FRCR Oncology Part 1: CANCER BIOLOGY, RADIOBIOLOGY - 12 (100 QUESTIONS, ANSWERS BELOW)

 

Cancer Biology (50 Questions)

1. Which mechanism underlies the synthetic lethality of PARP inhibitors in BRCA1-mutated cancers?
   A. Inhibition of non-homologous end joining
   B. Exploitation of defective homologous recombination
   C. Suppression of base excision repair
   D. Activation of mismatch repair
   E. Enhancement of nucleotide excision repair

2. What is the primary role of the NOTCH signalling pathway in cancer stem cell maintenance?
   A. Suppression of self-renewal
   B. Promotion of differentiation
   C. Enhancement of stemness and survival
   D. Inhibition of angiogenesis
   E. Reduction of metastatic potential

3. Which epigenetic regulator is frequently hypermethylated in colorectal cancer, leading to mismatch repair deficiency?
   A. MLH1
   B. APC
   C. SMAD4
   D. PTEN
   E. TP53

4. In the context of the tumour microenvironment, what is the primary function of cancer-associated fibroblasts (CAFs)?
   A. Direct cytotoxicity against tumour cells
   B. Secretion of matrix metalloproteinases to promote invasion
   C. Inhibition of immune cell infiltration
   D. Suppression of VEGF expression
   E. Enhancement of DNA repair

5. Which molecular alteration is most associated with resistance to EGFR tyrosine kinase inhibitors in non-small cell lung cancer?
   A. T790M mutation in EGFR
   B. Loss of PTEN expression
   C. Amplification of MYC
   D. Upregulation of p53
   E. Deletion of RB1

6. What is the primary consequence of MYC amplification in cancer cells?
   A. Inhibition of cell cycle progression
   B. Global transcriptional amplification
   C. Suppression of apoptosis
   D. Reduced glucose uptake
   E. Enhanced DNA repair

7. Which process is critical for the angiogenic switch in tumour progression?
   A. Downregulation of VEGF
   B. Upregulation of thrombospondin-1
   C. Balance shift towards pro-angiogenic factors
   D. Inhibition of HIF-1α
   E. Suppression of MMP activity

8. In cancer cells, what is the role of the IDH1 mutation in gliomas?
   A. Enhances oxidative phosphorylation
   B. Produces 2-hydroxyglutarate, altering epigenetics
   C. Inhibits glycolysis
   D. Promotes homologous recombination
   E. Suppresses angiogenesis

9. Which hallmark of cancer is most directly associated with the activation of telomerase?
   A. Evasion of apoptosis
   B. Replicative immortality
   C. Sustained angiogenesis
   D. Genomic instability
   E. Invasion and metastasis

10. What is the primary mechanism by which PTEN loss contributes to tumorigenesis?
    A. Activation of MAPK signalling
    B. Hyperactivation of PI3K/AKT pathway
    C. Inhibition of p53 transcription
    D. Suppression of DNA repair
    E. Enhancement of cell adhesion

11. Which cytokine is most critical for promoting an immunosuppressive tumour microenvironment?
    A. IL-2
    B. TGF-β
    C. IFN-γ
    D. IL-12
    E. TNF-α

12. What is the significance of the KRAS G12D mutation in pancreatic cancer?
    A. Inhibits MAPK signalling
    B. Constitutively activates RAS signalling
    C. Enhances apoptosis
    D. Suppresses glycolysis
    E. Reduces metastatic potential

13. Which protein is a key mediator of epithelial-to-mesenchymal transition (EMT) in cancer?
    A. E-cadherin
    B. Snail
    C. β-catenin
    D. p53
    E. VEGF

14. What is the primary role of the Hedgehog signalling pathway in basal cell carcinoma?
    A. Suppression of cell proliferation
    B. Promotion of uncontrolled growth
    C. Enhancement of DNA repair
    D. Inhibition of angiogenesis
    E. Reduction of immune evasion

15. Which metabolic adaptation allows cancer cells to survive in hypoxic conditions?
    A. Increased oxidative phosphorylation
    B. Upregulation of HIF-1α-driven glycolysis
    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 APC in colorectal cancer?
    A. Promotes Wnt signalling
    B. Inhibits β-catenin accumulation
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Activates p53 transcription

17. Which molecular marker is most commonly used to identify cancer stem cells in glioblastoma?
    A. CD133
    B. CD20
    C. CD56
    D. CD3
    E. CD19

18. What is the primary mechanism of action of immune checkpoint inhibitors in cancer therapy?
    A. Direct induction of apoptosis
    B. Blockade of PD-1/PD-L1 interaction
    C. Inhibition of VEGF signalling
    D. Suppression of DNA repair
    E. Enhancement of glycolysis

19. Which genetic alteration is most associated with hereditary breast and ovarian cancer syndrome?
    A. TP53 mutation
    B. BRCA1/2 mutation
    C. KRAS mutation
    D. MYC amplification
    E. PTEN deletion

20. What is the role of the NF-κB pathway in cancer?
    A. Inhibits inflammation
    B. Promotes cell survival and proliferation
    C. Enhances DNA repair
    D. Suppresses metastasis
    E. Reduces glycolysis

21. Which process is most critical for anoikis resistance in metastatic cancer cells?
    A. Upregulation of E-cadherin
    B. Activation of integrin signalling
    C. Inhibition of VEGF
    D. Suppression of MMPs
    E. Enhancement of p53 activity

22. What is the primary consequence of a loss-of-function mutation in the VHL gene in renal cell carcinoma?
    A. Inhibition of HIF-1α
    B. Constitutive activation of HIF-1α
    C. Suppression of angiogenesis
    D. Enhanced DNA repair
    E. Reduced cell proliferation

23. Which enzyme is critical for the glutamine metabolism in cancer cells?
    A. Glutaminase
    B. Hexokinase
    C. Lactate dehydrogenase
    D. Citrate synthase
    E. Pyruvate kinase

24. What is the role of the JAK/STAT pathway in cancer?
    A. Inhibits cytokine signalling
    B. Promotes proliferation and immune evasion
    C. Enhances apoptosis
    D. Suppresses angiogenesis
    E. Reduces DNA repair

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

26. What is the primary mechanism by which cancer cells evade immune surveillance?
    A. Upregulation of MHC class I
    B. Expression of immune checkpoint ligands
    C. Enhancement of NK cell activity
    D. Suppression of cytokine production
    E. Increased antigen presentation

27. Which molecular alteration is most associated with chronic myelogenous leukemia?
    A. BCR-ABL fusion
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

28. What is the primary role of the pentose phosphate pathway in cancer cells?
    A. ATP production
    B. NADPH and ribose-5-phosphate synthesis
    C. Lactate production
    D. Inhibition of glycolysis
    E. Enhancement of oxidative phosphorylation

29. Which process is most critical for the establishment of pre-metastatic niches?
    A. Suppression of MMPs
    B. Secretion of exosomes
    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 SMAD4 gene in pancreatic cancer?
    A. Activation of TGF-β signalling
    B. Inhibition of TGF-β signalling
    C. Enhancement of DNA repair
    D. Suppression of angiogenesis
    E. Increased apoptosis

31. Which protein is a key regulator of the G2/M 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 NF1 in neurofibromatosis?
    A. Promotes RAS signalling
    B. Inhibits RAS signalling
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Activates p53

33. Which metabolic enzyme is targeted by 2-deoxyglucose in cancer therapy?
    A. Hexokinase
    B. Pyruvate kinase
    C. Lactate dehydrogenase
    D. Glutaminase
    E. Citrate synthase

34. What is the primary mechanism of action of BRAF inhibitors in melanoma?
    A. Inhibition of MAPK signalling
    B. Activation of PI3K/AKT pathway
    C. Suppression of DNA repair
    D. Enhancement of apoptosis
    E. Inhibition of angiogenesis

35. Which process is most critical for the Warburg effect in cancer cells?
    A. Suppression of glycolysis
    B. Upregulation of HIF-1α and GLUT1
    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 LKB1 in lung cancer?
    A. Promotes mTOR signalling
    B. Inhibits mTOR signalling
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Activates p53

37. Which molecular alteration is most associated with mantle cell lymphoma?
    A. Cyclin D1 overexpression
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

38. What is the primary consequence of a mutation in the CTNNB1 gene in colorectal cancer?
    A. Inhibition of Wnt signalling
    B. Constitutive activation of β-catenin
    C. Suppression of angiogenesis
    D. Enhanced DNA repair
    E. Reduced cell proliferation

39. Which protein is a key mediator of DNA damage response in cancer cells?
    A. ATM
    B. VEGF
    C. Snail
    D. E-cadherin
    E. MMP-9

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

41. Which molecular alteration is most associated with Burkitt lymphoma?
    A. MYC translocation
    B. KRAS mutation
    C. TP53 deletion
    D. PTEN loss
    E. BCR-ABL fusion

42. What is the primary mechanism by which cancer cells achieve replicative immortality?
    A. Suppression of telomerase
    B. Activation of telomerase
    C. Inhibition of p53
    D. Enhancement of DNA repair
    E. Reduction of apoptosis

43. Which process is most critical for the formation of invadopodia in cancer cells?
    A. Upregulation of E-cadherin
    B. Actin cytoskeleton remodelling
    C. Inhibition of MMPs
    D. Suppression of VEGF
    E. Enhancement of p53 activity

44. What is the primary role of the tumour suppressor gene RB1 in retinoblastoma?
    A. Promotes E2F transcription
    B. Inhibits E2F transcription
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Activates p53

45. Which molecular alteration is most associated with hepatocellular carcinoma?
    A. TP53 mutation
    B. KRAS mutation
    C. MYC amplification
    D. PTEN loss
    E. CTNNB1 mutation

46. What is the primary consequence of a mutation in the PIK3CA gene in breast cancer?
    A. Inhibition of PI3K/AKT signalling
    B. Hyperactivation of PI3K/AKT 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 homologous recombination?
    A. Ku70/80
    B. RAD51
    C. DNA-PK
    D. PARP1
    E. XRCC1

48. What is the primary role of the tumour suppressor gene PTEN in glioblastoma?
    A. Promotes PI3K/AKT signalling
    B. Inhibits PI3K/AKT signalling
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Activates p53

49. Which molecular alteration is most associated with acute promyelocytic leukemia?
    A. PML-RARA fusion
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

50. What is the primary mechanism by which cancer cells resist apoptosis?
    A. Upregulation of BCL2
    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 mitotic catastrophe?
    A. Direct induction of apoptosis
    B. Aberrant mitosis due to unrepaired DNA damage
    C. Inhibition of protein synthesis
    D. Disruption of mitochondrial function
    E. Suppression of glycolysis

52. In a cell survival curve, what does the extrapolation number (n) represent?
    A. The dose required to reduce survival to 37%
    B. The number of cells surviving at zero dose
    C. The shoulder width of the curve
    D. The ratio of α to β
    E. The dose causing complete cell inactivation

53. Which factor most significantly influences the oxygen enhancement ratio (OER) in radiotherapy?
    A. Dose rate
    B. Linear energy transfer (LET)
    C. Fraction size
    D. Cell cycle phase
    E. Total dose

54. What is the primary advantage of using carbon ions over protons in radiotherapy?
    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 error-prone in response to radiation-induced double-strand breaks?
    A. Homologous recombination
    B. Non-homologous end joining
    C. Base excision repair
    D. Nucleotide excision repair
    E. Mismatch repair

56. What is the primary mechanism of radiation-induced bystander effect?
    A. Direct DNA damage in irradiated cells
    B. Release of reactive oxygen species from irradiated cells
    C. Intercellular signalling via gap junctions
    D. Inhibition of DNA repair in unirradiated cells
    E. Suppression of apoptosis in irradiated cells

57. In the Linear-Quadratic model, what does the β component represent?
    A. Single-hit cell killing
    B. Double-hit cell killing
    C. Repair of sublethal damage
    D. Oxygen-dependent damage
    E. Cell cycle redistribution

58. Which normal tissue is most susceptible to radiation-induced late effects?
    A. Skin
    B. Bone marrow
    C. Spinal cord
    D. Liver
    E. Lung

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

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

61. What is the biologically effective dose (BED) for a regimen of 50 Gy in 25 fractions with an α/β ratio of 3 Gy?
    A. 50 Gy
    B. 60 Gy
    C. 66.7 Gy
    D. 75 Gy
    E. 83.3 Gy

62. Which cell cycle phase is least sensitive to radiation-induced damage?
    A. G1
    B. S
    C. G2
    D. M
    E. G0

63. What is the primary advantage of stereotactic body radiotherapy (SBRT) over conventional fractionation?
    A. Reduced total dose
    B. Enhanced tumour control probability
    C. Increased normal tissue toxicity
    D. Lower cost
    E. Reduced treatment time

64. Which protein is most critical for sensing radiation-induced double-strand breaks?
    A. p53
    B. ATM
    C. RAD51
    D. DNA-PK
    E. PARP1

65. What is the primary mechanism of action of radiosensitisers like cisplatin?
    A. Inhibition of DNA repair
    B. Enhancement of apoptosis
    C. Suppression of glycolysis
    D. Reduction of hypoxia
    E. Inhibition of angiogenesis

66. Which factor most significantly influences the relative biological effectiveness (RBE) of radiation?
    A. Dose rate
    B. 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 ATR 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 high-dose per fraction radiotherapy?
    A. Acute mucositis
    B. Late fibrosis
    C. Erythema
    D. Desquamation
    E. Leukopenia

69. What is the primary mechanism of radiation-induced second malignancies?
    A. Direct induction of apoptosis
    B. Genomic instability from unrepaired DNA damage
    C. Inhibition of DNA repair
    D. Suppression of immune surveillance
    E. Enhancement of glycolysis

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

71. What is the equivalent dose in 2 Gy fractions (EQD2) for a regimen of 40 Gy in 5 fractions with an α/β ratio of 10 Gy?
    A. 48 Gy
    B. 56 Gy
    C. 64 Gy
    D. 72 Gy
    E. 80 Gy

72. Which repair pathway is most active in the S phase of the cell cycle?
    A. Non-homologous end joining
    B. Homologous recombination
    C. Base excision repair
    D. Nucleotide excision repair
    E. Mismatch repair

73. What is the primary advantage of intensity-modulated radiotherapy (IMRT) over 3D conformal radiotherapy?
    A. Reduced treatment time
    B. Improved dose conformity to tumour
    C. Lower cost
    D. Increased oxygen enhancement ratio
    E. Enhanced normal tissue toxicity

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

75. What is the primary mechanism of radiation-induced cardiac toxicity?
    A. Acute apoptosis of cardiomyocytes
    B. Chronic inflammation and fibrosis
    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 single-strand breaks?
    A. RAD51
    B. DNA-PK
    C. PARP1
    D. ATM
    E. BRCA2

77. What is the primary consequence of a mutation in the FANCA 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

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

79. What is the surviving fraction after 4 Gy of radiation if the D0 is 1.5 Gy?
    A. 0.05
    B. 0.07
    C. 0.14
    D. 0.25
    E. 0.37

80. Which normal tissue is most susceptible to radiation-induced acute effects?
    A. Spinal cord
    B. Bone marrow
    C. Kidney
    D. Liver
    E. Heart

81. What is the primary mechanism of action of radioprotectors like amifostine?
    A. Enhancement of DNA repair
    B. Scavenging of reactive oxygen species
    C. Inhibition of apoptosis
    D. Suppression of glycolysis
    E. Reduction of hypoxia

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

83. What is the primary consequence of a mutation in the BRCA2 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

84. Which normal tissue effect is most associated with low-dose per fraction radiotherapy?
    A. Late fibrosis
    B. Acute mucositis
    C. Myelopathy
    D. Cardiac toxicity
    E. Pneumonitis

85. What is the primary mechanism of radiation-induced neurotoxicity?
    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

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

87. What is the biologically effective dose (BED) for a regimen of 70 Gy in 35 fractions with an α/β ratio of 2 Gy?
    A. 70 Gy
    B. 84 Gy
    C. 98 Gy
    D. 112 Gy
    E. 126 Gy

88. Which protein is most critical for the repair of radiation-induced double-strand breaks in G2 phase?
    A. Ku70/80
    B. RAD51
    C. DNA-PK
    D. PARP1
    E. XRCC1

89. What is the primary advantage of proton therapy over carbon ion therapy?
    A. Higher RBE
    B. Lower cost and wider availability
    C. Increased oxygen enhancement ratio
    D. Enhanced fractionation requirement
    E. Reduced normal tissue sparing

90. Which factor most significantly influences the normal tissue tolerance dose?
    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 60 Gy in 10 fractions with an α/β ratio of 3 Gy?
    A. 72 Gy
    B. 84 Gy
    C. 96 Gy
    D. 108 Gy
    E. 120 Gy

92. Which repair pathway is most critical for repairing radiation-induced crosslinks?
    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 gastrointestinal toxicity?
    A. Acute apoptosis of crypt cells
    B. Chronic inflammation and fibrosis
    C. Direct DNA damage in endothelial cells
    D. Inhibition of mitochondrial function
    E. Suppression of glycolysis

94. Which factor most significantly influences the oxygen effect in radiotherapy?
    A. Dose rate
    B. Tumour hypoxia
    C. Fraction size
    D. Cell cycle phase
    E. Total dose

95. What is the primary consequence of a mutation in the TP53 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-LET radiation?
    A. Acute mucositis
    B. Late fibrosis
    C. Erythema
    D. Desquamation
    E. Leukopenia

97. What is the primary mechanism of action of hypoxia-activated prodrugs in radiotherapy?
    A. Enhancement of DNA repair
    B. Selective cytotoxicity in hypoxic cells
    C. Inhibition of apoptosis
    D. Suppression of glycolysis
    E. Reduction of normal tissue toxicity

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

99. What is the surviving fraction after 6 Gy of radiation if the D0 is 2 Gy?
    A. 0.05
    B. 0.09
    C. 0.14
    D. 0.25
    E. 0.37

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

Cancer Biology (50 Answers)

1. B. PARP inhibitors exploit defective homologous recombination in BRCA1-mutated cells, leading to synthetic lethality.

2. C. NOTCH signalling enhances stemness and survival in cancer stem cells.

3. A. Hypermethylation of MLH1 leads to mismatch repair deficiency in colorectal cancer.

4. B. CAFs secrete matrix metalloproteinases to promote tumour invasion.

5. A. T790M mutation in EGFR is the most common mechanism of resistance to EGFR TKIs.

6. B. MYC amplification drives global transcriptional amplification in cancer cells.

7. C. The angiogenic switch involves a shift towards pro-angiogenic factors like VEGF.

8. B. IDH1 mutation produces 2-hydroxyglutarate, altering epigenetic regulation in gliomas.

9. B. Telomerase activation enables replicative immortality, a hallmark of cancer.

10. B. PTEN loss hyperactivates the PI3K/AKT pathway, promoting tumorigenesis.

11. B. TGF-β promotes an immunosuppressive tumour microenvironment.

12. B. KRAS G12D constitutively activates RAS signalling in pancreatic cancer.

13. B. Snail is a key mediator of EMT, promoting invasion and metastasis.

14. B. Hedgehog signalling promotes uncontrolled growth in basal cell carcinoma.

15. B. HIF-1α-driven glycolysis allows cancer cells to survive hypoxia.

16. B. APC inhibits β-catenin accumulation, suppressing Wnt signalling.

17. A. CD133 is a common marker for glioblastoma cancer stem cells.

18. B. Immune checkpoint inhibitors block PD-1/PD-L1 interaction to enhance T-cell activity.

19. B. BRCA1/2 mutations are associated with hereditary breast and ovarian cancer syndrome.

20. B. NF-κB promotes cell survival and proliferation in cancer.

21. B. Integrin signalling enables anoikis resistance in metastatic cells.

22. B. VHL mutation leads to constitutive HIF-1α activation, promoting angiogenesis.

23. A. Glutaminase is critical for glutamine metabolism in cancer cells.

24. B. JAK/STAT promotes proliferation and immune evasion in cancer.

25. B. Histone deacetylase inhibitors target histone acetylation to alter gene expression.

26. B. Cancer cells evade immune surveillance by expressing immune checkpoint ligands like PD-L1.

27. A. BCR-ABL fusion is the hallmark of chronic myelogenous leukemia.

28. B. The pentose phosphate pathway produces NADPH and ribose-5-phosphate for biosynthesis.

29. B. Exosomes are critical for establishing pre-metastatic niches.

30. B. SMAD4 mutation inhibits TGF-β signalling in pancreatic cancer.

31. B. Chk1 regulates the G2/M checkpoint in response to DNA damage.

32. B. NF1 inhibits RAS signalling in neurofibromatosis.

33. A. 2-deoxyglucose targets hexokinase to inhibit glycolysis.

34. A. BRAF inhibitors block MAPK signalling in melanoma.

35. B. Upregulation of HIF-1α and GLUT1 drives the Warburg effect.

36. B. LKB1 inhibits mTOR signalling in lung cancer.

37. A. Cyclin D1 overexpression is associated with mantle cell lymphoma.

38. B. CTNNB1 mutation leads to constitutive β-catenin activation in colorectal cancer.

39. A. ATM is a key mediator of the DNA damage response.

40. B. The tumour microenvironment secretes survival signals to promote chemotherapy resistance.

41. A. MYC translocation is the hallmark of Burkitt lymphoma.

42. B. Activation of telomerase enables replicative immortality.

43. B. Actin cytoskeleton remodelling is critical for invadopodia formation.

44. B. RB1 inhibits E2F transcription, preventing cell cycle progression in retinoblastoma.

45. E. CTNNB1 mutation is commonly associated with hepatocellular carcinoma.

46. B. PIK3CA mutation hyperactivates PI3K/AKT signalling in breast cancer.

47. B. RAD51 is critical for homologous recombination in DNA damage response.

48. B. PTEN inhibits PI3K/AKT signalling in glioblastoma.

49. A. PML-RARA fusion is the hallmark of acute promyelocytic leukemia.

50. A. Upregulation of BCL2 inhibits apoptosis in cancer cells.

Radiobiology (50 Answers)

51. B. Mitotic catastrophe results from aberrant mitosis due to unrepaired DNA damage.

52. C. The extrapolation number (n) represents the shoulder width of the cell survival curve.

53. B. LET significantly influences OER, with lower OER for high-LET radiation.

54. B. Carbon ions have higher RBE, improving tumour control.

55. B. Non-homologous end joining is the most error-prone DSB repair pathway.

56. C. The bystander effect involves intercellular signalling via gap junctions.

57. B. The β component represents double-hit cell killing in the Linear-Quadratic model.

58. C. The spinal cord is most susceptible to late effects due to low α/β ratio.

59. B. Radiation-induced pneumonitis results from chronic inflammation and cytokine release.

60. C. Normal tissue repair capacity significantly influences the therapeutic ratio.

61. E. BED = 50 × (1 + 2/3) = 83.3 Gy.

62. B. S phase is the least radiosensitive due to active DNA repair.

63. B. SBRT enhances tumour control probability with high doses per fraction.

64. B. ATM is critical for sensing double-strand breaks.

65. A. Cisplatin inhibits DNA repair, enhancing radiation effects.

66. B. LET significantly influences RBE, with higher LET increasing RBE.

67. B. ATR mutation increases radiosensitivity due to impaired DNA damage response.

68. B. Late fibrosis is associated with high-dose per fraction radiotherapy.

69. B. Genomic instability from unrepaired DNA damage causes second malignancies.

70. C. Volume of tissue irradiated significantly influences NTCP.

71. B. EQD2 = 40 × (8 + 10)/(2 + 10) = 56 Gy.

72. B. Homologous recombination is most active in S phase.

73. B. IMRT improves dose conformity to the tumour.

74. B. Fractionation interval allows reoxygenation of hypoxic tumour cells.

75. B. Chronic inflammation and fibrosis cause radiation-induced cardiac toxicity.

76. C. PARP1 is critical for repairing single-strand breaks.

77. B. FANCA mutation increases radiosensitivity due to impaired DNA repair.

78. B. Fractionation interval allows repair of sublethal damage in normal tissues.

79. B. SF = e^(-4/1.5) ≈ 0.07.

80. B. Bone marrow is most susceptible to acute effects due to high cell turnover.

81. B. Amifostine scavenges reactive oxygen species to protect normal tissues.

82. B. Cell cycle progression influences redistribution in fractionated radiotherapy.

83. B. BRCA2 mutation increases radiosensitivity due to defective homologous recombination.

84. B. Acute mucositis is associated with low-dose per fraction radiotherapy.

85. B. Chronic inflammation and vascular damage cause radiation-induced neurotoxicity.

86. B. Treatment duration influences tumour cell repopulation.

87. D. BED = 70 × (1 + 2/2) = 112 Gy.

88. B. RAD51 is critical for DSB repair in G2 phase via homologous recombination.

89. B. Proton therapy is less costly and more widely available than carbon ion therapy.

90. C. Volume of tissue irradiated significantly influences tolerance dose.

91. D. EQD2 = 60 × (6 + 3)/(2 + 3) = 108 Gy.

92. D. Nucleotide excision repair is critical for repairing radiation-induced crosslinks.

93. A. Acute apoptosis of crypt cells causes radiation-induced gastrointestinal toxicity.

94. B. Tumour hypoxia significantly influences the oxygen effect.

95. C. TP53 mutation reduces apoptosis, decreasing radiation response.

96. B. Late fibrosis is associated with high-LET radiation due to dense damage.

97. B. Hypoxia-activated prodrugs are selectively cytotoxic in hypoxic cells.

98. B. Post-irradiation conditions influence repair of potentially lethal damage.

99. B. SF = e^(-6/2) ≈ 0.09.

100. B. ATM is critical for activating the DNA damage response to radiation.