Radiation Biology, Clinical Dosimetry, and Radiation Oncology Practice

Comprehensive vocabulary flashcards covering ionizing radiation exposure sources, DNA damage kinetics, molecular carcinogenesis, fractionation models, dosimetry metrics, and normal-tissue radiobiology.

Which item is identified in the notes as the largest overall source of radiation exposure?

A. Consumer products B. Terrestrial radiation C. Radon and thoron D. CT scans

C. Radon and thoron

Radon and thoron account for $37\%$ of overall radiation exposure, delivering an average annual effective dose of $2.28\,\text{mSv}$.

Which medical source is the largest in the exposure table?

A. Conventional X-ray/fluoroscopy B. Interventional fluoroscopy C. Nuclear medicine D. CT scans

D. CT scans

CT scans account for $24\%$ of total exposure, representing the single largest medical contributor in the exposure table.

Which source is associated with exposure that increases at higher elevations?

A. Radon B. Ingested radionuclides C. Cosmic rays D. Building materials

C. Cosmic rays

Cosmic radiation originates in deep space and increases in intensity at higher elevations and aircraft flight altitudes due to reduced atmospheric shielding.

Which is an example of internal radiation exposure?

A. Radioactive material is inhaled or ingested B. Radiation comes from cosmic rays outside the body C. Radiation comes from soil outside the body D. Exposure to an external radioactive object without entry into the body

A. Radioactive material is inhaled or ingested

Internal exposure occurs when radionuclides gain access inside the body through inhalation or ingestion.

What does the term 'hormesis' mean in the source notes?

A. The process of making oxygen unavailable to tumours B. The idea that a small radiation dose may be beneficial C. The repair of DNA double-strand breaks D. The idea that any dose always causes immediate sickness

B. The idea that a small radiation dose may be beneficial

Hormesis is the hypothesis suggesting that low, non-lethal doses of ionizing radiation stimulate protective cellular repair mechanisms.

The Chernobyl thyroid study notes report a relative risk of approximately what per $1\,\text{Gy}$?

A. $1.47$ B. $0.525$ C. $52.5$ D. $5.25$

D. $5.25$

The cited Chernobyl thyroid screening study observed a relative risk of approximately $5.25$ per $1\,\text{Gy}$ of radiation absorbed dose.

Which value is listed for natural background radiation in Canada?

A. $1\,\text{mSv}$ per year B. $7\,\text{mSv}$ per year C. $0.005\,\text{mSv}$ per year D. $1.8\,\text{mSv}$ per year

D. $1.8\,\text{mSv}$ per year

Natural background radiation exposure in Canada is listed as approximately $1.8\,\text{mSv}$ per year.

What public effective-dose limit is shown in the source notes?

A. $100\,\text{mSv}$ per year B. $15\,\text{mSv}$ per year C. $1\,\text{mSv}$ per year D. $50\,\text{mSv}$ per year

C. $1\,\text{mSv}$ per year

The established radiation protection limit for public effective dose is $1\,\text{mSv}$ per year.

Which statement best describes stochastic effects?

A. Severity increases with dose after a clear threshold B. Probability increases with dose, but severity is independent of dose and there is no threshold in the model C. They occur only above $100\,\text{Gy}$ D. They are always immediate and non-cancerous

B. Probability increases with dose, but severity is independent of dose and there is no threshold in the model

Stochastic effects (e.g., carcinogenesis and heritable mutations) increase in probability with dose without a threshold, while severity remains dose-independent.

Which statement best describes deterministic (tissue) effects?

A. Severity increases with dose and there is a practical threshold B. Probability increases but severity is dose independent C. They are limited to hereditary effects D. There is never a threshold

A. Severity increases with dose and there is a practical threshold

Deterministic effects possess a practical threshold dose below which damage is not clinically apparent, above which clinical severity escalates with increasing dose.

What cataract threshold is shown in the deterministic-effects notes?

A. About $10\,\text{mGy}$ B. About $100\,\text{Gy}$ C. About $1\,\text{Gy}$ D. About $0.001\,\text{Gy}$

C. About $1\,\text{Gy}$

Radiation-induced cataractogenesis exhibits a practical deterministic threshold of approximately $1\,\text{Gy}$.

What is the equivalent-dose formula in the notes?

A. $\text{Equivalent dose} = \text{dose} \div \text{treatment time}$ B. $\text{Equivalent dose} = \text{absorbed dose} \times w_T$ C. $\text{Equivalent dose} = \text{activity} \times \text{half-life}$ D. $\text{Equivalent dose} = \text{absorbed dose} \times w_R$

D. $\text{Equivalent dose} = \text{absorbed dose} \times w_R$

Equivalent dose adjusts physical absorbed dose $D$ by the radiation weighting factor $w_R$ to account for biological effectiveness, measured in sieverts ($\text{Sv}$).

What radiation weighting factor ($w_R$) is listed for alpha particles and fission fragments?

A. $2$ B. $20$ C. $5$ D. $1$

B. $20$

Densely ionizing high-LET radiation such as alpha particles and fission fragments have a radiation weighting factor of $w_R = 20$.

Which formula matches the source notes for effective dose to an exposed tissue?

A. $\text{Absorbed dose} + n$ B. $\text{Absorbed dose} \times \text{treatment time}$ C. $\text{Absorbed dose} \times w_R \times w_T$ D. $\text{Absorbed dose} \div w_R$

C. $\text{Absorbed dose} \times w_R \times w_T$

Effective dose accounts for both radiation quality ($w_R$) and individual tissue radiosensitivity ($w_T$), summing across all exposed organs.

What does the absolute-risk model assume? A. Only inherited mutations matter B. Cancer risk falls as dose rises C. Radiation multiplies background cancer incidence at every age by a factor D. Radiation adds a crop of cancers above the natural incidence

D. Radiation adds a crop of cancers above the natural incidence

The absolute-risk model assumes radiation adds a constant excess number of cancer cases directly on top of spontaneous background incidence.

What does the relative-risk model assume? A. Radiation increases the natural cancer incidence by a given factor after exposure B. Only leukemia can be induced C. Radiation produces cancers unrelated to natural incidence D. Risk is independent of age after exposure

A. Radiation increases the natural cancer incidence by a given factor after exposure

The relative-risk model posits that radiation exposure multiplies natural background incidence by a constant factor, predicting larger numbers of excess cancers at older ages.

What is the 'doubling dose' in heritable-risk assessment? A. Dose that doubles a tumour's physical size B. Dose that halves cell survival C. Radiation dose that produces as many mutations as occur spontaneously in one generation D. Dose required to double the treatment time

C. Radiation dose that produces as many mutations as occur spontaneously in one generation

The doubling dose is defined as the dose of ionizing radiation required to produce an excess mutation frequency equal to the spontaneous rate.

What is the main idea of the therapeutic ratio? A. The ratio of oxygen to carbon dioxide in carbogen B. Tumour response/control for a fixed level of normal-tissue damage C. Number of fractions divided by the total dose D. Normal-tissue damage for a fixed dose rate only

B. Tumour response/control for a fixed level of normal-tissue damage

The therapeutic ratio balances tumour control probability (TCP) against normal-tissue complication probability (NTCP), seeking maximal tumour ablation with acceptable toxicity.

Which sequence correctly lists the three stages of carcinogenesis? A. Invasion $\rightarrow$ initiation $\rightarrow$ fractionation B. Promotion $\rightarrow$ initiation $\rightarrow$ apoptosis C. Initiation $\rightarrow$ promotion $\rightarrow$ progression D. Progression $\rightarrow$ repair $\rightarrow$ senescence

C. Initiation $\rightarrow$ promotion $\rightarrow$ progression

Carcinogenesis progresses sequentially through initiation (DNA mutation), promotion (clonal cellular expansion), and progression (malignant transformation and invasion).

How does an oncogene typically contribute to cancer? A. It prevents all DNA synthesis B. Loss of function always blocks proliferation C. Gain of function or overexpression drives excessive growth/survival signalling D. It increases apoptosis in every cell

C. Gain of function or overexpression drives excessive growth/survival signalling

Oncogenes undergo gain-of-function mutations or overexpression, acting like an accelerator locked 'on' to promote autonomous cellular growth.

For a classic tumour-suppressor loss-of-function effect, how many copies often need to be inactivated? A. No copies of DNA B. Only one copy always C. Three copies D. Both copies

D. Both copies

Under Knudson's two-hit hypothesis, recessive tumour-suppressor genes require inactivation of both alleles to eliminate regulatory growth control.

Which HRAS point mutation is specifically highlighted in oncogene activation? A. RB1 is duplicated outside the chromosome B. Codon 12 valine is changed to glycine, turning HRAS OFF C. A BRCA2 deletion switches off VEGF D. Codon 12 glycine is changed to valine, locking HRAS ON

D. Codon 12 glycine is changed to valine, locking HRAS ON

A missense mutation at codon 12 substituting glycine with valine locks the HRAS protein into a constitutively active GTP-bound state.

What are 'double minutes' in the gene amplification notes? A. The first two minutes after a radiation exposure B. Extrachromosomal amplified DNA copies C. Amplified regions located only inside chromosomes D. The two copies of a tumour-suppressor gene

B. Extrachromosomal amplified DNA copies

Double minutes are small, circular, extrachromosomal DNA elements that lack centromeres and contain amplified oncogenes.

Which chromosome rearrangement/fusion is associated with chronic myelogenous leukemia (CML)? A. Chromosomes 1 and 2 creating ATM–TP53 B. Chromosomes 4 and 8 creating BRCA1–RB1 C. Philadelphia chromosome involving chromosomes 9 and 22, creating BCR–ABL1 D. Chromosomes 13 and 17 creating VEGF–TSP1

C. Philadelphia chromosome involving chromosomes 9 and 22, creating BCR–ABL1

The $t(9;22)$ reciprocal translocation generates the Philadelphia chromosome, encoding the constitutively active BCR–ABL1 tyrosine kinase.

What are gatekeeper genes? A. Genes that measure radiation dose B. Genes that only control angiogenesis C. Genes that directly regulate tumour growth by inhibiting division or promoting cell death D. Genes that only maintain cell adhesion

C. Genes that directly regulate tumour growth by inhibiting division or promoting cell death

Gatekeeper tumour suppressors (such as $p53$ and $RB1$) directly regulate the cell cycle, enforcing arrest checkpoints or apoptosis.

What are caretaker genes mainly responsible for? A. Maintaining genomic stability and limiting the accumulation of mutations B. Allowing cells to detach without apoptosis C. Directly accelerating cell division under all conditions D. Forming all blood vessels in a tumour

A. Maintaining genomic stability and limiting the accumulation of mutations

Caretaker genes (such as $BRCA1$, $BRCA2$, and $ATM$) identify and repair DNA damage, preserving genome integrity.

What does RB protein do at the G1–S checkpoint? A. Degrades extracellular matrix B. Blocks genes required for DNA synthesis C. Activates VEGF in all tumours D. Releases cytochrome c as an initiator caspase

B. Blocks genes required for DNA synthesis

Hypophosphorylated RB binds and inhibits E2F transcription factors, preventing entry into S-phase and DNA synthesis.

Which sequence describes the intrinsic (mitochondrial) apoptosis pathway? A. VEGF $\rightarrow$ TSP-1 $\rightarrow$ RB1 B. E-cadherin $\rightarrow$ ECM degradation $\rightarrow$ caspase-9 C. FasL $\rightarrow$ caspase-8 $\rightarrow$ cytochrome c $\rightarrow$ VEGF D. Cell stress/DNA damage $\rightarrow$ cytochrome c $\rightarrow$ Apaf-1 $\rightarrow$ caspase-9 $\rightarrow$ caspases 3, 6, 7

D. Cell stress/DNA damage $\rightarrow$ cytochrome c $\rightarrow$ Apaf-1 $\rightarrow$ caspase-9 $\rightarrow$ caspases 3, 6, 7

Internal cellular stress triggers mitochondrial cytochrome c release, apoptosome formation with Apaf-1, initiator caspase-$9$ activation, and cleavage by caspases $3$, $6$, and $7$.

Which sequence describes the extrinsic apoptosis pathway? A. DNA damage $\rightarrow$ cytochrome c $\rightarrow$ caspase-9 only B. VEGF binds a receptor $\rightarrow$ caspase-3 C. Bcl-2 releases cytochrome c $\rightarrow$ RB1 D. Fas ligand binds a death receptor $\rightarrow$ caspase-8 $\rightarrow$ effector caspases 3, 6, 7

D. Fas ligand binds a death receptor $\rightarrow$ caspase-8 $\rightarrow$ effector caspases 3, 6, 7

Extracellular ligands (e.g., FasL) bind transmembrane death receptors, activating initiator caspase-$8$ to cleave downstream effector caspases $3$, $6$, and $7$.

What is the biological role of VEGF in tumour progression? A. Directly cuts the extracellular matrix B. Activates apoptosis through caspase-8 C. Stimulates endothelial-cell growth and new blood-vessel formation D. Inhibits all blood-vessel formation

C. Stimulates endothelial-cell growth and new blood-vessel formation

Vascular Endothelial Growth Factor (VEGF) promotes endothelial proliferation and neovascularization to support tumour growth and nutrient exchange.

What is the correct metastatic-cascade order in the source notes? A. Local invasion $\rightarrow$ intravasation $\rightarrow$ survival in circulation $\rightarrow$ extravasation $\rightarrow$ colonization B. Colonization $\rightarrow$ intravasation $\rightarrow$ local invasion $\rightarrow$ apoptosis C. Extravasation $\rightarrow$ local invasion $\rightarrow$ initiation $\rightarrow$ promotion D. Angiogenesis $\rightarrow$ senescence $\rightarrow$ repair $\rightarrow$ metastasis

A. Local invasion $\rightarrow$ intravasation $\rightarrow$ survival in circulation $\rightarrow$ extravasation $\rightarrow$ colonization

Metastasis occurs sequentially: invading primary tissue, penetrating vascular walls (intravasation), surviving circulation, exiting vasculature (extravasation), and colonizing distant organs.

What is anoikis? A. Cellular immortalization B. Entry into a lymphatic vessel C. Apoptosis triggered when cells detach from their normal surroundings D. The process of new blood vessel formation

C. Apoptosis triggered when cells detach from their normal surroundings

Anoikis is a specialized form of programmed cell death triggered by the loss of cellular contact with the extracellular matrix.

What does the 'seed and soil' hypothesis explain? A. Every cancer grows equally well in every organ B. Only the tissue environment matters, never the cancer cell C. A metastatic cell must encounter a compatible tissue environment to grow successfully D. Metastasis occurs without cell survival

C. A metastatic cell must encounter a compatible tissue environment to grow successfully

Proposed by Stephen Paget, this concept states that circulating cancer cells ('seeds') require a compatible, receptive organ microenvironment ('soil') to colonize.

Which gene is mutated in ataxia-telangiectasia (A-T)? A. TP53 B. ATM C. PTCH1 D. RB1

B. ATM

Ataxia-telangiectasia is caused by autosomal recessive mutations in the $ATM$ gene, which codes for a serine/threonine kinase crucial in double-strand break repair.

What is the key radiation-related feature of ataxia-telangiectasia (A-T)? A. Selective hypersensitivity only to UV radiation B. Resistance to all radiation because ATM is overactive C. No sensitivity to DNA damage D. Marked hypersensitivity to ionizing radiation

D. Marked hypersensitivity to ionizing radiation

Inability to coordinate double-strand break repair renders cells and patients with A-T profoundly hypersensitive to ionizing radiation.

Which syndrome is associated with germline PTEN mutations in the rapid-memorization list? A. Ataxia-telangiectasia B. Gorlin syndrome C. Li-Fraumeni syndrome D. Cowden syndrome

D. Cowden syndrome

Cowden syndrome is an autosomal dominant condition linked to $PTEN$ mutations, causing multiple hamartomas and elevated risks of breast and thyroid cancer.

What is the DNA-repair problem associated with Fanconi anemia? A. Excess VEGF production B. Defective G1–S checkpoint from RB1 loss only C. Loss of all effector caspases D. Defective repair of DNA interstrand crosslinks

D. Defective repair of DNA interstrand crosslinks

Fanconi anemia is characterized by failure to resolve and repair DNA interstrand crosslinks, causing chromosomal instability and bone marrow failure.

How does the source distinguish radiosensitivity from radiation-induced cancer susceptibility? A. They are exactly the same concept B. Radiosensitivity means unusually severe normal-cell damage; cancer susceptibility means higher risk of a new cancer after exposure C. Cancer susceptibility means only acute skin reactions D. Radiosensitivity means a person cannot develop cancer

B. Radiosensitivity means unusually severe normal-cell damage; cancer susceptibility means higher risk of a new cancer after exposure

Radiosensitivity refers to immediate cellular/tissue toxicity from cell killing, while cancer susceptibility reflects elevated stochastic second-cancer risk.

How is mutated KRAS described in the source's radiotherapy-response section? A. Associated with increased radioresistance and lower complete response rates in rectal cancer after neoadjuvant chemoradiation B. A normal germline variant that always increases radiosensitivity C. Associated with guaranteed complete response D. A direct activator of E-cadherin

A. Associated with increased radioresistance and lower complete response rates in rectal cancer after neoadjuvant chemoradiation

KRAS mutations confer radioresistance, correlating clinically with reduced complete response rates following neoadjuvant treatment.

What does the abbreviation GARD stand for? A. Gross Anatomy Radiation Dose B. Genome-Based Model for Adjusting Radiotherapy Dose C. Gene Activation Repair Detector D. General Assessment of Radiation Damage

B. Genome-Based Model for Adjusting Radiotherapy Dose

GARD is a genomic model utilizing gene expression profiles (radiosensitivity index) to calculate personalized therapeutic radiation doses.

Which item is included among the source's five Rs of radiobiology? A. Recombination fraction B. Radiographic magnification C. Redistribution/reassortment D. Refraction

C. Redistribution/reassortment

The 5 Rs are Repair of sublethal damage, Redistribution/reassortment across cell-cycle phases, Repopulation, Reoxygenation, and intrinsic Radiosensitivity.

What does the Strandqvist plot relate? A. Total radiation dose and overall treatment time for the same biological effect B. Only number of mutations and age C. Only dose and tissue weighting factor D. Only tumour volume and blood flow

A. Total radiation dose and overall treatment time for the same biological effect

The Strandqvist plot demonstrates isoeffect relationships, plotting total required physical dose against overall treatment time.

Which formula is shown for the Ellis NSD model in the notes? A. $D = k_1 \times n^{0.24} \times T^{0.11}$ B. $D = k_1 \times T^{0.33}$ C. $D = n \times T^2$ D. $D = k_1 \div (n + T)$

A. $D = k_1 \times n^{0.24} \times T^{0.11}$

The Ellis Nominal Standard Dose formula relates total tolerance dose $D$ to fraction number $n$ (exponent $0.24$) and elapsed time $T$ (exponent $0.11$).

What is the alpha/beta ratio ($\alpha/\beta$)? A. The ratio of activity to half-life B. The percentage of cells that are oxygenated C. The ratio of tumour volume to normal tissue volume D. The dose at which the linear and quadratic components of radiation effect are equal

D. The dose at which the linear and quadratic components of radiation effect are equal

The $\alpha/\beta$ ratio is the physical dose where the linear ($\alpha D$) and quadratic ($\beta D^2$) contributions to cell killing are identical.

A low $\alpha/\beta$ ratio (e.g., $2\text{–}3\,\text{Gy}$) indicates that a tissue is: A. Always radioresistant at every dose B. Less sensitive to changes in fraction size C. Unaffected by dose per fraction D. More sensitive to changes in fraction size

D. More sensitive to changes in fraction size

Late-responding normal tissues have low $\alpha/\beta$ values, displaying marked sensitivity and escalating damage when fraction size increases.

Around when is accelerated repopulation estimated to begin for human head-and-neck squamous cell carcinoma (HNSCC)? A. Within $24\,\text{hours}$ of the first fraction B. Around day $28$ after radiotherapy starts C. After $5\,\text{years}$ in all patients D. Only after treatment ends

B. Around day $28$ after radiotherapy starts

Accelerated clonogenic repopulation begins approximately $4\,\text{weeks}$ (day $28$) into fractionated treatment, requiring roughly $0.6\,\text{Gy/day}$ to counteract.

What is hyperfractionation? A. More fractions per day using smaller doses per fraction, usually twice daily B. Fewer, larger fractions over a shorter course C. The same dose delivered once only D. Increasing dose rate continuously without fractionation

A. More fractions per day using smaller doses per fraction, usually twice daily

Hyperfractionation delivers smaller fraction doses ($< 1.8\,\text{Gy}$) more than once daily to spare late-reacting tissues while maintaining or escalating tumour control.

What is the main distinction between hyperfractionation and accelerated treatment? A. Both mean exactly the same schedule B. Acceleration always uses fewer fractions than conventional treatment C. Hyperfractionation uses smaller fractions to spare late tissue; acceleration shortens overall time to reduce repopulation D. Hyperfractionation uses only one fraction; acceleration uses no radiation

C. Hyperfractionation uses smaller fractions to spare late tissue; acceleration shortens overall time to reduce repopulation

Hyperfractionation decreases dose per fraction to spare late-reacting normal tissue; acceleration shortens total elapsed days to prevent tumour clonogen repopulation.

Which formula gives cell survival ($S$) after a single dose in the linear-quadratic model (LQM)? A. $S = e^{+(\alpha D + \beta D^2)}$ B. $S = D \div (\alpha/\beta)$ C. $S = e^{-(\alpha D + \beta D^2)}$ D. $S = \alpha D + \beta D^2$

C. $S = e^{-(\alpha D + \beta D^2)}$

In the LQM, survival fraction follows an exponential decrease driven by single-track lethal events ($\alpha D$) and two-track lethal lesions ($\beta D^2$).

Which formula calculates Biologically Effective Dose (BED) from fraction number and fraction dose? A. $\text{BED} = n d \left(1 + \frac{d}{\alpha/\beta}\right)$ B. $\text{BED} = \text{EQD2} \times (\alpha/\beta)$ C. $\text{BED} = n + d + \alpha/\beta$ D. $\text{BED} = D \div (n \times d)$

A. $\text{BED} = n d \left(1 + \frac{d}{\alpha/\beta}\right)$

BED standardizes biological dose across different fractionation regimens, where $n$ is fraction count and $d$ is dose per fraction.

Which formula is given to convert BED into EQD2? A. $\text{EQD2} = \alpha D + \beta D^2$ B. $\text{EQD2} = D \times n$ C. $\text{EQD2} = \frac{\text{BED}}{1 + \frac{2}{\alpha/\beta}}$ D. $\text{EQD2} = \text{BED} \left(1 + \frac{d}{\alpha/\beta}\right)$

C. $\text{EQD2} = \frac{\text{BED}}{1 + \frac{2}{\alpha/\beta}}$

EQD2 converts any BED to the equivalent total dose delivered in conventional $2\,\text{Gy}$ fractions.

What constitutes the Gross Tumour Volume (GTV)? A. The GTV plus microscopic disease B. The CTV expanded for geometric uncertainties C. The actual visible tumour D. All organs at risk

C. The actual visible tumour

The GTV is the demonstrable palpable or radiologically visible extent of malignant growth.

What constitutes the Clinical Target Volume (CTV)? A. The planning margin for setup uncertainty only B. The entire body exposed to radiation C. Only the visible tumour D. GTV plus potential microscopic disease

D. GTV plus potential microscopic disease

The CTV includes the demonstrable GTV plus surrounding subclinical microscopic malignant disease requiring eradication.

What is the Planning Target Volume (PTV) designed to account for? A. Geometric uncertainties such as patient movement, organ motion and setup variation B. Only DNA repair between fractions C. Only tumour histology D. Only tumour oxygenation

A. Geometric uncertainties such as patient movement, organ motion and setup variation

The PTV is a geometrical margin added to the CTV to ensure the prescribed dose is absorbed despite internal motion and setup variations.

What is carbogen in the source notes? A. Nitrogen mixed with helium B. $95\%$ oxygen and $5\%$ carbon dioxide C. $95\%$ carbon dioxide and $5\%$ oxygen D. $100\%$ oxygen at high pressure only

B. $95\%$ oxygen and $5\%$ carbon dioxide

Carbogen ($95\%\,\text{O}_2$ and $5\%\,\text{CO}_2$) is inhaled to enhance blood oxygenation while $CO_2$ prevents cerebral vasoconstriction, reversing tumour hypoxia.

Which sequence best describes cisplatin's radiosensitizing action in the notes? A. Removes guanine from DNA and improves replication B. Binds E-cadherin, increases cell adhesion, and prevents DNA damage C. Blocks oxygen delivery without affecting DNA D. Binds DNA, especially guanine; forms crosslinks that bend DNA; disrupts copying; adds to radiation damage

D. Binds DNA, especially guanine; forms crosslinks that bend DNA; disrupts copying; adds to radiation damage

Cisplatin forms intrastrand and interstrand crosslinks primarily on guanine, interfering with replication and inhibiting radiation repair.

What is a consequential late effect? A. A reversible resting state B. A tumour growth advantage from VEGF C. A late effect caused by unresolved severe acute injury, with no latent period D. An injury that always happens without any prior acute injury

C. A late effect caused by unresolved severe acute injury, with no latent period

Consequential late effects occur when persistent, severe acute epithelial injury fails to heal, leading directly into chronic fibrosis or ulceration without a latency period.

What does TD5/5 mean in the source notes? A. Total dose delivered in five fractions over five weeks B. Dose associated with a $5\%$ risk of severe complications within $5\,\text{years}$ C. Dose causing toxicity in $50\%$ of patients within $5\,\text{days}$ D. Dose causing $5\%$ tumour shrinkage in $5\,\text{weeks}$

B. Dose associated with a $5\%$ risk of severe complications within $5\,\text{years}$

TD5/5 defines the normal-tissue tolerance dose associated with a $5\%$ probability of severe complications within a $5\text{-year}$ observation interval.

Which is an example of a serial organ architecture in the notes? A. Spinal cord B. Bladder C. Lung D. Liver

A. Spinal cord

The spinal cord possesses a serial architecture where disabling a single critical functional subunit precipitates total organ failure; it is sensitive to maximum local point dose.

What exposure pattern is required for acute radiation syndrome (ARS) in the notes? A. Only exposure confined to one small patch of skin B. Only long-term low-dose background exposure C. Any dental X-ray D. Substantial whole-body or near-whole-body exposure

D. Substantial whole-body or near-whole-body exposure

ARS requires substantial, penetrating radiation exposure delivered to the whole body or major portion of the body within a short duration.

What whole-body dose range is listed for hematopoietic syndrome? A. About $2.5\text{–}5\,\text{Gy}$ B. Greater than $100\,\text{Gy}$ C. $0.005\text{–}0.02\,\text{Gy}$ D. Exactly $50\,\text{Gy}$

A. About $2.5\text{–}5\,\text{Gy}$

Hematopoietic syndrome occurs at whole-body doses of approximately $2.5\text{–}5\,\text{Gy}$, destroying bone marrow stem cells and causing severe cytopenia, infection, and hemorrhage.

What dose is associated with gastrointestinal ARS in the source notes? A. $2.5\,\text{mGy}$ B. Greater than $10\,\text{Gy}$ C. $0.1\,\text{Gy}$ D. $1\,\text{mGy}$

B. Greater than $10\,\text{Gy}$

GI syndrome occurs at whole-body doses exceeding $10\,\text{Gy}$, causing crypt stem cell death, mucosal denudation, and death within $3\text{–}10\,\text{days}$.

What dose range is associated with the cerebrovascular syndrome in the notes? A. $0.1\text{–}1\,\text{Gy}$ B. $5\text{–}10\,\text{mGy}$ C. More than $100\,\text{Gy}$ D. $2.5\text{–}5\,\text{Gy}$

C. More than $100\,\text{Gy}$

Cerebrovascular syndrome occurs at extreme doses above $100\,\text{Gy}$, leading to rapid neurological deterioration, cardiovascular collapse, and death within $24\text{–}48\,\text{hours}$.

What is the major effect of radiation exposure during the preimplantation stage? A. No sensitivity to radiation B. Greatest sensitivity to lethal effects; surviving embryos may develop normally C. Specific organ malformations are always the only effect D. Only growth restriction in late pregnancy

B. Greatest sensitivity to lethal effects; surviving embryos may develop normally

Preimplantation follows an 'all-or-none' rule: radiation causes lethal embryonic failure, or the blastocyst repairs fully and develops normally.

During which prenatal developmental stage is the risk of gross anatomical malformations emphasized? A. Only after adulthood B. Organogenesis, when major organs form and cells actively differentiate C. Only before fertilization D. Only after birth

B. Organogenesis, when major organs form and cells actively differentiate

Organogenesis is the period of active tissue differentiation and organ assembly, rendering the fetus highly vulnerable to structural teratogenic malformations.

How does radon commonly expose people to radiation?

A. External exposure from the ground only B. Inhalation C. Injection into the bloodstream D. External exposure from space

B. Inhalation

Radon is an inert radioactive gas that emanates from the decay of uranium in soil and rock, posing its primary hazard when inhaled into pulmonary tissue.

Which pair is associated with natural terrestrial radiation in the notes?

A. Earth's crust and building materials B. Nuclear medicine and consumer products C. Radon and dental X-rays D. Cosmic rays and CT scans

A. Earth's crust and building materials

Terrestrial radiation naturally originates from primordial radionuclides situated within rocks, soil, and building materials derived from the Earth's crust.

What radioactive material is mentioned in bananas?

A. Cobalt-60 B. Radon-222 C. Iodine-131 D. Potassium-40

D. Potassium-40

Bananas naturally contain potassium, including a small fixed fraction of the radioactive isotope $^{40}\text{K}$.

What event is described as the cause of the Chernobyl accident in the notes?

A. Unit 4 exploded and caught fire during a flawed safety test B. A hurricane damaged all reactor units C. A transport aircraft released radionuclides D. A CT scanner malfunctioned

A. Unit 4 exploded and caught fire during a flawed safety test

The accident at Chernobyl occurred when Reactor Unit 4 underwent an uncontrolled power surge, leading to steam explosions and graphite fires during a low-power turbine test.

What key lesson about Chernobyl contamination is emphasized in the notes?

A. Contamination was patchy and extended beyond 30 km B. Only people inside the reactor were exposed C. Contamination stopped exactly at the 30-km boundary D. Distance from the reactor guaranteed safety

A. Contamination was patchy and extended beyond 30 km

Atmospheric transport and rainfall created localized, irregular contamination hotspots that extended well past the arbitrary $30\,\text{km}$ evacuation zone.

According to the Chernobyl notes, what fraction of thyroid cancer cases in the cited study was attributed to radiation?

A. 75% B. 50% C. 37% D. 25%

A. 75%

In the cited screening cohort of individuals exposed as children or adolescents, approximately $75\%$ of detected thyroid malignancies were radiation-attributable.

Which value is listed for a chest CT in the common-dose table?

A. 7 mSv B. 1.8 mSv C. 0.1 mSv D. 0.005 mSv

A. 7 mSv

A standard diagnostic computed tomography (CT) scan of the chest delivers an effective dose of approximately $7\,\text{mSv}$.

Which value is listed for a chest X-ray in the common-dose table?

A. 1 mSv B. 0.02 mSv C. 0.1 mSv D. 7 mSv

C. 0.1 mSv

A two-view plain diagnostic chest radiograph delivers an average effective dose of approximately $0.1\,\text{mSv}$.

What annual dose limit is listed for a nuclear energy worker in the common-dose table?

A. 1 mSv B. 100 mSv C. 150 mSv D. 50 mSv

D. 50 mSv

The occupational annual effective dose limit for a nuclear energy worker is listed at $50\,\text{mSv}$ in any single year (with a 5-year cumulative limit of $100\,\text{mSv}$).

What does the radiation weighting factor ($w_R$) account for?

A. Differences in biological effect due to radiation type and energy/quality B. Differences in tumour size only C. Differences in treatment volume only D. Differences in patient age only

A. Differences in biological effect due to radiation type and energy/quality

The radiation weighting factor adjusts physical absorbed dose to reflect the relative biological effectiveness (RBE) of different radiation types and Linear Energy Transfer (LET) profiles.

What is the SI unit for equivalent dose and effective dose?

A. Gray (Gy) B. Becquerel (Bq) C. Coulomb per kilogram only D. Sievert (Sv)

D. Sievert (Sv)

While absorbed dose is quantified in grays ($\text{Gy}$), equivalent and effective doses use the sievert ($\text{Sv}$) to incorporate biological weighting.

What radiation weighting factor ($w_R$) is listed for photons?

A. 10 B. 20 C. 1 D. 2

C. 1

Electromagnetic radiations such as X-rays and gamma photons are sparsely ionizing (low-LET) and are assigned a reference radiation weighting factor of $w_R = 1$.

What radiation weighting factor ($w_R$) is listed for protons and charged pions in the source table?

A. 10 B. 1 C. 2 D. 20

C. 2

Protons and charged pions have an intermediate linear energy transfer and are assigned a radiation weighting factor of $w_R = 2$.

What is the sum of all tissue weighting factors ($w_T$) across the human body in the source table?

A. 1 B. 10 C. 0.5 D. 100

A. 1

Tissue weighting factors ($w_T$) represent fractional contributions to total radiation detriment and sum to exactly $1$ over the entire organism.

Which risk model is described as favored by BEIR for assessment of atomic-bomb survivors?

A. No-risk model B. Threshold-only deterministic model C. Time-dependent relative risk D. Absolute risk only

C. Time-dependent relative risk

The Biological Effects of Ionizing Radiation (BEIR) committee selected a time-dependent relative-risk model that modifies baseline risk according to attained age, age at exposure, and latency.

What does LSS stand for in the atomic-bomb survivor research?

A. Longitudinal Somatic Syndrome B. Low Sensitivity Screening C. Linear Survival Score D. Life Span Study

D. Life Span Study

The Life Span Study (LSS) is the long-term epidemiological investigation tracking approximately $120{,}000$ Hiroshima and Nagasaki atomic-bomb survivors.

What long-term temporal pattern is described for leukemia incidence among atomic-bomb survivors?

A. It never increased B. It increased at a constant rate forever C. It only appeared before exposure D. It rose relatively soon after exposure, then levelled off

D. It rose relatively soon after exposure, then levelled off

Leukemia showed a short latency period, peaking approximately $5\text{–}7\,\text{years}$ post-detonation before declining back toward baseline.

What long-term temporal pattern is described for solid cancers after atomic-bomb exposure?

A. They appeared later and continued increasing over time B. They occurred only in utero C. They peaked immediately and disappeared D. They were unaffected by time since exposure

A. They appeared later and continued increasing over time

Unlike leukemia, excess radiation-induced solid malignancies demonstrated a minimum latency of over a decade and remained elevated across the survivors' lifetimes.

What was the scale of the Mega Mouse project by the end of the study?

A. About 7 million mice B. About 45 mice C. About 120,000 mice D. About 3,300 mice

A. About 7 million mice

The Russell Mega Mouse project evaluated approximately $7\times 10^6$ mice to quantify heritable germline mutation rates induced by ionizing radiation.

According to the source notes, what interval in humans was suggested between irradiation and conception to minimize genetic consequences?

A. About 2 weeks B. About 5 years C. About 2 days D. About 6 months

D. About 6 months

A minimum delay of approximately $6\,\text{months}$ is recommended after therapeutic or significant radiation exposure before attempting conception to clear irradiated gametes.

According to the source notes, what is the ideal-dose goal on a therapeutic window diagram?

A. Lowest possible dose even if tumour control is poor B. 100% tumour control regardless of severe normal-tissue injury C. Zero tumour control with no normal tissue exposed D. High tumour control (about 80–90%) with low acceptable normal-tissue damage (about 20% or less)

D. High tumour control (about 80–90%) with low acceptable normal-tissue damage (about 20% or less)

The optimal therapeutic ratio optimizes TCP to around $80\text{–}90\%$ while maintaining NTCP below an acceptable threshold ($\le 20\%$).

What occurs during the initiation stage of carcinogenesis in the source notes?

A. A normal cell is exposed to something that alters DNA and the damage is not repaired B. A tumour shrinks after radiation C. Only a blood vessel is formed D. An established metastasis colonizes a distant organ

A. A normal cell is exposed to something that alters DNA and the damage is not repaired

Initiation involves the induction of an irreversible genetic mutation caused by an unrepaired or misrepaired carcinogen-induced DNA lesion.

What best describes the promotion stage of carcinogenesis?

A. Permanent death of the initiated cell B. Repair of all DNA damage C. Expansion of a clone or clump of initiated cells, often with long-term exposure D. Immediate metastatic spread to every organ

C. Expansion of a clone or clump of initiated cells, often with long-term exposure

Promotion is the non-mutagenic clonal expansion of initiated cells driven by mitogenic stimuli, hormones, or sustained inflammatory exposure.

Why can familial retinoblastoma develop after only one additional somatic mutation?

A. A second tumour always provides the mutation B. Both RB1 copies are always normal at birth C. The child already has one faulty RB1 copy D. RB1 is a viral promoter

C. The child already has one faulty RB1 copy

In familial retinoblastoma, a germline mutation knocks out one $RB1$ allele in every somatic cell, meaning only one additional 'hit' in a retinoblast is required for tumorigenesis.

What does LTR stand for in the retroviral oncogene-activation notes?

A. Low threshold radiation B. Long terminal repeat C. Late tissue reaction D. Linear tumour response

B. Long terminal repeat

Long Terminal Repeats (LTRs) are identical DNA sequences flanking retroviral genomes that act as strong promoters/enhancers capable of activating adjacent proto-oncogenes.

What does HSR refer to in the cytogenetic gene-amplification notes?

A. Homogeneously staining regions within a chromosome B. High-sensitivity radiographs C. A gene outside the chromosome D. A type of apoptosis caspase

A. Homogeneously staining regions within a chromosome

Homogeneously Staining Regions (HSRs) are intrachromosomal segments composed of amplified, duplicated gene segments that lack normal Giemsa banding patterns.

Which cellular state is an irreversible cell-cycle arrest where the cell remains metabolically active but ceases dividing?

A. Senescence B. Metastasis C. Quiescence D. Intravasation

A. Senescence

Senescence represents permanent mitotic arrest triggered by telomere shortening (replicative senescence) or severe DNA stress, unlike reversible quiescence ($G_0$).

Which caspases serve as the initiators in the apoptotic pathways?

A. Caspases 1, 2 and 4 B. Caspases 3, 6 and 7 C. Caspases 8 and 9 D. Caspases 5, 10 and 12

C. Caspases 8 and 9

Caspase-$8$ (extrinsic pathway) and caspase-$9$ (intrinsic pathway) are the initiator caspases that undergo auto-cleavage to activate downstream executioners.

Which caspases serve as the executioner (effector) caspases in apoptosis?

A. Caspases 1 and 2 B. Caspases 8 and 9 C. Caspases 10 and 12 D. Caspases 3, 6 and 7

D. Caspases 3, 6 and 7

Effector caspases ($3$, $6$, and $7$) systematically dismantle the cell by cleaving structural proteins, nuclear lamins, and ICAD.

Which group contains pro-apoptotic BCL-2 family proteins?

A. Bax, Bak, Bid and Bim B. VEGF, VHL and TSP-1 C. Bcl-2, Bcl-xL and Mcl-1 D. RB1, p16 and ATM

A. Bax, Bak, Bid and Bim

Bax, Bak, Bid, and Bim promote mitochondrial outer membrane permeabilization (MOMP), facilitating the release of cytochrome c into the cytoplasm.

Which group contains anti-apoptotic BCL-2 family proteins?

A. MRE11, NBN and RAD50 B. Caspases 3, 6 and 7 C. Bax, Bak, Bid and Bim D. Bcl-2, Bcl-xL and Mcl-1

D. Bcl-2, Bcl-xL and Mcl-1

Bcl-2, Bcl-xL, and Mcl-1 preserve mitochondrial membrane integrity by binding and neutralizing pro-apoptotic BH3-only proteins.

What is intravasation in the metastatic cascade?

A. Growth at a distant site B. Apoptosis after detachment C. Entry of tumour cells into blood or lymphatic vessels D. Exit of tumour cells from vessels into distant tissue

C. Entry of tumour cells into blood or lymphatic vessels

Intravasation is the active trans-endothelial migration of cancer cells across the vessel wall into the bloodstream or lymphatics.

What is extravasation in the metastatic cascade?

A. Tumour cells leave blood/lymphatic vessels and enter tissue B. Tumour cells degrade DNA C. Tumour cells enter vessels D. A tumour forms new vessels

A. Tumour cells leave blood/lymphatic vessels and enter tissue

Extravasation is the process whereby circulating tumour cells arrest in distant capillaries, penetrate endothelial barriers, and invade foreign parenchyma.

What is the defining characteristic of a nonsense mutation?

A. A mutation that substitutes one amino acid for another B. A gene copy added outside a chromosome C. A mutation that introduces a premature stop codon D. A normal gene sequence

C. A mutation that introduces a premature stop codon

A nonsense mutation alters a nucleotide triplet into a stop codon (UAA, UAG, or UGA), leading to premature polypeptide chain termination.

Which defect is associated with radiosensitive severe combined immunodeficiency (SCID) in the notes?

A. Accelerated tumour repopulation B. Defective non-homologous end joining (NHEJ) C. Increased E-cadherin adhesion D. Excessive TSP-1 expression

B. Defective non-homologous end joining (NHEJ)

Radiosensitive SCID arises from genetic mutations in non-homologous end joining machinery (such as Artemis/$DCLRE1C$, DNA-PKcs/$PRKDC$, or $LIG4$), impairing both V(D)J recombination and double-strand break repair.