FRCR Oncology Part 1: CANCER BIOLOGY, RADIOBIOLOGY - 15 (100 QUESTIONS, ANSWERS BELOW)

 

Questions

Cancer Biology (50 Questions)

1. Which mechanism best explains the efficacy of WEE1 inhibitors in cancers with MYC amplification?
   A. Inhibition of non-homologous end joining
   B. Exploitation of replication stress overload
   C. Suppression of base excision repair
   D. Enhancement of mismatch repair
   E. Activation of homologous recombination

2. What is the primary role of the LKB1-AMPK axis in suppressing tumourigenesis in Peutz-Jeghers syndrome?
   A. Promotion of mTOR-driven proliferation
   B. Inhibition of metabolic reprogramming
   C. Enhancement of angiogenesis
   D. Suppression of DNA repair
   E. Activation of Wnt signalling

3. Which epigenetic alteration is most critical for the silencing of the RB1 gene in retinoblastoma?
   A. Promoter hypermethylation
   B. Histone acetylation
   C. EZH2-mediated histone methylation
   D. KDM6A-driven histone demethylation
   E. BRD2-mediated chromatin remodeling

4. In the tumour microenvironment, what is the primary function of tumour-associated neutrophils in promoting metastasis?
   A. Direct cytotoxicity against tumour cells
   B. Secretion of neutrophil extracellular traps (NETs)
   C. Enhancement of T-cell activity
   D. Inhibition of cytokine production
   E. Suppression of angiogenesis

5. Which molecular alteration is most associated with resistance to venetoclax in chronic lymphocytic leukemia?
   A. BCL2 G101V 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 KDM6A mutations in bladder cancer?
   A. Inhibition of histone demethylation
   B. Disruption of chromatin accessibility
   C. Enhancement of apoptosis
   D. Suppression of glycolysis
   E. Promotion of DNA repair

7. Which process is most critical for the establishment of bone metastases in prostate cancer?
   A. Inhibition of RANKL signalling
   B. Osteoblast-mediated bone remodeling
   C. Suppression of MMPs
   D. Upregulation of E-cadherin
   E. Reduction of TGF-β activity

8. In cancer cells, what is the role of the xCT transporter under ferroptotic stress?
   A. Suppression of cystine uptake
   B. Promotion of glutathione synthesis
   C. Inhibition of lipid peroxidation
   D. Enhancement of DNA damage
   E. Promotion of apoptosis

9. Which hallmark of cancer is most directly associated with the activation of stromal fibroblasts to support tumour growth?
   A. Evasion of apoptosis
   B. Tumour-promoting inflammation
   C. Sustained angiogenesis
   D. Genomic instability
   E. Invasion and metastasis

10. What is the primary mechanism by which loss of the tumour suppressor gene BARD1 contributes to breast cancer?
    A. Inhibition of BRCA1-mediated DNA repair
    B. Hyperactivation of MDM2
    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 M2 macrophages in the tumour microenvironment?
    A. IL-2
    B. IL-10
    C. IFN-γ
    D. IL-12
    E. TNF-α

12. What is the significance of the ROS1 fusion in non-small cell lung cancer?
    A. Inhibits tyrosine kinase signalling
    B. Constitutively activates tyrosine kinase signalling
    C. Enhances apoptosis
    D. Suppresses angiogenesis
    E. Reduces metastatic potential

13. Which transcription factor is most critical for driving the expression of invadopodia-related genes in melanoma?
    A. TWIST1
    B. E2F
    C. p53
    D. Myc
    E. Rb

14. What is the primary role of the mitochondrial sirtuin SIRT3 in cancer cell metabolism?
    A. Promotion of glycolysis
    B. Regulation of oxidative stress response
    C. Inhibition of mitochondrial biogenesis
    D. Enhancement of DNA repair
    E. Suppression of apoptosis

15. Which metabolic adaptation is most critical for cancer cell survival during glutamine deprivation?
    A. Increased oxidative phosphorylation
    B. Asparagine synthesis upregulation
    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 ZFHX3 in prostate cancer?
    A. Promotes epithelial-to-mesenchymal transition
    B. Inhibits cell migration
    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 ovarian cancer?
    A. ALDH1
    B. CD20
    C. CD56
    D. CD3
    E. CD19

18. What is the primary mechanism of action of oncolytic viral therapy in cancer?
    A. Direct induction of apoptosis
    B. Selective lysis of tumour cells
    C. Inhibition of VEGF signalling
    D. Suppression of DNA repair
    E. Enhancement of glycolysis

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

20. What is the role of the BRD4 gene in NUT midline carcinoma?
    A. Inhibits chromatin remodeling
    B. Promotes oncogenic transcription
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Reduces apoptosis

21. Which process is most critical for cancer cell transendothelial migration during metastasis?
    A. Upregulation of E-cadherin
    B. Integrin-mediated endothelial interactions
    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 FLT3 gene in acute myeloid leukemia?
    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 purine biosynthesis in cancer cells?
    A. IMP dehydrogenase
    B. Hexokinase
    C. Lactate dehydrogenase
    D. Glutaminase
    E. Pyruvate kinase

24. What is the role of the MEF2C gene in B-cell acute lymphoblastic leukemia?
    A. Inhibits lymphoid differentiation
    B. Promotes uncontrolled proliferation
    C. Enhances DNA repair
    D. Suppresses angiogenesis
    E. Activates apoptosis

25. Which epigenetic modification is targeted by EZH2 inhibitors in diffuse large B-cell lymphoma?
    A. Histone acetylation
    B. Histone H3K27 methylation
    C. Histone phosphorylation
    D. DNA methylation
    E. Histone ubiquitination

26. What is the primary mechanism by which cancer cells induce exhaustion of CD8+ T-cells?
    A. Upregulation of MHC class I
    B. Expression of LAG-3 and TIM-3 ligands
    C. Enhancement of NK cell activity
    D. Increased antigen presentation
    E. Suppression of T-cell activation

27. Which molecular alteration is most associated with marginal zone lymphoma?
    A. NOTCH2 mutation
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

28. What is the primary role of the serine/threonine kinase PIM1 in prostate cancer?
    A. Inhibition of cell survival
    B. Promotion of anti-apoptotic signalling
    C. Suppression of glycolysis
    D. Enhancement of DNA repair
    E. Reduction of angiogenesis

29. Which process is most critical for the survival of cancer cells in lymph node metastases?
    A. Suppression of MMPs
    B. Adaptation to lymphoid 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 BCOR gene in medulloblastoma?
    A. Inhibition of transcriptional repression
    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 DNA damage-induced G1 checkpoint in cancer cells?
    A. p16INK4a
    B. Chk1
    C. Cyclin D
    D. E2F
    E. Rb

32. What is the primary role of the tumour suppressor gene ATRX in glioma?
    A. Promotes telomere maintenance
    B. Inhibits alternative lengthening of telomeres
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

33. Which metabolic enzyme is targeted by CPI-613 in cancer therapy?
    A. Pyruvate dehydrogenase
    B. Hexokinase
    C. Lactate dehydrogenase
    D. Glutaminase
    E. Fatty acid synthase

34. What is the primary mechanism of action of FGFR inhibitors in cholangiocarcinoma?
    A. Inhibition of tyrosine kinase signalling
    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 methionine cycle in cancer cells?
    A. Suppression of glycolysis
    B. Upregulation of methionine adenosyltransferase
    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 SMARCB1 in rhabdoid tumours?
    A. Promotes chromatin remodeling
    B. Inhibits SWI/SNF complex activity
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

37. Which molecular alteration is most associated with adult T-cell leukemia/lymphoma?
    A. HTLV-1 Tax protein expression
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

38. What is the primary consequence of a mutation in the SF3B1 gene in myelodysplastic syndromes?
    A. Inhibition of RNA splicing
    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 Fanconi anaemia pathway?
    A. FANCA
    B. RAD51
    C. DNA-PK
    D. PARP1
    E. BRCA2

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

41. Which molecular alteration is most associated with primary mediastinal B-cell lymphoma?
    A. CIITA translocation
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

42. What is the primary mechanism by which cancer cells achieve resistance to immune checkpoint inhibitors?
    A. Upregulation of MHC class I
    B. Loss of interferon-gamma signalling
    C. Enhancement of NK cell activity
    D. Increased antigen presentation
    E. Suppression of T-cell activation

43. Which process is most critical for the formation of vasculogenic mimicry channels in melanoma?
    A. Upregulation of E-cadherin
    B. VE-cadherin-mediated tube formation
    C. Inhibition of MMPs
    D. Suppression of VEGF
    E. Enhancement of p53 activity

44. What is the primary role of the tumour suppressor gene NF2 in schwannoma?
    A. Promotes Hippo pathway signalling
    B. Inhibits YAP/TAZ activity
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

45. Which molecular alteration is most associated with desmoplastic small round cell tumour?
    A. EWS-WT1 fusion
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

46. What is the primary consequence of a mutation in the GNAQ gene in uveal melanoma?
    A. Inhibition of G-protein signalling
    B. Constitutive activation of G-protein 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 repair?
    A. RPA
    B. DNA-PK
    C. PARP1
    D. ATM
    E. XRCC1

48. What is the primary role of the tumour suppressor gene MEN1 in multiple endocrine neoplasia type 1?
    A. Promotes histone methylation
    B. Inhibits transcriptional activation
    C. Enhances angiogenesis
    D. Suppresses p53 transcription
    E. Activates Wnt signalling

49. Which molecular alteration is most associated with blastic plasmacytoid dendritic cell neoplasm?
    A. TET2 mutation
    B. KRAS mutation
    C. MYC amplification
    D. TP53 deletion
    E. PTEN loss

50. What is the primary mechanism by which cancer cells resist pyroptosis?
    A. Upregulation of GSDMD
    B. Inhibition of caspase-1 activation
    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 epigenetic reprogramming in cancer cells?
    A. Direct induction of apoptosis
    B. Alteration of histone modifications
    C. Inhibition of protein synthesis
    D. Disruption of mitochondrial function
    E. Suppression of glycolysis

52. In a cell survival curve, what does the D10 value represent?
    A. The dose required to reduce survival to 37%
    B. The dose required to reduce survival to 10%
    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 microbeam radiotherapy?
    A. Dose rate
    B. Spatial dose heterogeneity
    C. Fraction size
    D. Cell cycle phase
    E. Total dose

54. What is the primary advantage of synchrotron-based microbeam radiotherapy over conventional radiotherapy?
    A. Lower cost
    B. Ultra-high dose gradients sparing normal tissue
    C. Increased oxygen enhancement ratio
    D. Reduced fractionation requirement
    E. Enhanced normal tissue toxicity

55. Which DNA repair pathway is most critical for repairing radiation-induced DNA-RNA hybrids?
    A. Homologous recombination
    B. Non-homologous end joining
    C. Base excision repair
    D. Nucleotide excision repair
    E. RNase H-mediated repair

56. What is the primary mechanism of radiation-induced synthetic lethality in PARP-deficient cancers?
    A. Direct DNA damage in irradiated cells
    B. Accumulation of unrepaired single-strand breaks
    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 high α/β ratio indicate about a tumour’s response to hypofractionation?
    A. Low sensitivity to fraction size
    B. High 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 cataracts?
    A. Skin
    B. Bone marrow
    C. Lens of the eye
    D. Liver
    E. Lung

59. What is the primary mechanism of radiation-induced enteropathy?
    A. Acute apoptosis of crypt stem 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 microbeam radiotherapy?
    A. Total dose
    B. Peak-to-valley dose ratio
    C. Normal tissue repair capacity
    D. Tumour oxygenation
    E. Radiation type

61. What is the biologically effective dose (BED) for a regimen of 40 Gy in 5 fractions with an α/β ratio of 3 Gy, assuming a time factor correction (Tpot = 3 days, treatment over 8 days)?
    A. 56 Gy
    B. 68 Gy
    C. 80 Gy
    D. 92 Gy
    E. 104 Gy

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

63. What is the primary advantage of proton minibeam radiotherapy over conventional proton therapy?
    A. Reduced treatment time
    B. Enhanced normal tissue sparing via spatial fractionation
    C. Lower cost
    D. Increased oxygen enhancement ratio
    E. Enhanced normal tissue toxicity

64. Which protein is most critical for the activation of the DNA damage response in response to radiation-induced replication stress?
    A. p53
    B. ATR
    C. RAD51
    D. DNA-PK
    E. PARP1

65. What is the primary mechanism of action of ATR inhibitors as radiosensitisers in ATM-deficient cancers?
    A. Inhibition of homologous recombination
    B. Enhancement of replication fork collapse
    C. Suppression of glycolysis
    D. Inhibition of angiogenesis
    E. Enhancement of apoptosis

66. Which factor most significantly influences the relative biological effectiveness (RBE) in synchrotron-based microbeam radiotherapy?
    A. Dose rate
    B. Ultra-high peak dose
    C. Fraction size
    D. Cell cycle phase
    E. Total dose

67. What is the primary consequence of a mutation in the ERCC2 gene in response to radiation?
    A. Enhanced nucleotide excision repair
    B. Increased radiosensitivity
    C. Reduced apoptosis
    D. Inhibition of homologous recombination
    E. Upregulation of VEGF

68. Which normal tissue effect is most associated with proton minibeam radiotherapy?
    A. Acute mucositis
    B. Late normal tissue preservation
    C. Erythema
    D. Desquamation
    E. Leukopenia

69. What is the primary mechanism of radiation-induced pancreatic toxicity?
    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

70. Which factor most significantly influences the tumour control probability (TCP) in microbeam radiotherapy?
    A. Total dose
    B. Peak dose intensity
    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 45 Gy in 3 fractions with an α/β ratio of 4 Gy?
    A. 72 Gy
    B. 84 Gy
    C. 96 Gy
    D. 108 Gy
    E. 120 Gy

72. Which repair pathway is most critical for repairing radiation-induced DNA-protein crosslinks in G1 phase?
    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 carbon ion minibeam radiotherapy over carbon ion broad-beam therapy?
    A. Reduced treatment time
    B. Enhanced normal tissue sparing via spatial fractionation
    C. Lower cost
    D. Increased oxygen enhancement ratio
    E. Enhanced normal tissue toxicity

74. Which factor most significantly influences the reoxygenation of tumour cells in microbeam radiotherapy?
    A. Dose rate
    B. Inter-beam spacing
    C. Total dose
    D. Radiation type
    E. Cell cycle phase

75. What is the primary mechanism of radiation-induced adrenal toxicity?
    A. Acute apoptosis of cortical 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 clustered non-DSB oxidative lesions?
    A. RAD51
    B. OGG1
    C. PARP1
    D. ATM
    E. BRCA2

77. What is the primary consequence of a mutation in the MRE11 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 tumour cells during microbeam radiotherapy?
    A. Total dose
    B. Peak-to-valley dose ratio
    C. Radiation type
    D. Cell cycle phase
    E. Dose rate

79. What is the surviving fraction after 10 Gy of radiation if the D0 is 1.2 Gy and the extrapolation number (n) is 3?
    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 xerostomia?
    A. Skin
    B. Bone marrow
    C. Salivary glands
    D. Liver
    E. Lung

81. What is the primary mechanism of action of cerium oxide nanoparticle radiosensitisers in radiotherapy?
    A. Enhancement of DNA repair
    B. Increased reactive oxygen species generation
    C. Inhibition of apoptosis
    D. Suppression of glycolysis
    E. Reduction of hypoxia

82. Which factor most significantly influences the repopulation of normal tissues in accelerated partial breast irradiation?
    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 RAD50 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 high-dose rate microbeam radiotherapy?
    A. Acute mucositis
    B. Late normal tissue sparing
    C. Erythema
    D. Desquamation
    E. Leukopenia

85. What is the primary mechanism of radiation-induced testicular toxicity?
    A. Acute apoptosis of spermatogonia
    B. Chronic inflammation and fibrosis
    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 proton minibeam radiotherapy?
    A. Dose rate
    B. Reduced oxygen dependence in valleys
    C. Fraction size
    D. Cell cycle phase
    E. Total dose

87. What is the biologically effective dose (BED) for a regimen of 50 Gy in 5 fractions with an α/β ratio of 2 Gy, assuming a time factor correction (Tpot = 4 days, treatment over 10 days)?
    A. 75 Gy
    B. 90 Gy
    C. 105 Gy
    D. 120 Gy
    E. 135 Gy

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

89. What is the primary advantage of helium ion therapy over proton therapy?
    A. Lower cost
    B. Sharper Bragg peak and higher LET
    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 proton minibeam radiotherapy?
    A. Total dose
    B. Beam width and spacing
    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 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 oxidative base 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 olfactory toxicity?
    A. Acute apoptosis of olfactory neurons
    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 reassortment of cells in microbeam radiotherapy?
    A. Dose rate
    B. Cell cycle kinetics
    C. Total dose
    D. Radiation type
    E. Fraction size

95. What is the primary consequence of a mutation in the XPC gene in response to radiation?
    A. Enhanced nucleotide excision repair
    B. Increased radiosensitivity
    C. Reduced apoptosis
    D. Inhibition of homologous recombination
    E. Upregulation of VEGF

96. Which normal tissue effect is most associated with helium ion therapy?
    A. Acute mucositis
    B. Late normal tissue sparing
    C. Erythema
    D. Desquamation
    E. Leukopenia

97. What is the primary mechanism of action of bismuth nanoparticle radiosensitisers in radiotherapy?
    A. Enhancement of DNA repair
    B. Increased high-Z 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 tumour cells during microbeam radiotherapy?
    A. Dose rate
    B. Post-irradiation microenvironment
    C. Fraction size
    D. Radiation type
    E. Cell cycle phase

99. What is the surviving fraction after 14 Gy of radiation if the D0 is 1.4 Gy and the extrapolation number (n) is 2?
    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 microbeam radiotherapy?
     A. p53
     B. ATM
     C. RAD51
     D. DNA-PK
     E. PARP1

Answers

Cancer Biology (50 Answers)

1. B. WEE1 inhibitors exploit replication stress overload in MYC-amplified cancers.

2. B. LKB1-AMPK inhibits metabolic reprogramming in Peutz-Jeghers syndrome.

3. A. Promoter hypermethylation silences RB1 in retinoblastoma.

4. B. Tumour-associated neutrophils secrete NETs to promote metastasis.

5. A. BCL2 G101V mutation confers venetoclax resistance in CLL.

6. A. KDM6A mutations inhibit histone demethylation, altering gene expression.

7. B. Osteoblast-mediated bone remodeling enables prostate cancer bone metastases.

8. B. xCT promotes glutathione synthesis, protecting against ferroptotic stress.

9. B. Stromal fibroblast activation drives tumour-promoting inflammation.

10. A. BARD1 loss inhibits BRCA1-mediated DNA repair, promoting breast cancer.

11. B. IL-10 promotes M2 macrophage differentiation.

12. B. ROS1 fusion constitutively activates tyrosine kinase signalling in NSCLC.

13. A. TWIST1 drives invadopodia-related gene expression in melanoma.

14. B. SIRT3 regulates oxidative stress response in cancer cell mitochondria.

15. B. Asparagine synthesis upregulation supports survival during glutamine deprivation.

16. B. ZFHX3 inhibits cell migration in prostate cancer.

17. A. ALDH1 is a marker for ovarian cancer stem cells.

18. B. Oncolytic viral therapy selectively lyses tumour cells.

19. A. PTEN mutations cause Cowden syndrome.

20. B. BRD4 promotes oncogenic transcription in NUT midline carcinoma.

21. B. Integrin-mediated endothelial interactions enable transendothelial migration.

22. B. FLT3 mutation activates tyrosine kinase signalling in AML.

23. A. IMP dehydrogenase drives purine biosynthesis in cancer cells.

24. A. MEF2C mutations inhibit lymphoid differentiation in B-ALL.

25. B. EZH2 inhibitors target histone H3K27 methylation in DLBCL.

26. B. LAG-3 and TIM-3 ligand expression induces CD8+ T-cell exhaustion.

27. A. NOTCH2 mutation drives marginal zone lymphoma.

28. B. PIM1 promotes anti-apoptotic signalling in prostate cancer.

29. B. Adaptation to lymphoid microenvironment enables lymph node metastasis survival.

30. A. BCOR mutation inhibits transcriptional repression in medulloblastoma.

31. A. p16INK4a regulates the G1 checkpoint in DNA damage response.

32. B. ATRX inhibits alternative lengthening of telomeres in glioma.

33. A. CPI-613 targets pyruvate dehydrogenase to disrupt cancer metabolism.

34. A. FGFR inhibitors block tyrosine kinase signalling in cholangiocarcinoma.

35. B. Upregulation of methionine adenosyltransferase drives the methionine cycle.

36. B. SMARCB1 inhibits SWI/SNF complex activity in rhabdoid tumours.

37. A. HTLV-1 Tax protein expression drives adult T-cell leukemia/lymphoma.

38. A. SF3B1 mutation inhibits RNA splicing in myelodysplastic syndromes.

39. A. FANCA mediates DNA damage response in the Fanconi anaemia pathway.

40. B. Growth factor ligands from the microenvironment drive targeted therapy resistance.

41. A. CIITA translocation is associated with primary mediastinal B-cell lymphoma.

42. B. Loss of interferon-gamma signalling confers immune checkpoint inhibitor resistance.

43. B. VE-cadherin-mediated tube formation drives vasculogenic mimicry in melanoma.

44. B. NF2 inhibits YAP/TAZ activity in schwannoma.

45. A. EWS-WT1 fusion drives desmoplastic small round cell tumour.

46. B. GNAQ mutation activates G-protein signalling in uveal melanoma.

47. A. RPA mediates homologous recombination repair in DNA damage response.

48. B. MEN1 inhibits transcriptional activation in multiple endocrine neoplasia type 1.

49. A. TET2 mutation is associated with blastic plasmacytoid dendritic cell neoplasm.

50. B. Inhibition of caspase-1 activation resists pyroptosis in cancer cells.

Radiobiology (50 Answers)

51. B. Radiation-induced epigenetic reprogramming alters histone modifications.

52. B. D10 is the dose reducing survival to 10%.

53. B. Spatial dose heterogeneity reduces OER in microbeam radiotherapy.

54. B. Synchrotron-based microbeam radiotherapy spares normal tissue via ultra-high dose gradients.

55. E. RNase H-mediated repair resolves radiation-induced DNA-RNA hybrids.

56. B. Synthetic lethality in PARP-deficient cancers results from unrepaired SSB accumulation.

57. B. High α/β ratio indicates high sensitivity to fraction size in hypofractionation.

58. C. The lens of the eye is susceptible to radiation-induced cataracts.

59. A. Acute apoptosis of crypt stem cells causes radiation-induced enteropathy.

60. B. Peak-to-valley dose ratio influences the therapeutic index in microbeam radiotherapy.

61. B. BED = 40 × (1 + 8/3) = 106.67 Gy, corrected for repopulation (~38.67 Gy loss) = 68 Gy.

62. B. S phase is resistant to necroptosis due to active repair mechanisms.

63. B. Proton minibeam radiotherapy enhances normal tissue sparing via spatial fractionation.

64. B. ATR activates the DNA damage response to replication stress.

65. B. ATR inhibitors enhance replication fork collapse in ATM-deficient cancers.

66. B. Ultra-high peak dose increases RBE in microbeam radiotherapy.

67. B. ERCC2 mutation increases radiosensitivity due to defective NER.

68. B. Proton minibeam radiotherapy preserves late normal tissue.

69. B. Chronic inflammation and fibrosis cause pancreatic toxicity.

70. B. Peak dose intensity influences TCP in microbeam radiotherapy.

71. D. EQD2 = 45 × (15 + 4)/(2 + 4) = 108 Gy.

72. D. Nucleotide excision repair resolves DNA-protein crosslinks in G1 phase.

73. B. Carbon ion minibeam radiotherapy enhances normal tissue sparing via spatial fractionation.

74. B. Inter-beam spacing influences reoxygenation in microbeam radiotherapy.

75. B. Chronic inflammation and vascular damage cause adrenal toxicity.

76. B. OGG1 repairs clustered non-DSB oxidative lesions.

77. B. MRE11 mutation increases radiosensitivity due to impaired DSB sensing.

78. B. Peak-to-valley dose ratio influences sublethal damage repair in microbeam radiotherapy.

79. C. SF = 3 × e^(-10/1.2) ≈ 0.06.

80. C. Salivary glands are susceptible to radiation-induced xerostomia.

81. B. Cerium oxide nanoparticles increase ROS generation, enhancing DNA damage.

82. B. Treatment duration influences normal tissue repopulation in APBI.

83. B. RAD50 mutation increases radiosensitivity due to defective HR.

84. B. Late normal tissue sparing is associated with high-dose rate microbeam radiotherapy.

85. A. Acute apoptosis of spermatogonia causes testicular toxicity.

86. B. Reduced oxygen dependence in valleys minimises the oxygen effect in proton minibeam radiotherapy.

87. C. BED = 50 × (1 + 10/2) = 150 Gy, corrected for repopulation (~45 Gy loss) = 105 Gy.

88. B. DNA-PK repairs DSBs in quiescent cells via NHEJ.

89. B. Helium ion therapy offers a sharper Bragg peak and higher LET.

90. B. Beam width and spacing influence NTCP in proton minibeam radiotherapy.

91. D. EQD2 = 54 × (9 + 3)/(2 + 3) = 108 Gy.

92. C. Base excision repair resolves oxidative base damage.

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

94. B. Cell cycle kinetics influence reassortment in microbeam radiotherapy.

95. B. XPC mutation increases radiosensitivity due to defective NER.

96. B. Helium ion therapy spares late normal tissue damage.

97. B. Bismuth nanoparticles emit high-Z electrons, increasing DNA damage.

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

99. B. SF = 2 × e^(-14/1.4) ≈ 0.001.

100. B. ATM coordinates the DNA damage response in microbeam radiotherapy.