated in retinoblastoma?
RB1
49What protein does RB1 encode?
pRB
50What is the normal function of pRB?
Prevents transition from G1 to S phase
51What causes retinoblastoma?
Mutation/deletion of both RB1 copies
52What is a key presenting sign of retinoblastoma?
Leukocoria
53What is the survival rate for retinoblastoma?
Greater than 95%
54What is neoplasia?
New growth
55What is a neoplasm?
A tumour that can be benign or malignant
56What is the difference between benign and malignant tumours?
Benign tumours remain localised; malignant tumours invade and metastasise
57Which feature distinguishes malignant tumours from benign ones?
Metastasis
58What is dedifferentiation in cancer cells?
Loss of specialised cell characteristics
59What is HER2?
A receptor tyrosine kinase involved in cell growth and differentiation
60What happens in HER2-positive breast cancer?
HER2 gene amplification (too many HER2 copies)
61How is HER2 amplification detected?
FISH testing
62Name HER2-targeted therapies
Trastuzumab, pertuzumab, and lapatinib
63What is angiogenesis?
Development of new blood vessels
64What is metastasis?
Spread of cancer cells to distant sites
65What is epithelial-to-mesenchymal transition (EMT)?
A process enabling cancer cell invasion and migration
66What is microsatellite instability (MSI)?
A form of genetic instability often due to DNA mismatch repair defects
67What causes mutations leading to cancer?
Spontaneous DNA replication errors or exposure to carcinogens
68Give examples of carcinogens
Asbestos, UV radiation, HPV, and H. pylori
69What are the main classes of cancer?
Carcinoma, sarcoma, and lymphoma/leukaemia
70What percentage of cancers are carcinomas?
About 90%
71What tissues do sarcomas arise from?
Connective tissues
72What cancer treatments are available?
Chemotherapy, radiation therapy, and surgery
73Why is tumour heterogeneity a challenge in treatment?
Different tumour cells respond differently, reducing treatment effectiveness
74What is personalised medicine in cancer?
Tailoring treatment based on tumour characteristics