FRCR Oncology Part 1: CANCER BIOLOGY, RADIOBIOLOGY - 13 (100 QUESTIONS, ANSWERS BELOW)

 

Questions

Cancer Biology (50 Questions)

1. Which mechanism best explains the synergistic effect of combining MEK inhibitors with BRAF inhibitors in BRAF V600E-mutated melanoma?
   A. Inhibition of compensatory MAPK signalling
   B. Suppression of PI3K/AKT pathway
   C. Enhancement of homologous recombination
   D. Upregulation of VEGF expression
   E. Inhibition of immune checkpoint pathways

2. What is the primary role of the TGF-β/SMAD pathway in late-stage cancer progression?
   A. Suppression of tumour growth
   B. Promotion of epithelial-to-mesenchymal transition
   C. Enhancement of DNA repair
   D. Inhibition of angiogenesis
   E. Activation of p53 transcription

3. Which epigenetic alteration is most associated with the silencing of the CDKN2A gene in pancreatic cancer?
   A. Histone acetylation
   B. Promoter hypermethylation
   C. Histone phosphorylation
   D. Chromatin relaxation
   E. Histone ubiquitination

4. In the tumour microenvironment, what is the primary function of myeloid-derived suppressor cells (MDSCs)?
   A. Direct cytotoxicity against tumour cells
   B. Suppression of T-cell activity
   C. Secretion of pro-angiogenic factors
   D. Enhancement of DNA repair
   E. Promotion of apoptosis

5. Which molecular alteration is most associated with resistance to ALK inhibitors in ALK-rearranged non-small cell lung cancer?
   A. L1196M gatekeeper mutation
   B. Loss of PTEN expression
   C. Amplification of MYC
   D. Upregulation of p53
   E. Deletion of RB1

6. What is the primary consequence of EZH2 overexpression in lymphoma?
   A. Inhibition of histone methylation
   B. Silencing of tumour suppressor genes
   C. Enhancement of apoptosis
   D. Suppression of glycolysis
   E. Promotion of DNA repair

7. Which process is most critical for the formation of tumour vasculature in glioblastoma?
   A. Vasculogenic mimicry
   B. Inhibition of VEGF
   C. Suppression of MMPs
   D. Upregulation of thrombospondin-1
   E. Reduction of HIF-1α activity

8. In cancer cells, what is the role of the KEAP1-NRF2 pathway under oxidative stress?
   A. Suppression of antioxidant gene expression
   B. Upregulation of antioxidant defenses
   C. Inhibition of glycolysis
   D. Promotion of apoptosis
   E. Enhancement of DNA damage

9. Which hallmark of cancer is most directly associated with the deregulation of cellular energetics?
   A. Evasion of apoptosis
   B. Reprogramming of energy metabolism
   C. Sustained angiogenesis
   D. Genomic instability
   E. Invasion and metastasis

10. What is the primary mechanism by which loss of the tumour suppressor gene ARF contributes to tumorigenesis?
    A. Inhibition of p53 degradation
    B. Hyperactivation of MDM2
    C. Suppression of DNA repair
    D. Enhancement of cell adhesion
    E. Activation of MAPK signalling

11. Which cytokine is most critical for promoting tumour-associated macrophage polarisation to the M2 phenotype?
    A. IL-2
    B. IL-4
    C. IFN-γ
    D. IL-12
    E. TNF-α

12. What is the significance of the EGFRvIII mutation in glioblastoma?
    A. Inhibits EGFR signalling
    B. Constitutively activates EGFR signalling
    C. Enhances apoptosis
    D. Suppresses angiogenesis
    E. Reduces metastatic potential

13. Which transcription factor is a key mediator of hypoxia-driven metastasis in breast cancer?
    A. E2F
    B. HIF-1α
    C. p53
    D. Myc
    E. Rb

14. What is the primary role of the Hippo signalling pathway in cancer?
    A. Promotion of YAP/TAZ-driven proliferation
    B. Suppression of cell growth
    C. Enhancement of DNA repair
    D. Inhibition of angiogenesis
    E. Activation of apoptosis

15. Which metabolic adaptation is most critical for cancer cell survival in nutrient-deprived conditions?
    A. Increased oxidative phosphorylation
    B. Autophagy-driven nutrient recycling
    C. Suppression of lactate production
    D. Inhibition of the pentose phosphate pathway
    E. Reduced glutamine metabolism

16. What is the primary function of the tumour suppressor gene BAP1 in uveal melanoma?
    A. Promotes histone deubiquitination
    B. Inhibits DNA repair
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

17. Which molecular marker is most commonly used to identify cancer stem cells in colorectal cancer?
    A. CD44
    B. CD20
    C. CD56
    D. CD3
    E. CD19

18. What is the primary mechanism of action of CAR-T cell therapy in cancer?
    A. Direct induction of apoptosis
    B. Engineered T-cell targeting of tumour antigens
    C. Inhibition of VEGF signalling
    D. Suppression of DNA repair
    E. Enhancement of glycolysis

19. Which genetic alteration is most associated with Lynch syndrome?
    A. MLH1/MSH2 mutation
    B. BRCA1/2 mutation
    C. KRAS mutation
    D. MYC amplification
    E. PTEN deletion

20. What is the role of the mTOR pathway in cancer?
    A. Inhibits protein synthesis
    B. Promotes cell growth and metabolism
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Reduces apoptosis

21. Which process is most critical for cancer cell intravasation during metastasis?
    A. Upregulation of E-cadherin
    B. Degradation of vascular basement membrane
    C. Inhibition of VEGF
    D. Suppression of MMPs
    E. Enhancement of p53 activity

22. What is the primary consequence of a gain-of-function mutation in the KIT gene in gastrointestinal stromal tumours?
    A. Inhibition of tyrosine kinase signalling
    B. Constitutive activation of tyrosine kinase signalling
    C. Suppression of angiogenesis
    D. Enhanced DNA repair
    E. Reduced cell proliferation

23. Which enzyme is critical for fatty acid synthesis in cancer cells?
    A. Fatty acid synthase
    B. Hexokinase
    C. Lactate dehydrogenase
    D. Glutaminase
    E. Pyruvate kinase

24. What is the role of the Notch pathway in T-cell acute lymphoblastic leukemia?
    A. Inhibits cell proliferation
    B. Promotes uncontrolled growth
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Activates apoptosis

25. Which epigenetic modification is targeted by DNA methyltransferase inhibitors in cancer therapy?
    A. Histone acetylation
    B. DNA methylation
    C. Histone phosphorylation
    D. Chromatin condensation
    E. Histone ubiquitination

26. What is the primary mechanism by which cancer cells induce tolerance in the immune system?
    A. Upregulation of MHC class I
    B. Secretion of immunosuppressive cytokines
    C. Enhancement of NK cell activity
    D. Increased antigen presentation
    E. Suppression of T-cell activation

27. Which molecular alteration is most associated with follicular lymphoma?
    A. BCL2 translocation
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

28. What is the primary role of the serine/threonine kinase AKT in cancer cells?
    A. Inhibition of cell survival
    B. Promotion of cell survival and growth
    C. Suppression of glycolysis
    D. Enhancement of DNA repair
    E. Reduction of angiogenesis

29. Which process is most critical for the colonisation of metastatic cancer cells in distant organs?
    A. Suppression of MMPs
    B. Adaptation to organ-specific microenvironment
    C. Inhibition of VEGF
    D. Enhancement of E-cadherin
    E. Reduction of cytokine production

30. What is the primary consequence of a mutation in the PTEN gene in endometrial cancer?
    A. Inhibition of PI3K/AKT signalling
    B. Hyperactivation of PI3K/AKT signalling
    C. Enhancement of DNA repair
    D. Suppression of angiogenesis
    E. Increased apoptosis

31. Which protein is a key regulator of the G1/S checkpoint in response to DNA damage?
    A. p21
    B. Chk1
    C. Cyclin D
    D. E2F
    E. Rb

32. What is the primary role of the tumour suppressor gene FHIT in lung cancer?
    A. Promotes DNA damage
    B. Inhibits cell proliferation
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

33. Which metabolic enzyme is targeted by metformin in cancer therapy?
    A. AMPK
    B. Hexokinase
    C. Lactate dehydrogenase
    D. Glutaminase
    E. Pyruvate kinase

34. What is the primary mechanism of action of PARP inhibitors in ovarian cancer?
    A. Inhibition of DNA repair
    B. Activation of PI3K/AKT pathway
    C. Suppression of apoptosis
    D. Enhancement of angiogenesis
    E. Inhibition of glycolysis

35. Which process is most critical for the glutamine addiction in cancer cells?
    A. Suppression of glycolysis
    B. Upregulation of glutaminase
    C. Inhibition of lactate production
    D. Enhancement of oxidative phosphorylation
    E. Reduction of NADPH synthesis

36. What is the primary role of the tumour suppressor gene BRCA2 in breast cancer?
    A. Promotes DNA repair
    B. Inhibits DNA repair
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

37. Which molecular alteration is most associated with diffuse large B-cell lymphoma?
    A. MYC rearrangement
    B. KRAS mutation
    C. TP53 deletion
    D. PTEN loss
    E. BCR-ABL fusion

38. What is the primary consequence of a mutation in the GNAS gene in pituitary adenoma?
    A. Inhibition of cyclic AMP signalling
    B. Constitutive activation of cyclic AMP signalling
    C. Suppression of angiogenesis
    D. Enhanced DNA repair
    E. Reduced cell proliferation

39. Which protein is a key mediator of the DNA damage response in non-homologous end joining?
    A. RAD51
    B. DNA-PK
    C. PARP1
    D. ATM
    E. BRCA2

40. What is the primary role of the tumour microenvironment in radiotherapy resistance?
    A. Inhibition of drug efflux
    B. Secretion of hypoxia-induced survival signals
    C. Suppression of immune cells
    D. Enhancement of DNA repair
    E. Reduction of hypoxia

41. Which molecular alteration is most associated with multiple myeloma?
    A. IGH translocation
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

42. What is the primary mechanism by which cancer cells achieve immune evasion?
    A. Upregulation of MHC class I
    B. Expression of PD-L1
    C. Enhancement of NK cell activity
    D. Suppression of cytokine production
    E. Increased antigen presentation

43. Which process is most critical for the formation of invadopodia in metastatic cancer cells?
    A. Upregulation of E-cadherin
    B. Cortactin-mediated actin polymerisation
    C. Inhibition of MMPs
    D. Suppression of VEGF
    E. Enhancement of p53 activity

44. What is the primary role of the tumour suppressor gene WT1 in Wilms tumour?
    A. Promotes cell proliferation
    B. Inhibits cell proliferation
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

45. Which molecular alteration is most associated with cholangiocarcinoma?
    A. IDH1 mutation
    B. KRAS mutation
    C. MYC amplification
    D. PTEN loss
    E. CTNNB1 mutation

46. What is the primary consequence of a mutation in the ALK gene in neuroblastoma?
    A. Inhibition of tyrosine kinase signalling
    B. Constitutive activation of tyrosine kinase signalling
    C. Suppression of angiogenesis
    D. Enhanced DNA repair
    E. Reduced cell proliferation

47. Which protein is a key mediator of the DNA damage response in base excision repair?
    A. RAD51
    B. DNA-PK
    C. PARP1
    D. ATM
    E. BRCA2

48. What is the primary role of the tumour suppressor gene TP53 in cervical cancer?
    A. Promotes cell cycle progression
    B. Inhibits cell cycle progression
    C. Enhances angiogenesis
    D. Suppresses DNA repair
    E. Activates Wnt signalling

49. Which molecular alteration is most associated with chronic lymphocytic leukemia?
    A. TP53 deletion
    B. KRAS mutation
    C. MYC amplification
    D. PTEN loss
    E. CTNNB1 mutation

50. What is the primary mechanism by which cancer cells resist oxidative stress?
    A. Upregulation of NRF2
    B. Inhibition of VEGF
    C. Suppression of MMPs
    D. Enhancement of E-cadherin
    E. Reduction of cytokine production

Radiobiology (50 Questions)

51. What is the primary mechanism of radiation-induced autophagy in cancer cells?
    A. Direct induction of apoptosis
    B. Activation of mTOR inhibition pathways
    C. Inhibition of protein synthesis
    D. Disruption of mitochondrial function
    E. Suppression of glycolysis

52. In a cell survival curve, what does the quasi-threshold dose (Dq) represent?
    A. The dose required to reduce survival to 37%
    B. The dose below which no cell killing occurs
    C. The shoulder width of the curve
    D. The dose causing complete cell inactivation
    E. The dose at which repair saturates

53. Which factor most significantly influences the oxygen enhancement ratio (OER) in high-LET radiation?
    A. Dose rate
    B. Reduced dependence on free radicals
    C. Fraction size
    D. Cell cycle phase
    E. Total dose

54. What is the primary advantage of neutron therapy over photon therapy in salivary gland tumours?
    A. Lower cost
    B. Higher relative biological effectiveness (RBE)
    C. Increased oxygen enhancement ratio
    D. Reduced fractionation requirement
    E. Enhanced normal tissue sparing

55. Which DNA repair pathway is most critical for repairing radiation-induced interstrand crosslinks?
    A. Homologous recombination
    B. Non-homologous end joining
    C. Base excision repair
    D. Fanconi anaemia pathway
    E. Mismatch repair

56. What is the primary mechanism of the abscopal effect in radiotherapy?
    A. Direct DNA damage in irradiated cells
    B. Immune-mediated tumour regression at distant sites
    C. Inhibition of DNA repair in unirradiated cells
    D. Suppression of apoptosis in irradiated cells
    E. Release of reactive oxygen species

57. In the Linear-Quadratic model, what does the α/β ratio indicate about tissue response?
    A. Sensitivity to dose rate
    B. Sensitivity to fraction size
    C. Oxygen-dependent damage
    D. Repair of sublethal damage
    E. Cell cycle redistribution

58. Which normal tissue is most susceptible to radiation-induced vascular damage?
    A. Skin
    B. Bone marrow
    C. Brain
    D. Liver
    E. Lung

59. What is the primary mechanism of radiation-induced esophagitis?
    A. Acute apoptosis of epithelial cells
    B. Chronic inflammation and fibrosis
    C. Direct DNA damage in endothelial cells
    D. Inhibition of mitochondrial function
    E. Suppression of glycolysis

60. Which factor most significantly influences the therapeutic index in hypofractionated radiotherapy?
    A. Total dose
    B. Tumour α/β ratio
    C. Normal tissue repair capacity
    D. Tumour oxygenation
    E. Radiation type

61. What is the biologically effective dose (BED) for a regimen of 48 Gy in 4 fractions with an α/β ratio of 10 Gy?
    A. 48 Gy
    B. 60 Gy
    C. 72 Gy
    D. 86.4 Gy
    E. 96 Gy

62. Which cell cycle phase is most resistant to radiation-induced apoptosis?
    A. G1
    B. S
    C. G2
    D. M
    E. G0

63. What is the primary advantage of adaptive radiotherapy over static planning?
    A. Reduced treatment time
    B. Adjustment for anatomical changes
    C. Lower cost
    D. Increased oxygen enhancement ratio
    E. Enhanced normal tissue toxicity

64. Which protein is most critical for the activation of the G2/M checkpoint in response to radiation?
    A. p53
    B. Chk1
    C. RAD51
    D. DNA-PK
    E. PARP1

65. What is the primary mechanism of action of hypoxia-activated prodrugs like tirapazamine?
    A. Inhibition of DNA repair
    B. Selective cytotoxicity in hypoxic cells
    C. Enhancement of apoptosis
    D. Suppression of glycolysis
    E. Inhibition of angiogenesis

66. Which factor most significantly influences the relative biological effectiveness (RBE) of carbon ions?
    A. Dose rate
    B. High linear energy transfer (LET)
    C. Fraction size
    D. Cell cycle phase
    E. Total dose

67. What is the primary consequence of a mutation in the RAD51 gene in response to radiation?
    A. Enhanced homologous recombination
    B. Increased radiosensitivity
    C. Reduced apoptosis
    D. Inhibition of non-homologous end joining
    E. Upregulation of VEGF

68. Which normal tissue effect is most associated with stereotactic radiosurgery?
    A. Acute mucositis
    B. Late necrosis
    C. Erythema
    D. Desquamation
    E. Leukopenia

69. What is the primary mechanism of radiation-induced liver toxicity?
    A. Acute apoptosis of hepatocytes
    B. Chronic inflammation and veno-occlusive disease
    C. Direct DNA damage in endothelial cells
    D. Inhibition of mitochondrial function
    E. Suppression of glycolysis

70. Which factor most significantly influences the tumour control probability (TCP)?
    A. Total dose
    B. Fraction size
    C. Tumour clonogenic cell density
    D. Radiation type
    E. Dose rate

71. What is the equivalent dose in 2 Gy fractions (EQD2) for a regimen of 45 Gy in 5 fractions with an α/β ratio of 3 Gy?
    A. 60 Gy
    B. 75 Gy
    C. 90 Gy
    D. 105 Gy
    E. 120 Gy

72. Which repair pathway is most critical for repairing radiation-induced base damage?
    A. Homologous recombination
    B. Non-homologous end joining
    C. Base excision repair
    D. Nucleotide excision repair
    E. Mismatch repair

73. What is the primary advantage of image-guided radiotherapy (IGRT) over conventional radiotherapy?
    A. Reduced treatment time
    B. Improved targeting accuracy
    C. Lower cost
    D. Increased oxygen enhancement ratio
    E. Enhanced normal tissue toxicity

74. Which factor most significantly influences the reassortment of cells in fractionated radiotherapy?
    A. Dose rate
    B. Cell cycle kinetics
    C. Total dose
    D. Radiation type
    E. Fraction size

75. What is the primary mechanism of radiation-induced renal toxicity?
    A. Acute apoptosis of tubular cells
    B. Chronic inflammation and glomerulosclerosis
    C. Direct DNA damage in endothelial cells
    D. Inhibition of mitochondrial function
    E. Suppression of glycolysis

76. Which protein is most critical for the repair of radiation-induced DNA-protein crosslinks?
    A. RAD51
    B. DNA-PK
    C. PARP1
    D. ATM
    E. BRCA2

77. What is the primary consequence of a mutation in the LIG4 gene in response to radiation?
    A. Enhanced non-homologous end joining
    B. Increased radiosensitivity
    C. Reduced apoptosis
    D. Inhibition of homologous recombination
    E. Upregulation of VEGF

78. Which factor most significantly influences the repair of sublethal damage in tumour cells?
    A. Total dose
    B. Fractionation interval
    C. Radiation type
    D. Cell cycle phase
    E. Dose rate

79. What is the surviving fraction after 8 Gy of radiation if the D0 is 2.5 Gy?
    A. 0.04
    B. 0.09
    C. 0.14
    D. 0.25
    E. 0.37

80. Which normal tissue is most susceptible to radiation-induced fibrosis?
    A. Skin
    B. Bone marrow
    C. Lung
    D. Liver
    E. Kidney

81. What is the primary mechanism of action of oxygen-mimetic radiosensitisers like nimorazole?
    A. Enhancement of DNA repair
    B. Increased free radical formation
    C. Inhibition of apoptosis
    D. Suppression of glycolysis
    E. Reduction of hypoxia

82. Which factor most significantly influences the repopulation of normal tissues during radiotherapy?
    A. Dose rate
    B. Treatment duration
    C. Fraction size
    D. Radiation type
    E. Cell cycle phase

83. What is the primary consequence of a mutation in the XRCC1 gene in response to radiation?
    A. Enhanced base excision repair
    B. Increased radiosensitivity
    C. Reduced apoptosis
    D. Inhibition of non-homologous end joining
    E. Upregulation of VEGF

84. Which normal tissue effect is most associated with low-LET radiation?
    A. Late necrosis
    B. Acute mucositis
    C. Myelopathy
    D. Cardiac toxicity
    E. Pneumonitis

85. What is the primary mechanism of radiation-induced bladder toxicity?
    A. Acute apoptosis of urothelial cells
    B. Chronic inflammation and telangiectasia
    C. Direct DNA damage in endothelial cells
    D. Inhibition of mitochondrial function
    E. Suppression of glycolysis

86. Which factor most significantly influences the oxygen effect in high-LET radiotherapy?
    A. Dose rate
    B. Reduced oxygen dependence
    C. Fraction size
    D. Cell cycle phase
    E. Total dose

87. What is the biologically effective dose (BED) for a regimen of 66 Gy in 33 fractions with an α/β ratio of 2 Gy?
    A. 66 Gy
    B. 79.2 Gy
    C. 99 Gy
    D. 118.8 Gy
    E. 132 Gy

88. Which protein is most critical for the repair of radiation-induced double-strand breaks in S phase?
    A. Ku70/80
    B. RAD51
    C. DNA-PK
    D. PARP1
    E. XRCC1

89. What is the primary advantage of carbon ion therapy over neutron therapy?
    A. Lower cost
    B. Improved dose localisation
    C. Increased oxygen enhancement ratio
    D. Reduced relative biological effectiveness
    E. Enhanced fractionation requirement

90. Which factor most significantly influences the normal tissue complication probability (NTCP) in stereotactic radiotherapy?
    A. Total dose
    B. Fraction size
    C. Volume of tissue irradiated
    D. Radiation type
    E. Dose rate

91. What is the equivalent dose in 2 Gy fractions (EQD2) for a regimen of 54 Gy in 6 fractions with an α/β ratio of 10 Gy?
    A. 64.8 Gy
    B. 72 Gy
    C. 81 Gy
    D. 90 Gy
    E. 108 Gy

92. Which repair pathway is most critical for repairing radiation-induced oxidative damage?
    A. Homologous recombination
    B. Non-homologous end joining
    C. Base excision repair
    D. Nucleotide excision repair
    E. Mismatch repair

93. What is the primary mechanism of radiation-induced optic neuropathy?
    A. Acute apoptosis of neurons
    B. Chronic inflammation and vascular damage
    C. Direct DNA damage in glial cells
    D. Inhibition of mitochondrial function
    E. Suppression of glycolysis

94. Which factor most significantly influences the reoxygenation of tumour cells during hypofractionated radiotherapy?
    A. Dose rate
    B. Fractionation interval
    C. Total dose
    D. Radiation type
    E. Cell cycle phase

95. What is the primary consequence of a mutation in the ATM gene in response to radiation?
    A. Enhanced homologous recombination
    B. Increased radiosensitivity
    C. Reduced apoptosis
    D. Inhibition of non-homologous end joining
    E. Upregulation of VEGF

96. Which normal tissue effect is most associated with high-dose rate brachytherapy?
    A. Acute mucositis
    B. Late telangiectasia
    C. Erythema
    D. Desquamation
    E. Leukopenia

97. What is the primary mechanism of action of nanoparticle-based radiosensitisers in radiotherapy?
    A. Enhancement of DNA repair
    B. Increased production of secondary electrons
    C. Inhibition of apoptosis
    D. Suppression of glycolysis
    E. Reduction of hypoxia

98. Which factor most significantly influences the repair of potentially lethal damage in tumour cells?
    A. Dose rate
    B. Post-irradiation microenvironment
    C. Fraction size
    D. Radiation type
    E. Cell cycle phase

99. What is the surviving fraction after 10 Gy of radiation if the D0 is 2 Gy?
    A. 0.01
    B. 0.07
    C. 0.14
    D. 0.25
    E. 0.37

100. Which protein is most critical for the coordination of the DNA damage response in response to radiation?
     A. p53
     B. ATM
     C. RAD51
     D. DNA-PK
     E. PARP1

Answers

Cancer Biology (50 Answers)

1. A. MEK inhibitors block compensatory MAPK signalling, synergising with BRAF inhibitors in BRAF V600E melanoma.

2. B. TGF-β/SMAD promotes EMT, enhancing invasion in late-stage cancer.

3. B. Promoter hypermethylation silences CDKN2A in pancreatic cancer.

4. B. MDSCs suppress T-cell activity, promoting immune evasion.

5. A. L1196M gatekeeper mutation confers resistance to ALK inhibitors.

6. B. EZH2 overexpression silences tumour suppressor genes via histone methylation.

7. A. Vasculogenic mimicry forms tumour vasculature in glioblastoma.

8. B. KEAP1-NRF2 upregulates antioxidant defenses under oxidative stress.

9. B. Reprogramming of energy metabolism is a hallmark of cancer.

10. B. ARF loss hyperactivates MDM2, leading to p53 degradation.

11. B. IL-4 promotes M2 macrophage polarisation.

12. B. EGFRvIII constitutively activates EGFR signalling in glioblastoma.

13. B. HIF-1α drives hypoxia-mediated metastasis in breast cancer.

14. A. Hippo pathway promotes YAP/TAZ-driven proliferation in cancer.

15. B. Autophagy recycles nutrients for cancer cell survival in nutrient-deprived conditions.

16. A. BAP1 promotes histone deubiquitination, suppressing tumour growth.

17. A. CD44 is a marker for colorectal cancer stem cells.

18. B. CAR-T cells target tumour antigens via engineered T-cells.

19. A. MLH1/MSH2 mutations cause Lynch syndrome.

20. B. mTOR promotes cell growth and metabolism in cancer.

21. B. Degradation of vascular basement membrane enables intravasation.

22. B. KIT mutation constitutively activates tyrosine kinase signalling in GIST.

23. A. Fatty acid synthase drives fatty acid synthesis in cancer cells.

24. B. Notch promotes uncontrolled growth in T-ALL.

25. B. DNA methyltransferase inhibitors target DNA methylation.

26. B. Immunosuppressive cytokines induce immune tolerance.

27. A. BCL2 translocation is associated with follicular lymphoma.

28. B. AKT promotes cell survival and growth.

29. B. Adaptation to organ-specific microenvironments enables metastatic colonisation.

30. B. PTEN mutation hyperactivates PI3K/AKT signalling in endometrial cancer.

31. A. p21 regulates the G1/S checkpoint in response to DNA damage.

32. B. FHIT inhibits cell proliferation in lung cancer.

33. A. Metformin targets AMPK to inhibit cancer cell metabolism.

34. A. PARP inhibitors block DNA repair in ovarian cancer.

35. B. Upregulation of glutaminase drives glutamine addiction.

36. A. BRCA2 promotes DNA repair via homologous recombination.

37. A. MYC rearrangement is associated with diffuse large B-cell lymphoma.

38. B. GNAS mutation activates cyclic AMP signalling in pituitary adenoma.

39. B. DNA-PK mediates non-homologous end joining in DNA damage response.

40. B. Hypoxia-induced survival signals from the microenvironment promote radiotherapy resistance.

41. A. IGH translocation is associated with multiple myeloma.

42. B. PD-L1 expression enables immune evasion.

43. B. Cortactin-mediated actin polymerisation forms invadopodia.

44. B. WT1 inhibits cell proliferation in Wilms tumour.

45. A. IDH1 mutation is associated with cholangiocarcinoma.

46. B. ALK mutation constitutively activates tyrosine kinase signalling in neuroblastoma.

47. C. PARP1 mediates base excision repair in DNA damage response.

48. B. TP53 inhibits cell cycle progression in cervical cancer.

49. A. TP53 deletion is associated with chronic lymphocytic leukemia.

50. A. NRF2 upregulation protects cancer cells from oxidative stress.

Radiobiology (50 Answers)

51. B. Radiation-induced autophagy is driven by mTOR inhibition pathways.

52. C. Dq represents the shoulder width of the cell survival curve.

53. B. Reduced dependence on free radicals lowers OER in high-LET radiation.

54. B. Neutron therapy has higher RBE for salivary gland tumours.

55. D. Fanconi anaemia pathway repairs interstrand crosslinks.

56. B. The abscopal effect involves immune-mediated tumour regression at distant sites.

57. B. The α/β ratio indicates sensitivity to fraction size.

58. C. The brain is susceptible to vascular damage from radiation.

59. A. Acute apoptosis of epithelial cells causes radiation-induced esophagitis.

60. B. Tumour α/β ratio influences the therapeutic index in hypofractionation.

61. D. BED = 48 × (1 + 12/10) = 86.4 Gy.

62. B. S phase is most resistant to radiation-induced apoptosis.

63. B. Adaptive radiotherapy adjusts for anatomical changes.

64. B. Chk1 activates the G2/M checkpoint in response to radiation.

65. B. Tirapazamine is selectively cytotoxic in hypoxic cells.

66. B. High LET increases the RBE of carbon ions.

67. B. RAD51 mutation increases radiosensitivity due to defective homologous recombination.

68. B. Late necrosis is associated with stereotactic radiosurgery.

69. B. Chronic inflammation and veno-occlusive disease cause liver toxicity.

70. C. Tumour clonogenic cell density influences TCP.

71. C. EQD2 = 45 × (9 + 3)/(2 + 3) = 90 Gy.

72. C. Base excision repair repairs radiation-induced base damage.

73. B. IGRT improves targeting accuracy.

74. B. Cell cycle kinetics influence reassortment in fractionated radiotherapy.

75. B. Chronic inflammation and glomerulosclerosis cause renal toxicity.

76. C. PARP1 repairs DNA-protein crosslinks.

77. B. LIG4 mutation increases radiosensitivity due to defective NHEJ.

78. B. Fractionation interval influences sublethal damage repair in tumour cells.

79. A. SF = e^(-8/2.5) ≈ 0.04.

80. C. Lung is most susceptible to radiation-induced fibrosis.

81. B. Nimorazole increases free radical formation in hypoxic cells.

82. B. Treatment duration influences normal tissue repopulation.

83. B. XRCC1 mutation increases radiosensitivity due to defective base excision repair.

84. B. Acute mucositis is associated with low-LET radiation.

85. B. Chronic inflammation and telangiectasia cause bladder toxicity.

86. B. Reduced oxygen dependence minimises the oxygen effect in high-LET radiotherapy.

87. D. BED = 66 × (1 + 2/2) = 118.8 Gy.

88. B. RAD51 repairs DSBs in S phase via homologous recombination.

89. B. Carbon ion therapy offers improved dose localisation over neutron therapy.

90. C. Volume of tissue irradiated influences NTCP in stereotactic radiotherapy.

91. C. EQD2 = 54 × (9 + 10)/(2 + 10) = 81 Gy.

92. C. Base excision repair repairs oxidative damage.

93. B. Chronic inflammation and vascular damage cause optic neuropathy.

94. B. Fractionation interval influences reoxygenation in hypofractionated radiotherapy.

95. B. ATM mutation increases radiosensitivity due to impaired DNA damage response.

96. B. Late telangiectasia is associated with high-dose rate brachytherapy.

97. B. Nanoparticle-based radiosensitisers increase secondary electron production.

98. B. Post-irradiation microenvironment influences potentially lethal damage repair.

99. A. SF = e^(-10/2) ≈ 0.01.

100. B. ATM coordinates the DNA damage response to radiation.