FRCR Oncology Part 1: CANCER BIOLOGY, RADIOBIOLOGY - 11 (100 QUESTIONS, ANSWERS BELOW)

 

Questions

Cancer Biology (50 Questions)

1. Which of the following best describes the role of the TP53 gene in cancer development?
   A. It promotes cell cycle progression by activating cyclin-dependent kinases.
   B. It acts as a transcription factor to induce apoptosis in response to DNA damage.
   C. It enhances angiogenesis by upregulating VEGF expression.
   D. It inhibits DNA repair by blocking homologous recombination.
   E. It activates proto-oncogenes to drive cell proliferation.

2. The Warburg effect in cancer cells is characterised by:
   A. Increased oxidative phosphorylation under aerobic conditions.
   B. Enhanced glucose uptake and glycolysis even in the presence of oxygen.
   C. Reduced lactate production due to mitochondrial dysfunction.
   D. Dependence on glutamine metabolism for ATP production.
   E. Inhibition of the pentose phosphate pathway.

3. Which oncogene is most commonly associated with non-small cell lung cancer?
   A. MYC
   B. KRAS
   C. BCL2
   D. BRCA1
   E. PTEN

4. Which of the following is a hallmark of cancer?
   A. Inhibition of angiogenesis
   B. Evasion of apoptosis
   C. Suppression of cell migration
   D. Enhanced contact inhibition
   E. Reduced genomic instability

5. What is the primary role of VEGF in tumour biology?
   A. Inhibition of cell proliferation
   B. Promotion of angiogenesis
   C. Induction of apoptosis
   D. Suppression of metastasis
   E. Enhancement of DNA repair

6. Which of the following is a proto-oncogene that, when mutated, promotes uncontrolled cell proliferation?
   A. RB1
   B. TP53
   C. PTEN
   D. EGFR
   E. BRCA1

7. A mutation in which gene is most likely to result in Li-Fraumeni syndrome?
   A. APC
   B. TP53
   C. KRAS
   D. MYC
   E. NF1

8. What is the primary function of the RB1 gene in the cell cycle?
   A. Promotes G1 to S phase transition
   B. Inhibits E2F transcription factors in G1
   C. Activates cyclin D expression
   D. Enhances DNA replication
   E. Induces apoptosis

9. Which oncogene is commonly amplified in neuroblastoma?
   A. HER2
   B. MYCN
   C. BCL2
   D. ALK
   E. KIT

10. Which phase of the cell cycle is regulated by the cyclin D-CDK4/6 complex?
    A. G0 to G1
    B. G1 to S
    C. S to G2
    D. G2 to M
    E. M to G1

11. What is the role of the BCL2 protein in cancer cells?
    A. Promotes cytochrome c release from mitochondria
    B. Inhibits apoptosis by binding pro-apoptotic proteins
    C. Activates caspase-3
    D. Enhances p53 transcriptional activity
    E. Inhibits angiogenesis

12. Which checkpoint is primarily responsible for detecting DNA damage before mitosis?
    A. G1/S checkpoint
    B. S phase checkpoint
    C. G2/M checkpoint
    D. Spindle assembly checkpoint
    E. Restriction point

13. What is the effect of a loss-of-function mutation in the ATM gene?
    A. Enhanced homologous recombination
    B. Increased radiosensitivity
    C. Reduced apoptosis
    D. Inhibition of non-homologous end joining
    E. Upregulation of VEGF

14. Which molecule is primarily responsible for promoting tumour angiogenesis?
    A. TGF-β
    B. VEGF-A
    C. IL-6
    D. TNF-α
    E. MMP-9

15. What is the role of matrix metalloproteinases (MMPs) in cancer progression?
    A. Inhibit cell migration
    B. Degrade extracellular matrix
    C. Suppress angiogenesis
    D. Enhance cell adhesion
    E. Induce cell cycle arrest

16. Which process is critical for the intravasation step of metastasis?
    A. Epithelial-to-mesenchymal transition
    B. Angiogenesis
    C. Anoikis resistance
    D. Homologous recombination
    E. Contact inhibition

17. What is the primary role of E-cadherin in cancer?
    A. Promotes cell invasion
    B. Maintains cell-cell adhesion
    C. Induces apoptosis
    D. Enhances glycolysis
    E. Activates oncogenes

18. Which cell type in the tumour microenvironment suppresses anti-tumour immunity?
    A. Cytotoxic T cells
    B. Regulatory T cells
    C. Natural killer cells
    D. Dendritic cells
    E. B cells

19. What is the role of PD-L1 expression in cancer cells?
    A. Enhances MHC class I presentation
    B. Inhibits T-cell activation
    C. Promotes NK cell activity
    D. Induces macrophage phagocytosis
    E. Activates B-cell proliferation

20. Which cytokine promotes inflammation in the tumour microenvironment?
    A. IL-10
    B. TGF-β
    C. IL-6
    D. IFN-γ
    E. IL-4

21. What is the significance of tumour-associated macrophages (TAMs)?
    A. They directly kill tumour cells
    B. They promote tumour growth and angiogenesis
    C. They inhibit MMP activity
    D. They enhance cytotoxic T-cell activity
    E. They reduce VEGF expression

22. Which epigenetic modification is most commonly associated with gene silencing in cancer?
    A. Histone acetylation
    B. DNA methylation
    C. Histone phosphorylation
    D. Chromatin relaxation
    E. Histone ubiquitination

23. What is the consequence of a BRCA1 mutation in breast cancer?
    A. Enhanced homologous recombination
    B. Increased genomic instability
    C. Reduced angiogenesis
    D. Inhibition of metastasis
    E. Upregulation of MYC

24. Which technique is used to detect microsatellite instability in colorectal cancer?
    A. Fluorescence in situ hybridisation
    B. Polymerase chain reaction
    C. Western blotting
    D. Spectral karyotyping
    E. Chromatin immunoprecipitation

25. What is the role of microRNAs in cancer?
    A. Directly repair DNA damage
    B. Regulate gene expression post-transcriptionally
    C. Promote protein synthesis
    D. Inhibit cell cycle checkpoints
    E. Enhance mitochondrial function

26. Which hallmark of cancer involves the ability to resist cell death?
    A. Sustained angiogenesis
    B. Evasion of apoptosis
    C. Genomic instability
    D. Replicative immortality
    E. Invasion and metastasis

27. What enables cancer cells to achieve replicative immortality?
    A. Telomerase activation
    B. Loss of p53
    C. VEGF overexpression
    D. MMP inhibition
    E. E-cadherin upregulation

28. Which process allows cancer cells to sustain proliferative signalling?
    A. Loss of contact inhibition
    B. Inhibition of cyclin D
    C. Upregulation of p21
    D. Suppression of RAS
    E. Activation of PTEN

29. What is the role of the tumour microenvironment in cancer progression?
    A. Inhibits cell migration
    B. Supports tumour growth and metastasis
    C. Enhances DNA repair
    D. Reduces glucose uptake
    E. Suppresses oncogene expression

30. What is the primary energy source for cancer cells exhibiting the Warburg effect?
    A. Oxidative phosphorylation
    B. Glycolysis
    C. Fatty acid oxidation
    D. Glutaminolysis
    E. Pentose phosphate pathway

31. Which enzyme is upregulated in cancer cells to support glycolysis?
    A. Hexokinase
    B. Cytochrome c oxidase
    C. Citrate synthase
    D. Acetyl-CoA carboxylase
    E. Succinate dehydrogenase

32. What is the role of glutamine in cancer cell metabolism?
    A. Inhibits glycolysis
    B. Provides carbon for biosynthesis
    C. Reduces lactate production
    D. Suppresses angiogenesis
    E. Enhances oxidative phosphorylation

33. Which pathway is critical for NADPH production in cancer cells?
    A. Glycolytic pathway
    B. Pentose phosphate pathway
    C. TCA cycle
    D. Fatty acid synthesis
    E. Urea cycle

34. What is a key characteristic of cancer stem cells?
    A. High radiosensitivity
    B. Self-renewal and tumour initiation
    C. Reduced metastatic potential
    D. Enhanced apoptosis
    E. Low expression of CD44

35. Which marker is commonly used to identify cancer stem cells in breast cancer?
    A. CD20
    B. CD44
    C. CD3
    D. CD19
    E. CD56

36. Why are cancer stem cells resistant to radiotherapy?
    A. Enhanced DNA repair mechanisms
    B. Reduced cell cycle activity
    C. Increased oxygen levels
    D. Suppressed glycolysis
    E. Decreased VEGF expression

37. What is the role of the Wnt signalling pathway in cancer stem cells?
    A. Inhibits self-renewal
    B. Promotes differentiation
    C. Enhances stemness
    D. Reduces metastasis
    E. Suppresses angiogenesis

38. Which pathway is activated by EGFR mutations in non-small cell lung cancer?
    A. PI3K/AKT
    B. JAK/STAT
    C. NF-κB
    D. Hedgehog
    E. Notch

39. What is the role of the MAPK pathway in cancer?
    A. Inhibits cell proliferation
    B. Promotes cell survival and growth
    C. Enhances apoptosis
    D. Suppresses metastasis
    E. Reduces angiogenesis

40. Which protein is a downstream target of the PI3K/AKT pathway?
    A. mTOR
    B. p53
    C. Rb
    D. BRCA1
    E. ATM

41. What is the effect of a PTEN mutation in cancer cells?
    A. Inhibits PI3K/AKT signalling
    B. Enhances apoptosis
    C. Increases PI3K/AKT activity
    D. Reduces DNA repair
    E. Suppresses glycolysis

42. Which factor is critical for the extravasation step of metastasis?
    A. Integrin expression
    B. Loss of p53
    C. Upregulation of p21
    D. Inhibition of VEGF
    E. Enhanced E-cadherin

43. What is the role of hypoxia-inducible factor 1 (HIF-1) in cancer?
    A. Inhibits glycolysis
    B. Promotes angiogenesis
    C. Enhances apoptosis
    D. Reduces cell migration
    E. Suppresses DNA repair

44. Which process is associated with tumour dormancy?
    A. Rapid cell proliferation
    B. Angiogenic switch
    C. Quiescent state of cancer cells
    D. Enhanced glycolysis
    E. Increased apoptosis

45. What is the primary driver of genomic instability in cancer?
    A. Telomerase inhibition
    B. DNA repair defects
    C. Enhanced apoptosis
    D. Reduced glycolysis
    E. Suppressed angiogenesis

46. Which of the following is TRUE about chromosomal aberrations post-irradiation?
    A. Dicentric chromosomes are stable and persist long-term.
    B. Translocations are always lethal to cells.
    C. Spectral karyotyping (SKY) detects stable aberrations decades later.
    D. Terminal deletions follow a linear dose-response curve.
    E. Chromosomal aberrations are independent of radiation type.

47. Which protein is critical for homologous recombination repair of DNA double-strand breaks?
    A. Ku70/80
    B. RAD51
    C. PARP1
    D. DNA-PK
    E. XRCC1

48. Which of the following is a proto-oncogene that, when mutated, promotes uncontrolled cell proliferation?
    A. RB1
    B. TP53
    C. PTEN
    D. EGFR
    E. BRCA1

49. What is the primary function of the RB1 gene in the cell cycle?
    A. Promotes G1 to S phase transition
    B. Inhibits E2F transcription factors in G1
    C. Activates cyclin D expression
    D. Enhances DNA replication
    E. Induces apoptosis

50. Which oncogene is commonly amplified in neuroblastoma?
    A. HER2
    B. MYCN
    C. BCL2
    D. ALK
    E. KIT

Radiobiology (50 Questions)

51. What is the primary mechanism by which ionising radiation causes cell death?
    A. Direct ionisation of cell membrane lipids
    B. Induction of double-strand DNA breaks
    C. Disruption of mitochondrial ATP production
    D. Inhibition of protein synthesis
    E. Activation of caspase-independent necrosis

52. In a cell survival curve, the D0 value represents:
    A. The dose required to reduce cell survival to 37% on the linear portion of the curve.
    B. The dose at which 50% of cells undergo apoptosis.
    C. The dose required to inactivate all cells in a population.
    D. The dose at which the curve transitions from exponential to linear.
    E. The threshold dose below which no cell killing occurs.

53. Which of the following statements about the oxygen enhancement ratio (OER) is TRUE?
    A. It is higher for low-LET radiation than high-LET radiation.
    B. It is negligible for alpha particles.
    C. It is independent of cell type or tissue.
    D. It decreases with increasing radiation dose.
    E. It is lower in hypoxic tumours than oxygenated tumours.

54. Which repair mechanism is primarily responsible for fixing radiation-induced double-strand DNA breaks in the G1 phase?
    A. Homologous recombination
    B. Non-homologous end joining
    C. Base excision repair
    D. Nucleotide excision repair
    E. Mismatch repair

55. The biologically effective dose (BED) for a radiotherapy regimen is calculated using which model?
    A. Linear-Quadratic model
    B. Multi-target model
    C. Single-hit model
    D. Oxygen enhancement model
    E. Relative biological effectiveness model

56. The effect of fractionation in radiotherapy on normal tissues is:
    A. It increases acute toxicity due to higher total dose.
    B. It spares normal tissues by allowing repair of sublethal damage.
    C. It enhances late toxicity by accumulating DNA damage.
    D. It reduces the therapeutic ratio by killing more tumour cells.
    E. It has no impact on normal tissue response.

57. The alpha/beta ratio for late-responding normal tissues is typically:
    A. Greater than 10 Gy
    B. Between 8 and 10 Gy
    C. Between 2 and 4 Gy
    D. Less than 1 Gy
    E. Equal to the tumour alpha/beta ratio

58. Which type of radiation has the highest relative biological effectiveness (RBE)?
    A. X-rays
    B. Gamma rays
    C. Protons
    D. Alpha particles
    E. Electrons

59. In radiobiology, the term ‘reoxygenation’ refers to:
    A. Increased oxygen delivery to normal tissues during fractionation.
    B. Restoration of oxygen levels in hypoxic tumour cells between fractions.
    C. Enhanced radiosensitivity due to high LET radiation.
    D. Reduction in OER during radiotherapy.
    E. Oxygen depletion in tumours post-irradiation.

60. The cell cycle phase most sensitive to radiation-induced damage is:
    A. G1
    B. S
    C. G2/M
    D. G0
    E. Early M

61. The tolerance dose of the kidney to radiation is highly dependent on:
    A. The total dose delivered in a single fraction.
    B. The volume of tissue irradiated.
    C. The use of high-LET radiation.
    D. The patient’s age.
    E. The presence of concurrent chemotherapy.

62. Which of the following statements about the bystander effect in radiobiology is TRUE?
    A. It occurs only with high-LET radiation.
    B. It involves direct DNA damage in irradiated cells.
    C. It causes damage in unirradiated cells via intercellular signalling.
    D. It is independent of gap junction communication.
    E. It enhances the therapeutic ratio in radiotherapy.

63. The primary advantage of carbon ion therapy over photon therapy is:
    A. Lower cost and wider availability.
    B. Reduced entrance dose and sharper Bragg peak.
    C. Higher OER compared to protons.
    D. Decreased RBE in the target volume.
    E. No requirement for fractionation.

64. Which type of DNA damage is most lethal following ionising radiation?
    A. Single-strand breaks
    B. Double-strand breaks
    C. Base damage
    D. DNA crosslinks
    E. Pyrimidine dimers

65. What is the primary source of reactive oxygen species (ROS) in irradiated cells?
    A. Mitochondrial dysfunction
    B. Radiolysis of water
    C. Lipid peroxidation
    D. Protein oxidation
    E. Nuclear membrane disruption

66. Which type of radiation has the highest linear energy transfer (LET)?
    A. X-rays
    B. Protons
    C. Carbon ions
    D. Gamma rays
    E. Electrons

67. What is the effect of high-LET radiation on DNA?
    A. Causes sparse, easily repaired damage
    B. Produces clustered, complex damage
    C. Induces only single-strand breaks
    D. Reduces ROS production
    E. Enhances homologous recombination

68. Which protein is essential for non-homologous end joining (NHEJ)?
    A. RAD51
    B. BRCA2
    C. DNA-PK
    D. PARP1
    E. ATR

69. What is the consequence of defective homologous recombination in irradiated cells?
    A. Increased radiosensitivity
    B. Enhanced cell survival
    C. Reduced apoptosis
    D. Inhibition of NHEJ
    E. Decreased ROS production

70. Which repair pathway corrects base damage from ionising radiation?
    A. Base excision repair
    B. Nucleotide excision repair
    C. Mismatch repair
    D. Homologous recombination
    E. Non-homologous end joining

71. What is the role of the MRN complex in DNA repair?
    A. Inhibits DNA-PK activity
    B. Senses double-strand breaks
    C. Promotes base excision repair
    D. Suppresses apoptosis
    E. Enhances glycolysis

72. In a cell survival curve, the shoulder region represents:
    A. Exponential cell killing
    B. Repair of sublethal damage
    C. Complete cell inactivation
    D. Oxygen-independent killing
    E. High-LET radiation effects

73. What does the D37 value indicate in radiobiology?
    A. Dose killing 37% of cells
    B. Dose reducing survival to 37%
    C. Dose causing 63% cell death
    D. Threshold dose for apoptosis
    E. Dose for complete DNA repair

74. Which cell type is most radiosensitive?
    A. Neurons
    B. Muscle cells
    C. Lymphocytes
    D. Fibroblasts
    E. Hepatocytes

75. What is the primary determinant of cellular radiosensitivity?
    A. Cell size
    B. DNA repair capacity
    C. Mitochondrial density
    D. Glycolytic rate
    E. Cell membrane thickness

76. Which of the 4Rs of radiobiology refers to the repair of sublethal damage between fractions?
    A. Reoxygenation
    B. Redistribution
    C. Repair
    D. Repopulation
    E. Radiosensitisation

77. What is the benefit of redistribution in fractionated radiotherapy?
    A. Increases normal tissue toxicity
    B. Enhances tumour cell killing
    C. Reduces DNA repair
    D. Inhibits angiogenesis
    E. Decreases OER

78. Which factor reduces the efficacy of radiotherapy in rapidly proliferating tumours?
    A. Reoxygenation
    B. Repopulation
    C. Repair
    D. Redistribution
    E. Radiosensitisation

79. What is the primary advantage of hypofractionation in radiotherapy?
    A. Reduces total treatment time
    B. Increases late toxicity
    C. Enhances repopulation
    D. Decreases tumour control
    E. Inhibits DNA repair

80. What is the oxygen enhancement ratio (OER) for X-rays?
    A. 1.0
    B. 1.5
    C. 2.5–3.0
    D. 4.0
    E. 5.0

81. Why is the OER lower for high-LET radiation?
    A. Less dependence on ROS
    B. Increased single-strand breaks
    C. Enhanced DNA repair
    D. Reduced apoptosis
    E. Higher energy deposition

82. What is the relative biological effectiveness (RBE) of protons compared to X-rays?
    A. 0.5
    B. 1.1
    C. 2.0
    D. 3.0
    E. 4.0

83. Which factor increases the RBE of radiation?
    A. Lower LET
    B. Higher dose rate
    C. Increased fractionation
    D. Higher LET
    E. Reduced oxygen levels

84. Which organ has the lowest tolerance to radiation?
    A. Skin
    B. Lung
    C. Spinal cord
    D. Liver
    E. Kidney

85. What is the primary mechanism of radiation-induced fibrosis?
    A. Acute apoptosis
    B. Chronic inflammation
    C. DNA cross-linking
    D. Mitochondrial failure
    E. Glycolytic inhibition

86. Which normal tissue effect is classified as an early reaction?
    A. Radiation pneumonitis
    B. Skin erythema
    C. Myelopathy
    D. Cardiac fibrosis
    E. Cataract formation

87. What is the tolerance dose (TD5/5) for whole-liver irradiation?
    A. 10 Gy
    B. 20 Gy
    C. 30 Gy
    D. 40 Gy
    E. 50 Gy

88. What is the biologically effective dose (BED) for a regimen of 60 Gy in 30 fractions (α/β = 10 Gy)?
    A. 60 Gy
    B. 72 Gy
    C. 80 Gy
    D. 90 Gy
    E. 100 Gy

89. Which tumour type has a high α/β ratio?
    A. Prostate cancer
    B. Breast cancer
    C. Glioblastoma
    D. Chordoma
    E. Sarcoma

90. What is the primary advantage of intensity-modulated radiotherapy (IMRT)?
    A. Reduced treatment time
    B. Improved dose conformity
    C. Lower cost
    D. Increased OER
    E. Enhanced repopulation

91. Which agent is used as a radiosensitiser in head and neck cancer?
    A. Bevacizumab
    B. Cisplatin
    C. Rituximab
    D. Trastuzumab
    E. Imatinib

92. What is the primary benefit of proton therapy?
    A. Higher RBE than carbon ions
    B. Reduced exit dose
    C. Increased OER
    D. Lower cost than IMRT
    E. Enhanced fractionation

93. Which feature of carbon ion therapy improves tumour control?
    A. Lower LET
    B. Higher RBE
    C. Reduced fractionation
    D. Increased OER
    E. Enhanced reoxygenation

94. What is the primary limitation of stereotactic body radiotherapy (SBRT)?
    A. Inability to target small lesions
    B. Risk of late toxicities
    C. Low tumour control probability
    D. Requirement for low doses
    E. Reduced normal tissue sparing

95. Which technique minimises organ motion in lung radiotherapy?
    A. Gating
    B. IMRT
    C. Brachytherapy
    D. 2D planning
    E. Electron therapy

96. What is the primary cause of radiation-induced second malignancies?
    A. Acute apoptosis
    B. Genomic instability
    C. Enhanced glycolysis
    D. Suppressed angiogenesis
    E. Reduced DNA repair

97. Which syndrome is associated with increased radiosensitivity due to ATM mutations?
    A. Li-Fraumeni syndrome
    B. Ataxia-telangiectasia
    C. Lynch syndrome
    D. Fanconi anaemia
    E. Xeroderma pigmentosum

98. What is the bystander effect in radiobiology?
    A. Direct DNA damage in irradiated cells
    B. Damage to unirradiated cells via signalling
    C. Enhanced repair in irradiated cells
    D. Reduced apoptosis in hypoxic cells
    E. Increased OER in normal tissues

99. Which factor increases the risk of radiation-induced pneumonitis?
    A. Low V20
    B. High V20
    C. Single-fraction delivery
    D. Reduced LET
    E. Increased OER

100. What is the equivalent dose in 2 Gy fractions (EQD2) for 50 Gy in 5 fractions (α/β = 3 Gy)?
     A. 60 Gy
     B. 75 Gy
     C. 90 Gy
     D. 100 Gy
     E. 120 Gy

Cancer Biology (50 Answers)

1. B. TP53 is a tumour suppressor gene that induces apoptosis or cell cycle arrest in response to DNA damage.

2. B. The Warburg effect describes aerobic glycolysis, where cancer cells preferentially use glycolysis for energy.

3. B. KRAS mutations are frequent in non-small cell lung cancer, driving uncontrolled proliferation.

4. B. Evasion of apoptosis is a key hallmark of cancer, enabling tumour survival.

5. B. VEGF promotes angiogenesis, supporting tumour growth by ensuring blood supply.

6. D. EGFR is a proto-oncogene; mutations lead to uncontrolled growth.

7. B. TP53 mutations cause Li-Fraumeni syndrome, increasing cancer risk.

8. B. RB1 inhibits E2F, preventing G1/S progression.

9. B. MYCN amplification is characteristic of neuroblastoma.

10. B. Cyclin D-CDK4/6 drives G1/S transition.

11. B. BCL2 inhibits apoptosis, promoting cancer cell survival.

12. C. G2/M checkpoint ensures DNA integrity before mitosis.

13. B. ATM mutations impair DNA damage response, increasing radiosensitivity.

14. B. VEGF-A drives angiogenesis in tumours.

15. B. MMPs degrade ECM, facilitating invasion and metastasis.

16. A. EMT enables cancer cells to invade blood vessels.

17. B. E-cadherin loss promotes metastasis by reducing adhesion.

18. B. Regulatory T cells suppress immune responses.

19. B. PD-L1 inhibits T cells, aiding immune evasion.

20. C. IL-6 drives inflammation, supporting tumour growth.

21. B. TAMs support tumour progression.

22. B. DNA methylation silences tumour suppressor genes.

23. B. BRCA1 mutations impair DNA repair, causing instability.

24. B. PCR detects microsatellite instability.

25. B. MicroRNAs regulate gene expression, impacting cancer pathways.

26. B. Evasion of apoptosis is a hallmark.

27. A. Telomerase maintains telomeres, enabling unlimited division.

28. A. Loss of contact inhibition sustains proliferation.

29. B. The microenvironment aids tumour progression.

30. B. Glycolysis is preferred in the Warburg effect.

31. A. Hexokinase drives glucose metabolism.

32. B. Glutamine supports biosynthetic pathways.

33. B. The pentose phosphate pathway generates NADPH.

34. B. Cancer stem cells self-renew and initiate tumours.

35. B. CD44 is a breast cancer stem cell marker.

36. A. Enhanced DNA repair confers resistance.

37. C. Wnt signalling maintains stemness.

38. A. EGFR activates PI3K/AKT, driving proliferation.

39. B. MAPK promotes survival and growth.

40. A. mTOR is activated by PI3K/AKT.

41. C. PTEN loss activates PI3K/AKT.

42. A. Integrins facilitate extravasation.

43. B. HIF-1 upregulates VEGF, promoting angiogenesis.

44. C. Dormancy involves a quiescent state.

45. B. DNA repair defects cause genomic instability.

46. C. SKY is effective for detecting stable aberrations like translocations long after irradiation.

47. B. RAD51 facilitates strand invasion in homologous recombination.

48. D. EGFR is a proto-oncogene; mutations lead to uncontrolled growth.

49. B. RB1 inhibits E2F, preventing G1/S progression.

50. B. MYCN amplification is characteristic of neuroblastoma.

Radiobiology Answers (50 Answers)

51. B. Double-strand DNA breaks are the primary lethal lesions caused by ionising radiation.

52. A. D0 is the dose that reduces survival to 37% (1/e) on the linear portion of the curve.

53. B. OER is lower for high-LET radiation like alpha particles, as they cause dense ionisation less dependent on oxygen.

54. B. Non-homologous end joining is the primary repair mechanism for double-strand breaks in G1.

55. A. The Linear-Quadratic model underpins BED calculations, accounting for linear and quadratic cell killing.

56. B. Fractionation allows normal tissues to repair sublethal damage, improving tolerance.

57. C. Late-responding tissues have low alpha/beta ratios (2–4 Gy), indicating sensitivity to fraction size.

58. D. Alpha particles have high LET and thus the highest RBE.

59. B. Reoxygenation improves tumour radiosensitivity by oxygenating hypoxic cells between fractions.

60. C. G2/M is the most radiosensitive phase due to active DNA replication and repair.

61. B. Kidney tolerance is volume-dependent, with small volumes tolerating higher doses.

62. C. The bystander effect involves damageElimination de células no irradiadas mediante señalización intercelular.

63. B. Carbon ions offer better normal tissue sparing and a sharper Bragg peak.

64. B. Double-strand breaks are the most lethal.

65. B. Radiolysis of water generates ROS.

66. C. Carbon ions have high LET.

67. B. High-LET radiation causes complex damage.

68. C. DNA-PK is critical for NHEJ.

69. A. Defective HR increases radiosensitivity.

70. A. Base excision repair corrects base damage.

71. B. The MRN complex detects DSBs.

72. B. The shoulder reflects sublethal damage repair.

73. B. D37 is the dose reducing survival to 37%.

74. C. Lymphocytes are highly radiosensitive.

75. B. DNA repair capacity determines radiosensitivity.

76. C. Repair occurs between fractions.

77. B. Redistribution sensitises cells in radiosensitive phases.

78. B. Repopulation allows tumour regrowth.

79. A. Hypofractionation shortens treatment duration.

80. C. OER for X-rays is typically 2.5–3.0.

81. A. High-LET radiation relies less on oxygen-mediated ROS.

82. B. Proton RBE is approximately 1.1.

83. D. Higher LET increases RBE.

84. C. The spinal cord has low tolerance (e.g., ~45 Gy).

85. B. Chronic inflammation drives fibrosis.

86. B. Skin erythema occurs early (days to weeks).

87. C. Whole-liver TD5/5 is ~30 Gy.

88. B. BED = 60 × (1 + 2/10) = 72 Gy.

89. C. Glioblastoma has a high α/β (~10 Gy).

90. B. IMRT improves dose conformity.

91. B. Cisplatin enhances radiation effects.

92. B. Protons reduce exit dose via the Bragg peak.

93. B. Carbon ions have higher RBE.

94. B. SBRT risks late toxicities due to high doses per fraction.

95. A. Gating accounts for respiratory motion.

96. B. Genomic instability drives second malignancies.

97. B. Ataxia-telangiectasia involves ATM mutations.

98. B. The bystander effect involves damage to unirradiated cells through signalling.

99. B. High V20 (lung volume receiving ≥20 Gy) increases pneumonitis risk.

100. C. EQD2 = 50 × (10 + 3)/(2 + 3) = 90 Gy.