Arab Board Oncology Part 1 key terms

A gene that, when mutated or overexpressed, drives uncontrolled cell growth. Oncogenes typically arise from normal proto-oncogenes and act dominantly, so an alteration in one copy can contribute to cancer development.

A gene whose normal function restrains cell division or repairs DNA damage. Cancer usually requires loss of both copies, so these genes behave recessively at the cellular level and are often inactivated by deletion or mutation.

The model stating that inherited cancer syndromes need one germline mutation plus a second somatic event to inactivate both copies of a tumour suppressor gene, explaining earlier onset and bilateral disease in hereditary retinoblastoma.

A genetic alteration that directly gives a cancer cell a growth or survival advantage and contributes to the malignant phenotype. Targeting a driver mutation with matched therapy can produce tumour shrinkage.

A situation where loss of either of two genes alone is tolerable, but losing both kills the cell. This principle underlies PARP inhibitor use in tumours with homologous recombination deficiency such as BRCA-mutated cancers.

A monoclonal antibody that blocks inhibitory receptors such as CTLA-4, PD-1 or PD-L1, releasing brakes on T cells so the immune system attacks tumour cells. Effects may be delayed and can include autoimmune toxicity.

The number of somatic mutations per megabase of tumour DNA. A high burden often generates more neoantigens and predicts better response to immune checkpoint blockade, though thresholds and assays vary between studies and laboratories.

Treatment in which a patient's T lymphocytes are genetically engineered to express a chimeric antigen receptor recognising a specific tumour antigen, then expanded and reinfused. Main risks include cytokine release syndrome and neurotoxicity.

Autoimmune toxicities caused by immune checkpoint blockade, commonly affecting skin, gut, thyroid, liver and lungs. They can occur weeks after treatment ends and are managed with corticosteroids and, in severe cases, additional immunosuppression.

The ratio between the dose of a drug that causes unacceptable toxicity and the dose that produces the desired effect. A narrow index means small dose changes can cause harm or loss of efficacy.

The principle that chemotherapy kills a constant fraction, not a fixed number, of cancer cells per dose. Repeated cycles are therefore needed to reduce residual disease, and it underpins combination and adjuvant chemotherapy.

The amount of drug delivered per unit of time, usually expressed as milligrams per square metre per week. Reducing dose or delaying cycles lowers dose intensity and may compromise cure rates in chemotherapy-sensitive tumours.

Dividing a radiation dose into several smaller treatments, usually given once daily. This spares normal tissues that repair damage well while still allowing tumour cell killing, and it is described mathematically by the linear-quadratic model.

A mathematical description of cell survival after radiation in which killing depends on dose and on the alpha/beta ratio of the tissue. It explains why fraction size matters more for late-responding normal tissues.

The ratio of radiation dose needed to achieve the same cell kill in low versus normal oxygen conditions. Oxygen fixes radiation-induced DNA damage, so hypoxic tumour cells are relatively radioresistant, supporting approaches that improve oxygenation.

The SI unit of absorbed radiation dose, equal to one joule per kilogram. It quantifies the physical energy deposited in tissue, while the sievert quantifies biological effect for radiation protection purposes.

A technique using antibodies tagged with a chromogen to detect specific proteins in tissue sections. It helps confirm tumour type and origin and assesses predictive markers such as hormone receptors, HER2 and mismatch repair proteins.

The pathological description of whether cancer cells reach the cut edge of a surgically removed specimen. R0 means no tumour at the margin, R1 microscopic involvement and R2 macroscopic residual disease, all with prognostic importance.

A pathologist's assessment of how closely tumour cells resemble the normal tissue of origin, usually based on differentiation, mitotic activity and nuclear features. Higher grade generally indicates more aggressive behaviour and poorer prognosis.

Fragments of tumour-derived DNA detectable in blood plasma. It can be used to monitor response, detect resistance mutations and identify residual disease, though sensitivity is limited when tumour burden is low.

A change in the length of short repeated DNA sequences caused by defective mismatch repair. It occurs in Lynch syndrome and some sporadic tumours and predicts strong benefit from immune checkpoint inhibitors regardless of tumour type.

A protein or other substance measurable in blood that is produced by certain cancers or in response to them. Markers such as AFP or CA-125 help with monitoring and sometimes diagnosis, but most are too non-specific for screening.

A semi-quantitative measure of tracer accumulation on PET imaging, normalised to injected activity and body size. Higher values suggest more metabolically active tissue, but uptake is not specific for malignancy.

Magnetic resonance imaging that combines several sequences, such as T2-weighted, diffusion-weighted and dynamic contrast-enhanced images, to characterise tissue. It improves detection and local staging, notably for prostate cancer.

The system describing extent of disease by primary tumour size and invasion (T), regional lymph node involvement (N) and distant metastasis (M). The combined score groups patients and guides prognosis and treatment choice.

Response Evaluation Criteria in Solid Tumours: a standardised method measuring change in the sum of target lesion diameters on imaging. It defines complete response, partial response, stable disease and progressive disease for solid tumours in trials.

A six-point scale from 0 to 5 describing a patient's functional ability, from fully active to dead. It guides treatment intensity, eligibility for trials and prognosis independently of tumour stage.

Analysis in which participants are evaluated in the group to which they were randomised, regardless of whether they received the assigned treatment. It preserves randomisation and gives a realistic estimate of real-world effectiveness.

In survival analysis, the ratio of the instantaneous risk of an event in one group compared with another over time. A value below one indicates lower risk in the treatment group.

The number of patients who must receive an intervention for one additional patient to benefit. It is the reciprocal of the absolute risk reduction, and lower values indicate greater clinical benefit.

A range of values around an estimate that is likely to contain the true population value with a specified probability, commonly 95%. Its width reflects precision and helps judge the clinical importance of findings.

The number of new cases of a disease arising in a defined population over a stated period, usually expressed per 100,000 person-years. It measures the risk of developing disease and allows comparison between populations.

The apparent survival gain created when screening advances diagnosis earlier without postponing death. Survival measured from diagnosis lengthens, so mortality rather than survival is the preferred endpoint in screening studies.

Detection of a cancer that would never have caused symptoms or death during the patient's lifetime. It leads to unnecessary treatment and inflates survival statistics, and is an important harm of screening programmes.

Fever with an absolute neutrophil count below 0.5 × 10⁹/L, or expected to fall below that level. It is an oncologic emergency requiring prompt blood cultures and empirical broad-spectrum antibiotics.

A metabolic emergency caused by rapid destruction of malignant cells, producing hyperkalaemia, hyperphosphataemia, hyperuricaemia and hypocalcaemia. It can cause acute kidney injury and arrhythmias and is prevented with hydration and hypouricaemic agents.

Compression of the spinal cord or cauda equina by tumour, causing back pain, weakness, sensory loss and sphincter dysfunction. It needs urgent imaging and corticosteroids with definitive radiotherapy or surgery to preserve function.

Obstruction of the superior vena cava by tumour or thrombus, producing facial and upper limb swelling, distended neck veins and breathlessness. Management includes supportive measures and urgent treatment of the underlying malignancy.

A patient's voluntary agreement to a procedure or treatment after receiving understandable information about its purpose, benefits, risks, alternatives and the right to refuse. It requires decision-making capacity and proper documentation.

A six-step protocol for breaking bad news: setting up the interview, assessing perception, obtaining invitation, giving knowledge, addressing emotions and summarising strategy. It structures difficult conversations in oncology practice.