EBOT cheat sheet

TNM staging: T = primary tumour size/invasion, N = regional nodes, M = distant metastasis; prefix c = clinical, p = pathological, y = post-neoadjuvant, r = recurrent.

Grade describes differentiation (G1 well to G4 undifferentiated); stage describes anatomical extent. Grade is a biological descriptor, not a substitute for stage.

Performance status: ECOG 0 fully active to 4 completely disabled; 5 = dead. Karnofsky 100 to 0 in steps of 10. Documented PS drives treatment intensity and trial eligibility.

Tissue diagnosis before definitive systemic therapy is mandatory except in emergencies (e.g., superior vena cava syndrome with a known histology, or a clearly palliative setting where biopsy is unsafe).

A single biopsy may under-represent tumour heterogeneity; predictive biomarker testing (e.g., ER, HER2, EGFR, PD-L1, MSI) should be done on adequate tissue, preferably a recent metastatic site.

Response criteria: RECIST 1.1 uses sum of longest diameters of target lesions; complete response = disappearance of all target lesions and nodes <10 mm short axis; progressive disease = ≥20% increase and ≥5 mm absolute increase.

Paraneoplastic syndromes are remote effects not explained by local invasion or metastasis: hypercalcaemia (PTHrP, squamous), SIADH (small cell), Cushing (ectopic ACTH), Lambert-Eaton (small cell).

Diagnostic staging must precede curative-intent local therapy; PET-CT changes stage and management in a substantial minority of NSCLC, lymphoma and head-and-neck cancers.

Cytotoxic chemotherapy is cell-cycle phase-dependent or -independent; log-kill kinetics means fraction of cells killed is constant, so dose intensity and schedule matter more than single-dose size.

Nadir typically occurs 7-14 days after chemotherapy; febrile neutropenia is a medical emergency requiring immediate empirical broad-spectrum antibiotics.

Targeted agents require a matching molecular alteration (e.g., EGFR/ALK in NSCLC, BRAF V600E in melanoma, HER2 amplification, BCR-ABL1). Test before treating; absence of the target predicts non-response.

Immune checkpoint inhibitors (anti-CTLA-4, anti-PD-1, anti-PD-L1) can produce immune-related adverse events in any organ; colitis, pneumonitis, hepatitis, thyroiditis and hypophysitis are classic. Grade 3-4 irAEs generally require drug interruption, corticosteroids, and specialist input.

Pseudo-progression in immunotherapy is an apparent increase in tumour size or new lesions followed by response; confirm with repeat imaging before abandoning a potentially effective drug.

Antibody-drug conjugates combine a targeting antibody with a cytotoxic payload; toxicities are a mix of antigen-driven and payload-driven effects (e.g., interstitial lung disease, neuropathy, cytopenias).

Pharmacogenomics: DPYD deficiency increases fluoropyrimidine toxicity; UGT1A1*28 increases irinotecan toxicity; TPMT/NUDT15 deficiency increases thiopurine toxicity.

Hormonal therapy (tamoxifen, aromatase inhibitors, androgen deprivation) is systemic therapy; in premenopausal women aromatase inhibitors require ovarian suppression.

Radiation dose is measured in gray (Gy); 1 Gy = 1 joule per kilogram. Fractionation exploits the 4 R's: repair, redistribution, repopulation, reoxygenation.

Conventional fractionation is ~1.8-2 Gy per fraction; hypofractionation uses larger doses per fraction (e.g., 5-8 Gy) with fewer fractions; SABR/SBRT uses ablative doses with steep dose gradients.

The alpha/beta ratio describes tissue radiosensitivity: late-responding tissues have low alpha/beta (~3 Gy), tumours and early-responding tissues higher (~10 Gy). This underpins hypofractionation safety.

Acute radiation toxicity occurs during or within weeks of treatment (mucositis, dermatitis, diarrhoea); late toxicity occurs months to years later (fibrosis, xerostomia, radiation myelopathy, second malignancy).

Radiation recall is an inflammatory reaction in a previously irradiated field triggered by a systemic agent (e.g., doxorubicin, gemcitabine, taxanes) given later.

Stereotactic radiosurgery delivers a single high dose to a small intracranial target; SBRT delivers a few fractions to extracranial targets with image guidance and motion management.

Brachytherapy places a radioactive source in or near the tumour; dose falls off with distance (inverse square law), sparing distant normal tissue.

Radiotherapy is locoregional but not always local: total body irradiation is used for conditioning, and prophylactic cranial irradiation reduces brain relapse in small cell lung cancer.

Margin status: R0 = no residual tumour, R1 = microscopic residual, R2 = macroscopic residual. R0 is the goal of curative resection.

Sentinel lymph node biopsy identifies the first draining node(s) with dye or radiotracer; a positive sentinel node may spare completion lymphadenectomy in selected melanoma and breast cancer cases.

Neoadjuvant therapy is given before surgery to downstage, test in vivo response, and increase resectability; adjuvant therapy is given after surgery to eradicate micrometastasis.

Multidisciplinary tumour board decisions integrate stage, histology, biomarkers, performance status, comorbidity and patient preference; documented MDT discussion is standard of care for complex cases.

Watch-and-wait strategies (e.g., rectal cancer after complete clinical response, some lymphomas, low-risk thyroid cancer) require strict protocolised surveillance.

Surgical oncology principles include en bloc resection, avoidance of tumour spillage, adequate lymph node sampling for accurate staging, and reconstruction planning.

Perioperative risk assessment (ASA class, cardiopulmonary reserve, frailty) determines fitness for resection; minimally invasive approaches are chosen on oncological equivalence, not convenience.

Postoperative complications that alter oncological outcome include anastomotic leak, surgical site infection and delayed adjuvant therapy; timing of adjuvant treatment matters for survival in many cancers.

Pain ladder: non-opioid (paracetamol/NSAID) for mild pain; weak opioid for moderate; strong opioid (morphine, oxycodone, fentanyl, hydromorphone) for severe pain. Titrate to effect and treat breakthrough pain.

Opioid adverse effects: constipation is not self-limiting and requires prophylactic laxatives; nausea and sedation usually tolerance-develop; respiratory depression is the feared toxicity.

Opioid rotation uses equianalgesic dose tables and a 25-50% dose reduction for incomplete cross-tolerance when switching between opioids.

Naloxone reverses opioid-induced respiratory depression but must be titrated to restore breathing without precipitating severe pain or withdrawal.

Antiemetic prophylaxis for highly emetogenic chemotherapy: 5-HT3 antagonist + NK1 antagonist + dexamethasone, often with olanzapine; rescue antiemetic is not a substitute for prophylaxis.

Malignant bowel obstruction in advanced cancer is often managed medically (antisecretory octreotide, dexamethasone, analgesics, antiemetics) rather than surgically.

Palliative care is appropriate alongside curative treatment and improves quality of life; it is not synonymous with end-of-life care or with stopping active treatment.

Advance care planning and goals-of-care discussions should be documented; surrogate decision-makers apply substituted judgement where the patient lacks capacity.

Febrile neutropenia: single temperature ≥38.3 °C or ≥38.0 °C sustained over 1 hour with ANC <0.5 ×10⁹/L (or expected to fall). Start empirical anti-pseudomonal beta-lactam within 60 minutes.

Spinal cord compression: back pain, motor weakness, sensory level, bladder/bowel dysfunction. Give dexamethasone immediately and obtain urgent MRI of the whole spine; definitive treatment is surgery or radiotherapy.

Superior vena cava syndrome: facial/upper limb swelling, distension of neck veins, dyspnoea. Urgent imaging; treat with radiotherapy, stenting, or systemic therapy depending on histology; thrombolysis if thrombotic.

Tumour lysis syndrome: hyperuricaemia, hyperkalaemia, hyperphosphataemia, hypocalcaemia, renal failure. Prevention with hydration and allopurinol (or rasburicase for high risk) is key.

Hypercalcaemia of malignancy: IV fluids plus bisphosphonate or denosumab; calcitonin for rapid but transient control. Correct for albumin.

Neutropenic sepsis, disseminated intravascular coagulation, and immune effector cell-associated neurotoxicity syndrome (ICANS) and cytokine release syndrome (CRS) after CAR-T are oncologic emergencies requiring protocolised grading and treatment.

Malignant pericardial effusion and cardiac tamponade present with hypotension, distended neck veins and muffled heart sounds; urgent pericardiocentesis is diagnostic and therapeutic.

Immune-related adverse events can be life-threatening (grade 4 colitis, pneumonitis, myocarditis); high-dose corticosteroids and, for steroid-refractory cases, infliximab or other immunosuppression are used.

Phase I: safety, dose-finding, maximum tolerated dose. Phase II: efficacy signal and further safety. Phase III: comparative effectiveness against standard of care. Phase IV: post-marketing surveillance.

Randomisation with allocation concealment reduces selection bias; blinding reduces performance and detection bias; intention-to-treat analysis preserves randomisation benefits.

p-value: probability of observing the result (or more extreme) if the null hypothesis is true; it is not the probability that the null is true or that the result will replicate.

Type I error (alpha) = false positive; type II error (beta) = false negative; power = 1 − beta. Sample size depends on effect size, variance, alpha and power.

Hazard ratio compares time-to-event between groups; a HR of 1 means no difference; confidence interval excluding 1 indicates statistical significance at the corresponding alpha.

Absolute risk reduction and number needed to treat (NNT = 1/ARR) convey clinical importance better than relative risk alone.

Levels of evidence: systematic reviews/meta-analyses of RCTs rank highest; single RCTs, cohort studies, case-control studies, case series and expert opinion descend in strength.

Surrogate endpoints (response rate, progression-free survival) may not predict overall survival benefit; regulatory and clinical decisions should weigh both.

Bias types to recognise: lead-time bias, length-time bias, selection bias, attrition bias, publication bias, and confounding by indication.

Informed consent requires capacity, adequate information (diagnosis, options, risks, benefits, alternatives including no treatment), voluntariness and documentation.

Capacity is decision-specific and time-specific; it is assessed by ability to understand, retain, weigh and communicate a decision, not by diagnosis alone.

Confidentiality may be breached only with consent or where legally required or justified to prevent serious harm; disclose the minimum necessary information.

Breaking bad news: establish what the patient knows and wants to know, give information in chunks, check understanding, respond to emotion, and agree next steps.

Medical error disclosure: patients should be told about harmful errors promptly, honestly and with an explanation and apology; this is an ethical and often legal duty.

Conflict of interest must be declared and managed; it includes financial ties, gifts, and institutional or personal relationships that could bias judgement.

Patient safety in oncology: verify patient identity, drug, dose, route and rate at every chemotherapy administration (independent double-check); use standardised order sets and error reporting.

Research ethics: IRB/ethics approval, valid informed consent, risk minimisation, equipoise, and respect for vulnerable populations (children, prisoners, cognitively impaired adults).