FRCR Oncology Part 1: CANCER BIOLOGY, RADIOBIOLOGY - 14 (100 QUESTIONS, ANSWERS BELOW)

 

Questions

Cancer Biology (50 Questions)

1. Which mechanism best explains the therapeutic efficacy of ATR inhibitors in cancers with ARID1A mutations?
   A. Exploitation of synthetic lethality via defective homologous recombination
   B. Inhibition of non-homologous end joining
   C. Suppression of base excision repair
   D. Enhancement of replication stress
   E. Activation of mismatch repair

2. What is the primary role of the YAP/TAZ-Hippo pathway interaction in mediating resistance to anti-EGFR therapy in colorectal cancer?
   A. Suppression of cell proliferation
   B. Upregulation of compensatory survival pathways
   C. Inhibition of angiogenesis
   D. Enhancement of DNA repair
   E. Promotion of apoptosis

3. Which epigenetic regulator is most critical for the silencing of the MGMT gene in temozolomide-resistant glioblastoma?
   A. DNMT1-mediated promoter methylation
   B. HDAC2-driven histone deacetylation
   C. EZH2-mediated histone methylation
   D. KDM5A-driven histone demethylation
   E. BRD4-mediated chromatin remodeling

4. In the tumour microenvironment, what is the primary function of tumour-derived extracellular vesicles in modulating anti-tumour immunity?
   A. Enhancement of cytotoxic T-cell activity
   B. Transfer of immunosuppressive miRNAs to immune cells
   C. Promotion of antigen presentation
   D. Inhibition of cytokine production
   E. Activation of NK cell responses

5. Which molecular alteration is most associated with acquired resistance to osimertinib in EGFR-mutated non-small cell lung cancer?
   A. C797S mutation in EGFR
   B. Loss of PTEN expression
   C. Amplification of MET
   D. Upregulation of p53
   E. Deletion of RB1

6. What is the primary consequence of ASXL1 mutations in acute myeloid leukemia?
   A. Inhibition of histone methylation
   B. Disruption of chromatin remodeling
   C. Enhancement of apoptosis
   D. Suppression of glycolysis
   E. Promotion of DNA repair

7. Which process is most critical for the establishment of brain metastases in triple-negative breast cancer?
   A. Inhibition of VEGF
   B. Astrocyte-mediated blood-brain barrier disruption
   C. Suppression of MMPs
   D. Upregulation of E-cadherin
   E. Reduction of HIF-1α activity

8. In cancer cells, what is the role of the SLC7A11 transporter under oxidative stress conditions?
   A. Suppression of cystine uptake
   B. Promotion of glutathione synthesis
   C. Inhibition of glycolysis
   D. Enhancement of DNA damage
   E. Promotion of apoptosis

9. Which hallmark of cancer is most directly associated with the activation of immune evasion via MHC class I downregulation?
   A. Evasion of apoptosis
   B. Avoiding immune destruction
   C. Sustained angiogenesis
   D. Genomic instability
   E. Invasion and metastasis

10. What is the primary mechanism by which loss of the tumour suppressor gene SETD2 contributes to renal cell carcinoma?
    A. Inhibition of histone methylation
    B. Disruption of DNA damage repair
    C. Enhancement of cell adhesion
    D. Suppression of p53 transcription
    E. Activation of MAPK signalling

11. Which cytokine is most critical for promoting the differentiation of Th17 cells in the tumour microenvironment?
    A. IL-2
    B. IL-6
    C. IFN-γ
    D. IL-12
    E. TNF-α

12. What is the significance of the FGFR3-TACC3 fusion in bladder cancer?
    A. Inhibits FGFR signalling
    B. Constitutively activates FGFR signalling
    C. Enhances apoptosis
    D. Suppresses angiogenesis
    E. Reduces metastatic potential

13. Which transcription factor is most critical for driving the expression of stemness genes in pancreatic cancer stem cells?
    A. SOX2
    B. E2F
    C. p53
    D. Myc
    E. Rb

14. What is the primary role of the PTEN-induced kinase 1 (PINK1) in cancer cell mitochondrial dynamics?
    A. Promotion of mitochondrial fission
    B. Regulation of mitophagy
    C. Inhibition of oxidative phosphorylation
    D. Enhancement of DNA repair
    E. Suppression of apoptosis

15. Which metabolic adaptation is most critical for cancer cell survival during matrix detachment in metastasis?
    A. Increased oxidative phosphorylation
    B. Reductive carboxylation of glutamine
    C. Suppression of lactate production
    D. Inhibition of the pentose phosphate pathway
    E. Upregulation of fatty acid oxidation

16. What is the primary function of the tumour suppressor gene KMT2D in follicular lymphoma?
    A. Promotes histone methylation
    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 hepatocellular carcinoma?
    A. EpCAM
    B. CD20
    C. CD56
    D. CD3
    E. CD19

18. What is the primary mechanism of action of bispecific T-cell engagers (BiTEs) in cancer therapy?
    A. Direct induction of apoptosis
    B. Bridging T-cells to tumour cells
    C. Inhibition of VEGF signalling
    D. Suppression of DNA repair
    E. Enhancement of glycolysis

19. Which genetic alteration is most associated with Li-Fraumeni syndrome?
    A. TP53 mutation
    B. BRCA1/2 mutation
    C. MLH1/MSH2 mutation
    D. MYC amplification
    E. PTEN deletion

20. What is the role of the SMARCA4 gene in small cell lung cancer?
    A. Inhibits chromatin remodeling
    B. Promotes transcriptional activation
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Reduces apoptosis

21. Which process is most critical for cancer cell extravasation during metastasis?
    A. Upregulation of E-cadherin
    B. Selectin-mediated endothelial adhesion
    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 IDH2 gene in acute myeloid leukemia?
    A. Inhibition of 2-hydroxyglutarate production
    B. Epigenetic dysregulation via 2-hydroxyglutarate
    C. Suppression of angiogenesis
    D. Enhanced DNA repair
    E. Reduced cell proliferation

23. Which enzyme is critical for one-carbon metabolism in cancer cells?
    A. Serine hydroxymethyltransferase
    B. Hexokinase
    C. Lactate dehydrogenase
    D. Glutaminase
    E. Pyruvate kinase

24. What is the role of the RUNX1 gene in acute myeloid leukemia?
    A. Inhibits hematopoietic differentiation
    B. Promotes uncontrolled proliferation
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Activates apoptosis

25. Which epigenetic modification is targeted by BET inhibitors in cancer therapy?
    A. Histone acetylation
    B. Bromodomain-mediated chromatin binding
    C. Histone phosphorylation
    D. DNA methylation
    E. Histone ubiquitination

26. What is the primary mechanism by which cancer cells induce regulatory T-cell expansion?
    A. Upregulation of MHC class I
    B. Secretion of TGF-β and IL-10
    C. Enhancement of NK cell activity
    D. Increased antigen presentation
    E. Suppression of T-cell activation

27. Which molecular alteration is most associated with Philadelphia chromosome-positive acute lymphoblastic leukemia?
    A. BCR-ABL1 fusion
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

28. What is the primary role of the serine/threonine kinase Aurora A in cancer cells?
    A. Inhibition of mitotic progression
    B. Promotion of centrosome amplification
    C. Suppression of glycolysis
    D. Enhancement of DNA repair
    E. Reduction of angiogenesis

29. Which process is most critical for the survival of circulating tumour cells in the bloodstream?
    A. Suppression of MMPs
    B. Resistance to shear stress
    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 TET2 gene in myelodysplastic syndromes?
    A. Inhibition of DNA demethylation
    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 spindle assembly checkpoint in cancer cells?
    A. Mad2
    B. Chk1
    C. Cyclin D
    D. E2F
    E. Rb

32. What is the primary role of the tumour suppressor gene FANCD2 in Fanconi anaemia-associated cancers?
    A. Promotes DNA crosslink repair
    B. Inhibits cell proliferation
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

33. Which metabolic enzyme is targeted by CB-839 in cancer therapy?
    A. Glutaminase
    B. Hexokinase
    C. Lactate dehydrogenase
    D. Pyruvate kinase
    E. Fatty acid synthase

34. What is the primary mechanism of action of CDK4/6 inhibitors in breast cancer?
    A. Inhibition of G1/S transition
    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 serine synthesis pathway in cancer cells?
    A. Suppression of glycolysis
    B. Upregulation of phosphoglycerate dehydrogenase
    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 STK11 in pancreatic cancer?
    A. Promotes mTOR signalling
    B. Inhibits AMPK signalling
    C. Enhances angiogenesis
    D. Regulates cellular energy homeostasis
    E. Activates Wnt signalling

37. Which molecular alteration is most associated with anaplastic large cell lymphoma?
    A. NPM-ALK fusion
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

38. What is the primary consequence of a mutation in the PTPN11 gene in juvenile myelomonocytic leukemia?
    A. Inhibition of RAS signalling
    B. Constitutive activation of RAS 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 nucleotide excision repair?
    A. XPC
    B. RAD51
    C. DNA-PK
    D. PARP1
    E. BRCA2

40. What is the primary role of the tumour microenvironment in resistance to immunotherapy?
    A. Inhibition of drug efflux
    B. Secretion of immunosuppressive metabolites
    C. Enhancement of DNA repair
    D. Suppression of hypoxia
    E. Promotion of T-cell infiltration

41. Which molecular alteration is most associated with Waldenström macroglobulinemia?
    A. MYD88 L265P mutation
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

42. What is the primary mechanism by which cancer cells achieve metabolic symbiosis in the tumour microenvironment?
    A. Upregulation of E-cadherin
    B. Differential expression of lactate transporters
    C. Inhibition of VEGF
    D. Suppression of MMPs
    E. Enhancement of p53 activity

43. Which process is most critical for the formation of tumour microtubes in glioblastoma?
    A. Upregulation of E-cadherin
    B. GAP43-mediated intercellular connectivity
    C. Inhibition of MMPs
    D. Suppression of VEGF
    E. Enhancement of p53 activity

44. What is the primary role of the tumour suppressor gene TSC1 in tuberous sclerosis-associated cancers?
    A. Promotes mTOR signalling
    B. Inhibits mTOR signalling
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

45. Which molecular alteration is most associated with intrahepatic cholangiocarcinoma?
    A. FGFR2 fusion
    B. KRAS mutation
    C. MYC amplification
    D. PTEN loss
    E. CTNNB1 mutation

46. What is the primary consequence of a mutation in the NOTCH1 gene in chronic lymphocytic leukemia?
    A. Inhibition of NOTCH signalling
    B. Constitutive activation of NOTCH 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 mismatch repair?
    A. MSH2
    B. RAD51
    C. DNA-PK
    D. PARP1
    E. BRCA2

48. What is the primary role of the tumour suppressor gene PBRM1 in renal cell carcinoma?
    A. Promotes chromatin remodeling
    B. Inhibits chromatin remodeling
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

49. Which molecular alteration is most associated with hairy cell leukemia?
    A. BRAF V600E mutation
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

50. What is the primary mechanism by which cancer cells resist ferroptosis?
    A. Upregulation of GPX4
    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 immunogenic cell death in cancer cells?
    A. Direct induction of apoptosis
    B. Release of damage-associated molecular patterns
    C. Inhibition of protein synthesis
    D. Disruption of mitochondrial function
    E. Suppression of glycolysis

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

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

54. What is the primary advantage of alpha particle therapy over beta particle therapy in targeted radionuclide therapy?
    A. Lower cost
    B. Higher linear energy transfer (LET)
    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 clustered DNA damage?
    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 adaptive immunity in combination with immunotherapy?
    A. Direct DNA damage in irradiated cells
    B. Upregulation of tumour neoantigens
    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 a low α/β ratio indicate about a tissue’s response to fractionation?
    A. High sensitivity to fraction size
    B. Low sensitivity to fraction size
    C. Oxygen-dependent damage
    D. Rapid repair of sublethal damage
    E. Cell cycle redistribution

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

59. What is the primary mechanism of radiation-induced salivary gland dysfunction?
    A. Acute apoptosis of acinar 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 FLASH radiotherapy?
    A. Total dose
    B. Ultra-high dose rate
    C. Normal tissue repair capacity
    D. Tumour oxygenation
    E. Radiation type

61. What is the biologically effective dose (BED) for a regimen of 36 Gy in 3 fractions with an α/β ratio of 4 Gy, assuming a time factor correction (Tpot = 5 days, treatment over 7 days)?
    A. 54 Gy
    B. 67.5 Gy
    C. 78 Gy
    D. 90 Gy
    E. 108 Gy

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

63. What is the primary advantage of lattice radiotherapy over conventional stereotactic radiotherapy?
    A. Reduced treatment time
    B. Spatially fractionated dose delivery
    C. Lower cost
    D. Increased oxygen enhancement ratio
    E. Enhanced normal tissue toxicity

64. Which protein is most critical for the activation of the intra-S phase checkpoint in response to radiation?
    A. p53
    B. ATR
    C. RAD51
    D. DNA-PK
    E. PARP1

65. What is the primary mechanism of action of PARP inhibitors as radiosensitisers in BRCA-deficient cancers?
    A. Inhibition of homologous recombination
    B. Trapping of PARP at DNA damage sites
    C. Enhancement of apoptosis
    D. Suppression of glycolysis
    E. Inhibition of angiogenesis

66. Which factor most significantly influences the relative biological effectiveness (RBE) in alpha particle therapy?
    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 PALB2 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 spatially fractionated radiotherapy?
    A. Acute mucositis
    B. Late vascular sparing
    C. Erythema
    D. Desquamation
    E. Leukopenia

69. What is the primary mechanism of radiation-induced ovarian toxicity?
    A. Acute apoptosis of oocytes
    B. Chronic inflammation and fibrosis
    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) in hypofractionated radiotherapy?
    A. Total dose
    B. Tumour α/β ratio
    C. Clonogenic cell density
    D. Radiation type
    E. Dose rate

71. What is the equivalent dose in 2 Gy fractions (EQD2) for a regimen of 50 Gy in 5 fractions with an α/β ratio of 2 Gy?
    A. 75 Gy
    B. 90 Gy
    C. 100 Gy
    D. 125 Gy
    E. 150 Gy

72. Which repair pathway is most critical for repairing radiation-induced DNA-histone crosslinks?
    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 MR-guided radiotherapy over CT-guided radiotherapy?
    A. Reduced treatment time
    B. Superior soft tissue contrast
    C. Lower cost
    D. Increased oxygen enhancement ratio
    E. Enhanced normal tissue toxicity

74. Which factor most significantly influences the reassortment of cells in hypofractionated 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 pituitary dysfunction?
    A. Acute apoptosis of endocrine cells
    B. Chronic inflammation and vascular damage
    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 complex DNA damage?
    A. RAD51
    B. DNA-PK
    C. PARP1
    D. ATM
    E. BRCA2

77. What is the primary consequence of a mutation in the NBS1 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 during FLASH radiotherapy?
    A. Total dose
    B. Ultra-high dose rate
    C. Radiation type
    D. Cell cycle phase
    E. Fractionation interval

79. What is the surviving fraction after 12 Gy of radiation if the D0 is 1.8 Gy and the extrapolation number (n) is 2?
    A. 0.01
    B. 0.03
    C. 0.06
    D. 0.12
    E. 0.25

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

81. What is the primary mechanism of action of gold nanoparticle radiosensitisers in radiotherapy?
    A. Enhancement of DNA repair
    B. Increased photoelectric effect
    C. Inhibition of apoptosis
    D. Suppression of glycolysis
    E. Reduction of hypoxia

82. Which factor most significantly influences the repopulation of tumour cells in accelerated 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 BLM 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 rate brachytherapy?
    A. Acute mucositis
    B. Late fibrosis
    C. Erythema
    D. Desquamation
    E. Leukopenia

85. What is the primary mechanism of radiation-induced thyroid dysfunction?
    A. Acute apoptosis of follicular cells
    B. Chronic inflammation and vascular damage
    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 carbon ion radiotherapy?
    A. Dose rate
    B. Minimal oxygen dependence
    C. Fraction size
    D. Cell cycle phase
    E. Total dose

87. What is the biologically effective dose (BED) for a regimen of 42 Gy in 7 fractions with an α/β ratio of 3 Gy, assuming a time factor correction (Tpot = 4 days, treatment over 9 days)?
    A. 54 Gy
    B. 66 Gy
    C. 78 Gy
    D. 90 Gy
    E. 108 Gy

88. Which protein is most critical for the repair of radiation-induced double-strand breaks in G0 phase?
    A. RAD51
    B. DNA-PK
    C. PARP1
    D. ATM
    E. BRCA2

89. What is the primary advantage of boron neutron capture therapy over conventional photon therapy?
    A. Lower cost
    B. Selective high-LET damage to tumour cells
    C. Increased oxygen enhancement ratio
    D. Reduced fractionation requirement
    E. Enhanced normal tissue toxicity

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

91. What is the equivalent dose in 2 Gy fractions (EQD2) for a regimen of 48 Gy in 4 fractions with an α/β ratio of 4 Gy?
    A. 64 Gy
    B. 80 Gy
    C. 96 Gy
    D. 112 Gy
    E. 128 Gy

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

94. Which factor most significantly influences the reoxygenation of tumour cells in FLASH radiotherapy?
    A. Dose rate
    B. Transient oxygen sparing
    C. Total dose
    D. Radiation type
    E. Cell cycle phase

95. What is the primary consequence of a mutation in the CHEK2 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 alpha particle therapy?
    A. Acute mucositis
    B. Late normal tissue sparing
    C. Erythema
    D. Desquamation
    E. Leukopenia

97. What is the primary mechanism of action of hafnium oxide nanoparticle radiosensitisers in radiotherapy?
    A. Enhancement of DNA repair
    B. Increased high-energy electron emission
    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 normal tissues?
    A. Dose rate
    B. Post-irradiation microenvironment
    C. Fraction size
    D. Radiation type
    E. Cell cycle phase

99. What is the surviving fraction after 15 Gy of radiation if the D0 is 1.5 Gy and the extrapolation number (n) is 1.5?
    A. 0.0001
    B. 0.001
    C. 0.01
    D. 0.05
    E. 0.10

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

Answers

Cancer Biology (50 Answers)

1. D. ATR inhibitors enhance replication stress in ARID1A-mutated cancers, leading to cell death.

2. B. YAP/TAZ upregulates compensatory survival pathways, mediating anti-EGFR resistance.

3. A. DNMT1-mediated MGMT promoter methylation confers temozolomide resistance.

4. B. Tumour-derived EVs transfer immunosuppressive miRNAs to immune cells.

5. A. C797S mutation in EGFR drives osimertinib resistance.

6. B. ASXL1 mutations disrupt chromatin remodeling, promoting leukemogenesis.

7. B. Astrocyte-mediated blood-brain barrier disruption enables brain metastases.

8. B. SLC7A11 promotes glutathione synthesis, protecting against oxidative stress.

9. B. MHC class I downregulation enables immune destruction avoidance.

10. B. SETD2 loss disrupts DNA damage repair, driving renal cell carcinoma.

11. B. IL-6 promotes Th17 cell differentiation in the tumour microenvironment.

12. B. FGFR3-TACC3 fusion constitutively activates FGFR signalling.

13. A. SOX2 drives stemness gene expression in pancreatic cancer stem cells.

14. B. PINK1 regulates mitophagy, maintaining mitochondrial homeostasis.

15. B. Reductive carboxylation of glutamine supports survival during matrix detachment.

16. A. KMT2D promotes histone methylation, suppressing tumour growth.

17. A. EpCAM is a marker for hepatocellular carcinoma cancer stem cells.

18. B. BiTEs bridge T-cells to tumour cells, enhancing cytotoxicity.

19. A. TP53 mutations cause Li-Fraumeni syndrome.

20. B. SMARCA4 promotes transcriptional activation in small cell lung cancer.

21. B. Selectin-mediated endothelial adhesion enables extravasation.

22. B. IDH2 mutation produces 2-hydroxyglutarate, causing epigenetic dysregulation.

23. A. Serine hydroxymethyltransferase drives one-carbon metabolism.

24. A. RUNX1 mutations inhibit hematopoietic differentiation in AML.

25. B. BET inhibitors target bromodomain-mediated chromatin binding.

26. B. TGF-β and IL-10 secretion induces regulatory T-cell expansion.

27. A. BCR-ABL1 fusion drives Philadelphia chromosome-positive ALL.

28. B. Aurora A promotes centrosome amplification, driving mitotic errors.

29. B. Resistance to shear stress enables circulating tumour cell survival.

30. A. TET2 mutation inhibits DNA demethylation, promoting myelodysplastic syndromes.

31. A. Mad2 regulates the spindle assembly checkpoint.

32. A. FANCD2 promotes DNA crosslink repair in Fanconi anaemia.

33. A. CB-839 targets glutaminase to inhibit glutamine metabolism.

34. A. CDK4/6 inhibitors block G1/S transition in breast cancer.

35. B. Upregulation of phosphoglycerate dehydrogenase drives serine synthesis.

36. D. STK11 regulates energy homeostasis via AMPK in pancreatic cancer.

37. A. NPM-ALK fusion drives anaplastic large cell lymphoma.

38. B. PTPN11 mutation activates RAS signalling in JMML.

39. A. XPC mediates nucleotide excision repair in DNA damage response.

40. B. Immunosuppressive metabolites from the microenvironment resist immunotherapy.

41. A. MYD88 L265P mutation drives Waldenström macroglobulinemia.

42. B. Differential lactate transporter expression enables metabolic symbiosis.

43. B. GAP43-mediated connectivity forms tumour microtubes in glioblastoma.

44. B. TSC1 inhibits mTOR signalling in tuberous sclerosis.

45. A. FGFR2 fusion is associated with intrahepatic cholangiocarcinoma.

46. B. NOTCH1 mutation activates NOTCH signalling in CLL.

47. A. MSH2 mediates mismatch repair in DNA damage response.

48. B. PBRM1 inhibits chromatin remodeling in renal cell carcinoma.

49. A. BRAF V600E mutation drives hairy cell leukemia.

50. A. GPX4 upregulation inhibits ferroptosis in cancer cells.

Radiobiology (50 Answers)

51. B. Immunogenic cell death releases DAMPs, triggering immune responses.

52. B. The α component represents single-hit cell killing.

53. B. Transient oxygen depletion reduces OER in FLASH radiotherapy.

54. B. Alpha particles have higher LET, causing dense DNA damage.

55. A. Homologous recombination repairs clustered DNA damage.

56. B. Radiation upregulates neoantigens, enhancing adaptive immunity.

57. A. Low α/β ratio indicates high sensitivity to fraction size.

58. C. The spinal cord is susceptible to radiation-induced demyelination.

59. A. Acute apoptosis of acinar cells causes salivary gland dysfunction.

60. B. Ultra-high dose rate enhances the therapeutic index in FLASH radiotherapy.

61. C. BED = 36 × (1 + 12/4) = 108 Gy, corrected for repopulation (~30 Gy loss) = 78 Gy.

62. B. S phase is resistant to mitotic catastrophe due to active repair.

63. B. Lattice radiotherapy delivers spatially fractionated doses.

64. B. ATR activates the intra-S phase checkpoint.

65. B. PARP inhibitors trap PARP at DNA damage sites, enhancing radiosensitivity.

66. B. High LET increases RBE in alpha particle therapy.

67. B. PALB2 mutation increases radiosensitivity due to defective HR.

68. B. Spatially fractionated radiotherapy spares vascular damage.

69. A. Acute oocyte apoptosis causes ovarian toxicity.

70. C. Clonogenic cell density influences TCP in hypofractionation.

71. D. EQD2 = 50 × (10 + 2)/(2 + 2) = 125 Gy.

72. D. Nucleotide excision repair repairs DNA-histone crosslinks.

73. B. MR-guided radiotherapy offers superior soft tissue contrast.

74. B. Cell cycle kinetics influence reassortment in hypofractionation.

75. B. Chronic inflammation and vascular damage cause pituitary dysfunction.

76. B. DNA-PK repairs complex DNA damage.

77. B. NBS1 mutation increases radiosensitivity due to impaired DSB sensing.

78. B. Ultra-high dose rate alters sublethal damage repair in FLASH radiotherapy.

79. B. SF = n × e^(-12/1.8) = 2 × 0.0013 ≈ 0.03.

80. C. The mandible is susceptible to osteoradionecrosis.

81. B. Gold nanoparticles enhance the photoelectric effect, increasing DNA damage.

82. B. Treatment duration influences tumour cell repopulation.

83. B. BLM mutation increases radiosensitivity due to defective HR.

84. B. Late fibrosis is associated with low-dose rate brachytherapy.

85. B. Chronic inflammation and vascular damage cause thyroid dysfunction.

86. B. Minimal oxygen dependence reduces the oxygen effect in carbon ion therapy.

87. C. BED = 42 × (1 + 6/3) = 126 Gy, corrected for repopulation (~48 Gy loss) = 78 Gy.

88. B. DNA-PK repairs DSBs in G0 phase via NHEJ.

89. B. Boron neutron capture therapy delivers selective high-LET damage.

90. B. Dose rate influences NTCP in FLASH radiotherapy.

91. C. EQD2 = 48 × (12 + 4)/(2 + 4) = 96 Gy.

92. D. Nucleotide excision repair repairs pyrimidine dimers.

93. B. Chronic inflammation and vascular damage cause auditory toxicity.

94. B. Transient oxygen sparing influences reoxygenation in FLASH radiotherapy.

95. B. CHEK2 mutation increases radiosensitivity due to impaired checkpoint activation.

96. B. Alpha particle therapy spares late normal tissue damage.

97. B. Hafnium oxide nanoparticles emit high-energy electrons.

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

99. B. SF = 1.5 × e^(-15/1.5) ≈ 0.001.

100. B. ATM coordinates the DNA damage response to high-LET radiation.