Arab Board Oncology Part 1 cheat sheet

Hallmarks include sustained proliferation, evasion of growth suppressors, resistance to apoptosis, replicative immortality, angiogenesis, invasion/metastasis, genomic instability, immune evasion, and deregulated metabolism.

Oncogenes are gain-of-function; tumour suppressor genes are loss-of-function and usually require biallelic inactivation (two-hit).

G1/S checkpoint involves RB and p53; G2/M checkpoint involves ATM/ATR and CHK1/CHK2.

Intrinsic apoptosis: BAX/BAK permeabilize mitochondria, cytochrome c release activates caspase-9. Extrinsic: Fas/TRAIL activates caspase-8.

Hypoxia stabilizes HIF-1α, driving VEGF and angiogenesis.

Warburg effect: cancer cells favor aerobic glycolysis even with oxygen.

EMT: loss of E-cadherin and gain of vimentin promotes invasion and metastasis.

Telomerase reactivation maintains telomeres and supports replicative immortality.

Carcinogenesis stages: initiation (irreversible genetic damage), promotion (clonal expansion), progression (additional mutations, invasion).

Direct carcinogens are active as parent compounds; indirect carcinogens (procarcinogens) require metabolic activation, often by cytochrome P450.

Knudson two-hit: hereditary retinoblastoma inherits one RB1 mutation; bilateral/early tumours; sporadic requires two somatic hits.

Driver mutations confer growth advantage; passenger mutations are neutral and accumulate with genomic instability.

Hereditary syndromes: BRCA1/2 (HBOC), MMR (Lynch), TP53 (Li-Fraumeni), APC (FAP), MEN1/RET (MEN).

Recurrent translocations: t(9;22) BCR-ABL in CML; t(15;17) PML-RARA in APL; t(8;21) RUNX1-RUNX1T1 in AML.

Genomic instability phenotypes include microsatellite instability (MMR loss) and chromosomal instability (aneuploidy).

Promoter hypermethylation can silence tumour suppressor genes, an epigenetic mechanism without DNA sequence change.

CD8+ T cells recognize antigen on MHC I; CD4+ T cells recognize antigen on MHC II.

CTLA-4 inhibits T-cell activation early in lymph nodes; PD-1/PD-L1 inhibits effector T cells in peripheral tissues.

Checkpoint inhibitors include ipilimumab (CTLA-4), nivolumab/pembrolizumab (PD-1), and atezolizumab/durvalumab (PD-L1).

Predictive biomarkers for checkpoint blockade include MSI-high/dMMR, high TMB, and PD-L1 expression (context dependent).

CAR-T cells are engineered to bind surface antigens independent of MHC; cytokine release syndrome and neurotoxicity are key toxicities.

Immunoediting phases: elimination, equilibrium, escape.

Tumour microenvironment can suppress immunity via Tregs, myeloid-derived suppressor cells, M2 macrophages, and TGF-β.

Immune-related adverse events can affect skin, colon, liver, lung, thyroid, and pituitary; early steroids are used for severe events.

Cell-cycle-specific drugs act in a specific phase (antimetabolites S phase; taxanes M phase); cell-cycle-nonspecific drugs act throughout.

Alkylating agents crosslink DNA; examples include cyclophosphamide, cisplatin, and melphalan.

Antimetabolites include methotrexate, 5-fluorouracil, and gemcitabine; they interfere with nucleotide synthesis.

Topoisomerase I inhibitors: irinotecan/topotecan; topoisomerase II inhibitors: etoposide/anthracyclines.

Anthracyclines cause cumulative dose-dependent cardiotoxicity; dexrazoxane can reduce risk.

Cisplatin toxicities: nephrotoxicity, ototoxicity, peripheral neuropathy, and severe emesis.

High-dose methotrexate requires leucovorin rescue and urine alkalinization.

5-FU toxicity is increased in dihydropyrimidine dehydrogenase deficiency.

Absorbed dose unit: 1 Gy = 1 J/kg. Equivalent dose: 1 Sv = absorbed dose × radiation weighting factor.

Linear quadratic model: S = exp(−αD − βD²). α/β ratio is high for early-responding tissues and tumours, low for late-responding tissues.

Fractionation exploits the 4 R's: repair, redistribution, repopulation, reoxygenation.

Oxygen enhancement ratio (OER) is about 2.5–3 for sparsely ionizing radiation; hypoxia reduces radiosensitivity.

Inverse square law: dose rate from a point source is inversely proportional to the square of distance.

BED = D × (1 + D/(α/β)) for fractionated radiotherapy; it compares schedules using the same α/β.

Brachytherapy delivers dose by placing sources near or inside the tumour; dose falls off steeply with distance.

Normal tissue tolerance depends on dose per fraction, total dose, volume irradiated, and intrinsic radiosensitivity.

H&E staining shows tissue architecture and cell morphology; formalin fixation preserves structure but can degrade nucleic acids.

Grade describes differentiation and mitotic activity; stage describes anatomical extent and is generally the stronger prognostic factor.

R0: no residual tumour at margins; R1: microscopic residual; R2: macroscopic residual.

Lymphovascular invasion and perineural invasion are adverse prognostic features.

Frozen section provides rapid intraoperative diagnosis, mainly for margin status or metastasis.

Immunohistochemistry identifies cell lineage and predictive markers, e.g., cytokeratin, CD45, ER, HER2.

Special stains: mucin (PAS/AB), melanin (Fontana-Masson), iron (Perls), amyloid (Congo red).

TNM staging is pathological (pTNM) when based on resection specimens; clinical staging uses imaging and examination.

PCR detects specific DNA/RNA sequences; RT-PCR quantifies RNA; digital PCR offers absolute quantification.

FISH detects gene rearrangements and amplifications, e.g., HER2 amplification, ALK/ROS1 rearrangements.

Next-generation sequencing enables multigene panels and detection of mutations, fusions, copy-number changes, and TMB.

Liquid biopsy uses circulating tumour DNA/cells; useful for monitoring and resistance detection; sensitivity falls with low tumour burden.

Tumour markers: CEA (colorectal), CA19-9 (pancreatic), AFP (hepatocellular), hCG (germ cell), PSA (prostate), CA-125 (ovarian).

Tumour markers are generally not diagnostic alone; benign conditions can elevate them and early cancers may not.

MSI/dMMR testing predicts Lynch syndrome and immunotherapy benefit.

HER2 status is assessed by IHC and/or ISH; IHC 3+ is positive, IHC 2+ requires ISH.

CT is preferred for staging lung, liver, and bone lesions; iodinated contrast can cause allergic reactions and nephropathy.

MRI has superior soft-tissue contrast; gadolinium contrast carries a risk of nephrogenic systemic fibrosis in severe renal impairment.

FDG PET-CT detects glucose-avid tumours; false positives occur with inflammation/infection; false negatives occur with low-avidity tumours.

Ultrasound is useful for thyroid, breast, and abdominal lesions; operator dependent.

Bone scan (Tc-99m) detects osteoblastic metastases; false positives occur with trauma, infection, and degenerative disease.

RECIST 1.1 uses CT/MRI; target lesions are measurable, up to five total and two per organ.

Response categories by target lesion sum: CR disappearance; PR ≥30% decrease; PD ≥20% increase or new lesions; SD between PR and PD.

TNM: T = primary tumour extent, N = regional nodes, M = distant metastasis.

Stage groups combine T, N, M, and sometimes grade or biomarkers into prognostic categories.

RECIST 1.1 target lesions: up to 5 total, max 2 per organ; longest diameter sum is tracked.

RECIST response: CR = disappearance; PR = ≥30% decrease; PD = ≥20% increase from nadir and ≥5 mm absolute increase, or new lesions; SD otherwise.

Non-target lesions are assessed qualitatively; unequivocal progression can define PD even without target lesion change.

iRECIST adds immune response criteria to avoid stopping immunotherapy for pseudoprogression; confirmation is required.

PET response uses metabolic activity; Deauville score is used in lymphoma.

Downstaging refers to reduction in stage after neoadjuvant therapy; it differs from response assessment.

Sensitivity = TP/(TP+FN); specificity = TN/(TN+FP); PPV = TP/(TP+FP); NPV = TN/(TN+FN).

Relative risk = incidence in exposed / incidence in unexposed; odds ratio approximates RR for rare outcomes.

Hazard ratio compares hazard rates over time; HR = 1 means no difference.

p-value is the probability of observing data at least as extreme if the null hypothesis is true; it is not the probability the null is true.

Type I error = α (false positive); type II error = β (false negative); power = 1 − β.

95% confidence interval excludes the null value if the p-value is <0.05 (for a two-sided test).

Kaplan-Meier estimates survival over time; log-rank test compares survival curves.

Cox proportional hazards model estimates hazard ratios adjusting for covariates.

Phase I: safety, dose-finding, pharmacokinetics; phase II: efficacy and further safety; phase III: comparative effectiveness; phase IV: post-marketing surveillance.

Randomization balances known and unknown confounders; allocation concealment prevents selection bias.

Blinding reduces performance and detection bias; double-blind means both participants and investigators are unaware.

Intention-to-treat analysis preserves randomization; per-protocol analysis can introduce bias.

Confounding occurs when a third variable is associated with both exposure and outcome.

Systematic reviews and meta-analyses pool studies; heterogeneity is assessed with I² and forest plots.

Levels of evidence: systematic reviews of RCTs > individual RCTs > cohort studies > case-control > case series.

CONSORT reporting standards apply to randomized trials.

Incidence counts new cases per population per time; prevalence counts all existing cases at a point or period.

Crude rates reflect population age structure; age-standardized rates allow comparison across populations.

Mortality rate = deaths from cancer per population per time; case fatality = deaths among diagnosed cases.

Relative risk compares incidence in exposed versus unexposed; attributable risk is the excess incidence in exposed.

Case-control studies estimate odds ratios; cohort studies estimate relative risks.

Screening can increase measured incidence by detecting preclinical disease (lead-time bias).

Cancer registries provide population-based incidence, mortality, and survival data.

Herd immunity reduces transmission when a sufficient proportion is immune.

Primary prevention reduces exposure (tobacco, HPV, HBV, alcohol, obesity); secondary prevention is screening and early detection.

HPV vaccination prevents cervical and other HPV-related cancers; it does not treat existing infection.

HBV vaccination reduces hepatocellular carcinoma risk.

Smoking cessation lowers lung and other cancer risks; risk declines over time after quitting.

Breast screening: mammography every 1–2 years in appropriate age groups; false positives and overdiagnosis are harms.

Colorectal screening: colonoscopy or FIT; FIT positive requires colonoscopy.

Cervical screening: cytology and/or HPV testing; HPV testing is more sensitive.

Lung screening with low-dose CT is for high-risk smokers; it reduces lung cancer mortality.

PSA screening remains controversial because of overdiagnosis and false positives.

Febrile neutropenia: fever ≥38.3°C once or ≥38.0°C sustained plus ANC <500/µL or expected to fall; urgent cultures and empirical antibiotics.

G-CSF reduces duration of neutropenia and febrile neutropenia risk; primary prophylaxis is based on regimen risk.

Antiemetics: 5-HT3 antagonists, NK1 antagonists, dexamethasone, olanzapine; match to emetogenic risk.

Mucositis management includes oral care, analgesia, and nutritional support; palifermin is used in selected settings.

Cancer-associated VTE: low-molecular-weight heparin or DOACs are used for treatment; DOACs have interactions.

Bone health: bisphosphonates or denosumab for bone metastases; monitor calcium and renal function.

Palliative care improves quality of life and can be integrated early with anticancer therapy.

Psychosocial support includes screening for distress, depression, and anxiety.

WHO analgesic ladder: non-opioid → weak opioid → strong opioid, with adjuvants at any step.

Opioid dosing: titrate to effect; manage constipation with laxatives; naloxone reverses overdose.

Spinal cord compression: urgent MRI and dexamethasone; neurosurgery or radiotherapy may be needed.

SVC syndrome: facial swelling, distended neck veins, dyspnoea; urgent imaging and supportive care.

Tumour lysis syndrome: hyperkalaemia, hyperphosphataemia, hyperuricaemia, hypocalcaemia; prevent with hydration and allopurinol/rasburicase.

Hypercalcaemia of malignancy: IV fluids, bisphosphonates, and calcitonin for severe cases.

Malignant pericardial effusion can cause tamponade; urgent pericardiocentesis may be lifesaving.

Airway obstruction from tumour requires urgent assessment; steroids, radiotherapy, or stenting may be used.

Informed consent requires capacity, disclosure of diagnosis/treatment/alternatives/risks/benefits, understanding, and voluntariness.

Confidentiality can be breached only with consent or when required by law/public safety.

Decision-making capacity: understand information, appreciate consequences, reason, and communicate a choice.

Breaking bad news can use SPIKES: setting, perception, invitation, knowledge, emotions, strategy.

Research ethics: institutional review board approval, informed consent, risk minimization, and equipoise.

Conflicts of interest must be disclosed and managed; they can affect judgment and public trust.

End-of-life care includes advance care planning, symptom control, and respect for patient values.

Cultural competence and interpreter services improve communication and equity.