Therapeutics 2 : synopsis 1. Basic principles of cancer chemotherapeutic agents 2. General introduction of cancer chemotherapeutic agents ( classification, basic moa , indications and common adrs ) 3. Chemo induced nausea and vomiting 4. Management of breast cancer and leukaemia

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Therapeutics 2 — Cancer Chemotherapy: Complete Synopsis

TOPIC 1 — Basic Principles of Cancer Chemotherapy

1.1 Rationale and Goals

Cancer chemotherapy aims to cause apoptosis or lethal cytotoxic events in cancer cells, halting tumor growth. The attack targets DNA or metabolic pathways critical to cell replication (e.g., purine and pyrimidine synthesis for DNA/RNA).

Most classical agents are non-selective — they affect all proliferating cells, not just neoplastic ones. This is why most carry steep dose-response curves for both benefit and toxicity. Newer targeted therapies (kinase inhibitors, growth factor blockers) have a more favorable adverse effect profile. Immuno-oncology agents (checkpoint inhibitors) allow the patient's own immune system to attack cancer cells but cause autoimmune toxicities rather than myelosuppressive toxicities.

Treatment goals exist on a spectrum:

Goal	Definition
Cure	Long-term disease-free survival; requires eradication of every neoplastic cell
Control	Prevent enlargement/spread; treat as chronic disease
Palliation	Alleviate symptoms in advanced disease without extending survival

— Lippincott Illustrated Reviews: Pharmacology, p. 1211–1212

1.2 Types of Chemotherapy by Timing

Type	Definition
Adjuvant chemotherapy	Given after surgery/radiation to attack residual micrometastases
Neoadjuvant chemotherapy	Given before surgery to shrink the tumor
Maintenance chemotherapy	Lower doses given to prolong remission

1.3 Combination Chemotherapy Principles

Single-drug therapy is inferior to combination therapy in most cancers. Combination regimens are chosen based on:

Different mechanisms of action → additive/synergistic cytotoxicity
Non-overlapping toxicities → allows full doses of each drug
Broader coverage of heterogeneous tumor populations
Prevention of resistance development

Example: R-CHOP for non-Hodgkin lymphoma = Rituximab + Cyclophosphamide + Hydroxydaunorubicin (doxorubicin) + Oncovin (vincristine) + Prednisone Dosages are calculated per body surface area (BSA) and given in intermittent cycles to allow immune system recovery.

— Lippincott Illustrated Reviews: Pharmacology, p. 1213–1214

1.4 Cell Cycle Specificity

Cell Cycle Status	Description
Cell cycle-specific	Effective only against actively dividing cells (S, M phase) — antimetabolites, taxanes, vinca alkaloids
Cell cycle-nonspecific	Toxic in cycling and non-cycling cells — alkylating agents; useful for low-growth-fraction tumors

Rapidly dividing cells (high growth fraction) are more chemosensitive.
Non-dividing cells (G₀) generally survive most chemotherapeutic agents.
Tumor growth follows a Gompertzian curve — small tumors grow faster and are more sensitive; large tumors grow slower and are relatively resistant.

Drug resistance mechanisms include: decreased drug uptake, increased drug efflux (P-glycoprotein), enhanced DNA repair, target enzyme overexpression, and altered apoptotic pathways.

TOPIC 2 — Classification of Chemotherapeutic Agents: MOA, Indications, ADRs

2.1 Alkylating Agents

MOA: Form covalent bonds with DNA bases (guanine N-7 position), causing crosslinks and strand breaks → inhibit DNA replication. Cell cycle nonspecific.

Drug	Key Indications	Key ADRs
Cyclophosphamide	Lymphomas, breast cancer, leukemia	Myelosuppression, hemorrhagic cystitis (prevented by mesna), alopecia, sterility
Ifosfamide	Sarcomas, testicular cancer	Hemorrhagic cystitis (use mesna), nephrotoxicity, neurotoxicity
Busulfan	CML (conditioning for BMT)	Myelosuppression, pulmonary fibrosis, hyperpigmentation
Cisplatin	Testicular, ovarian, lung, bladder	Nephrotoxicity (dose-limiting), ototoxicity, peripheral neuropathy, N/V
Carboplatin	Lung, ovarian, head/neck	Myelosuppression (dose-limiting), less nephrotoxicity than cisplatin
Nitrosoureas (carmustine, lomustine)	Brain tumors (cross BBB)	Myelosuppression (delayed), pulmonary fibrosis

Secondary malignancies are a class-wide concern — platinum agents and topoisomerase inhibitors (etoposide) can cause therapy-related AML.

2.2 Antimetabolites

MOA: Structurally mimic normal metabolites (purines, pyrimidines, folate), interfering with DNA/RNA synthesis. Cell cycle specific (S phase).

Drug	MOA	Key Indications	Key ADRs
Methotrexate (MTX)	Inhibits DHFR → blocks folate metabolism → ↓ thymidylate + purines	ALL, osteosarcoma, lymphoma, RA	Myelosuppression, mucositis, nephrotoxicity (high dose), hepatotoxicity — reversed by leucovorin rescue
5-Fluorouracil (5-FU)	Inhibits thymidylate synthase → ↓ dTMP	Colorectal, gastric, breast cancer	Diarrhea, mucositis, myelosuppression (bolus), hand-foot syndrome (infusion), coronary vasospasm
Capecitabine	Oral prodrug converted to 5-FU in tumor cells	Colorectal, breast cancer	Hand-foot syndrome, diarrhea
6-Mercaptopurine (6-MP)	Inhibits purine synthesis	ALL maintenance	Myelosuppression, hepatotoxicity — reduce dose by 50–75% with allopurinol
Cytarabine (Ara-C)	Incorporated into DNA → chain termination	AML, ALL	Myelosuppression, cerebellar toxicity (high dose)
Fludarabine	Purine analogue, inhibits DNA polymerase	CLL, indolent lymphomas	Myelosuppression, severe immunosuppression (opportunistic infections)
Gemcitabine	Nucleoside analogue; blocks ribonucleotide reductase	Pancreatic, lung, bladder cancer	Myelosuppression, flu-like syndrome, pulmonary toxicity

2.3 Antitumour Antibiotics

MOA: DNA intercalation, free radical generation, topoisomerase II inhibition.

Drug	MOA	Indications	Key ADRs
Doxorubicin (Adriamycin)	DNA intercalation + Topo II inhibition + free radicals	Breast, sarcoma, leukemia, lymphoma	Cardiotoxicity (dose-dependent, irreversible) — CHF; monitor LVEF; use dexrazoxane for cardiac protection; red urine
Daunorubicin	Same as doxorubicin	AML, ALL	Cardiotoxicity
Idarubicin	Same	AML	Cardiotoxicity
Bleomycin	DNA strand breaks via oxidative mechanism	Testicular cancer, Hodgkin lymphoma	Pulmonary fibrosis (dose-limiting), skin reactions; minimal myelosuppression
Mitomycin C	DNA cross-linking (alkylating)	Gastric, bladder cancer	Myelosuppression, hemolytic uremic syndrome

2.4 Plant-Derived Agents

Vinca Alkaloids (Cell cycle specific — M phase)

MOA: Bind β-tubulin → inhibit microtubule polymerization → mitotic spindle arrest

Drug	Indications	Key ADRs
Vincristine	ALL, lymphomas, Wilms tumor	Peripheral neuropathy (dose-limiting), minimal myelosuppression
Vinblastine	Testicular cancer, Hodgkin lymphoma	Myelosuppression (dose-limiting), less neuropathy
Vinorelbine	Lung cancer, breast cancer	Myelosuppression, constipation

Taxanes (Cell cycle specific — M phase)

MOA: Stabilize microtubules → prevent depolymerization → mitotic arrest

Drug	Indications	Key ADRs
Paclitaxel	Breast, ovarian, lung cancer	Neutropenia, peripheral neuropathy, hypersensitivity reactions (premedicate with dexamethasone + diphenhydramine + H₂ blocker)
Docetaxel	Breast, prostate, gastric cancer	Neutropenia, fluid retention/edema (premedicate with dexamethasone)

Topoisomerase Inhibitors

MOA:

Topo I inhibitors (irinotecan, topotecan): prevent DNA religation → strand breaks
Topo II inhibitors (etoposide, teniposide): cause DNA double-strand breaks

Drug	Indications	Key ADRs
Etoposide	Testicular, lung cancer	Myelosuppression, secondary AML
Irinotecan	Colorectal cancer	Severe diarrhea (acute cholinergic or delayed; treat with atropine or loperamide), myelosuppression
Topotecan	Ovarian, lung cancer	Myelosuppression

2.5 Hormonal Agents and Antagonists

MOA: Tumors sensitive to hormones can be blocked by removing hormonal stimulation or using receptor antagonists.

Drug	Class	Indication	ADRs
Tamoxifen	Selective estrogen receptor modulator (SERM)	ER+ breast cancer	Hot flashes, thromboembolism, endometrial cancer
Anastrozole / Letrozole / Exemestane	Aromatase inhibitors	Postmenopausal ER+ breast cancer	Osteoporosis, arthralgias, hot flashes
Leuprolide / Goserelin	LHRH agonists	Prostate cancer, breast cancer	Tumor flare initially, hot flashes, bone loss
Bicalutamide / Flutamide	Androgen receptor antagonists	Prostate cancer	Gynecomastia, hepatotoxicity
Prednisone / Dexamethasone	Glucocorticoids	ALL, lymphoma, multiple myeloma	Immunosuppression, hyperglycemia, osteoporosis

2.6 Targeted / Biologic Agents

Drug Class	Examples	MOA	Indications
Monoclonal antibodies	Rituximab (anti-CD20), Trastuzumab (anti-HER2), Bevacizumab (anti-VEGF)	Receptor/antigen blocking, ADCC	Lymphoma, HER2+ breast cancer, colorectal cancer
Tyrosine kinase inhibitors	Imatinib, Dasatinib	Block BCR-ABL, c-Kit, PDGFR	CML, GIST
EGFR inhibitors	Erlotinib, Gefitinib	Block EGFR signalling	NSCLC
Checkpoint inhibitors	Pembrolizumab (anti-PD-1), Nivolumab	Restore T-cell antitumour activity	Melanoma, NSCLC, TNBC, many solid tumours
Proteasome inhibitors	Bortezomib, Carfilzomib	Inhibit proteasome → promote apoptosis	Multiple myeloma
Immunomodulators	Thalidomide, Lenalidomide	Antiangiogenic, immune modulation	Multiple myeloma

2.7 General ADR Summary by System

System	Common ADRs	Causative Agents
Haematological	Myelosuppression (nadir 7–14 days), anaemia, thrombocytopenia	Most cytotoxic agents
Cardiac	Cardiomyopathy / CHF	Anthracyclines (doxorubicin), trastuzumab
Pulmonary	Pulmonary fibrosis	Bleomycin, busulfan, nitrosoureas
Renal	Nephrotoxicity	Cisplatin, ifosfamide, MTX (high dose)
Bladder	Hemorrhagic cystitis	Cyclophosphamide, ifosfamide → prevent with mesna
Neurological	Peripheral neuropathy	Vincristine, taxanes, cisplatin
GI	N/V, mucositis, diarrhoea	Most agents
Dermatological	Alopecia, hand-foot syndrome	Cyclophosphamide, 5-FU/capecitabine
Reproductive	Sterility, teratogenicity	Alkylating agents

TOPIC 3 — Chemotherapy-Induced Nausea and Vomiting (CINV)

3.1 Epidemiology and Clinical Relevance

70–80% of patients undergoing chemotherapy experience CINV.
10–42% experience anticipatory vomiting (before drug administration — conditioned response).
Young patients and women are more susceptible than older patients and men.
Uncontrolled CINV leads to: dehydration, electrolyte imbalances, nutrient depletion, treatment refusal.

3.2 Types of CINV

Type	Onset	Mechanism
Acute	0–24 hours post-chemo	5-HT₃ receptor activation (serotonin from enterochromaffin cells)
Delayed	24–120 hours post-chemo	Substance P / NK-1 receptor activation
Anticipatory	Before drug given	Conditioned reflex — previous emetic experience

3.3 Emetic Potential of Agents

Emetogenicity	Agents
High (>90%)	Cisplatin, dacarbazine, cyclophosphamide (high dose), doxorubicin
Moderate (30–90%)	Carboplatin, irinotecan, oxaliplatin, doxorubicin (lower dose)
Low (<30%)	Taxanes, etoposide, 5-FU, gemcitabine
Minimal (<10%)	Vincristine, bleomycin, bevacizumab

3.4 Neuroanatomical Pathways

Two key brainstem sites:

Chemoreceptor trigger zone (CTZ) — area postrema, 4th ventricle floor, outside BBB → detects emetic chemicals in blood/CSF; contains D₂ and 5-HT₃ receptors.
Vomiting centre — lateral reticular formation of medulla → coordinates motor vomiting; receives input from CTZ, vestibular system, GI tract, and cortex.

Peripheral mechanism: Chemotherapy damages GI enterochromaffin cells → releases serotonin → activates 5-HT₃ receptors on vagal/splanchnic afferents → signals to medulla.

3.5 Antiemetic Drug Classes

Class	Drugs	MOA	Use
5-HT₃ antagonists	Ondansetron (Zofran), Granisetron, Palonosetron, Dolasetron	Block 5-HT₃ receptors in CTZ and gut	First-line for acute CINV
NK-1 antagonists	Aprepitant, Fosaprepitant (Emend); Netupitant, Rolapitant	Block substance P / NK-1 receptors in CNS	Delayed CINV; combined with 5-HT₃ antagonist + dexamethasone
Corticosteroids	Dexamethasone	Unknown antiemetic mechanism; synergistic	All emetic levels — used as adjunct
Dopamine (D₂) antagonists	Prochlorperazine (Compazine), Metoclopramide	Block D₂ receptors in CTZ	Moderate CINV; rescue
Atypical antipsychotics	Olanzapine	Multiple receptor blockade (D₂, 5-HT₃, H₁)	Highly refractory CINV; adjunct
Cannabinoids	Dronabinol, Nabilone	CB₁ receptor agonists	Refractory or anticipatory CINV
Benzodiazepines	Lorazepam	Anxiolytic, amnestic	Anticipatory CINV
Anticholinergics/H₁	Scopolamine, Dimenhydrinate	Anticholinergic, H₁ block	Motion sickness; not for CTZ-mediated

3.6 Antiemetic Protocol Summary

Emetic Risk	Recommended Regimen
High	5-HT₃ antagonist + NK-1 antagonist + Dexamethasone ± Olanzapine
Moderate	5-HT₃ antagonist + Dexamethasone ± NK-1 antagonist
Low	Dexamethasone alone or D₂ antagonist
Minimal	No routine prophylaxis
Anticipatory	Benzodiazepine (lorazepam) before treatment; behavioural therapy

— Lippincott Illustrated Reviews: Pharmacology, p. 1429–1431

TOPIC 4 — Management of Breast Cancer and Leukaemia

4.1 Breast Cancer Management

Risk Factors

Older age, female sex, BRCA1/BRCA2 mutations (50–85% lifetime risk)
Early menarche, late menopause, nulliparity, late first pregnancy (prolonged estrogen exposure)
Li-Fraumeni syndrome (p53), Cowden syndrome (PTEN), PALB2/CHEK2 mutations
Previous atypical hyperplasia, lobular carcinoma in situ
Ionizing radiation, combined HRT, alcohol

Molecular Subtypes

Subtype	Features	Prognosis
Luminal A	ER+/PR+, HER2−, low grade	Best prognosis; high endocrine therapy sensitivity
Luminal B	ER+/PR+, HER2+/−, higher grade	Worse than Luminal A; some chemo benefit
HER2-enriched	ER−/PR−, HER2+	Intermediate; treat with anti-HER2 agents
Triple-negative (TNBC)	ER−, PR−, HER2−	Worst prognosis; no endocrine/HER2 target; chemotherapy backbone

Staging: TNM System (I–IV)

Stage I & II: early-stage; Stage III: locally advanced; Stage IV: metastatic

Treatment Approach

Surgery:

Lumpectomy + radiation (breast-conserving) vs. mastectomy — equivalent survival in early disease
Sentinel lymph node biopsy for nodal staging

Systemic Therapy:

Modality	Agents	Indication
Adjuvant chemotherapy	Anthracycline-based (AC) + taxane (e.g., AC → paclitaxel)	High-risk early breast cancer
Neoadjuvant chemotherapy	Same regimens; adds pembrolizumab for TNBC	Locally advanced; improves breast conservation
Endocrine therapy — premenopausal	Tamoxifen 20 mg/day × 5–10 years ± LHRH agonist	ER+/PR+ breast cancer
Endocrine therapy — postmenopausal	Aromatase inhibitors (anastrozole 1 mg, letrozole 2.5 mg, exemestane 25 mg daily)	ER+/PR+; ~30% reduction in recurrence vs tamoxifen
HER2-targeted	Trastuzumab (Herceptin) + pertuzumab + taxane	HER2+ cancer; coadminister trastuzumab with taxane
TNBC	Pembrolizumab + chemotherapy (neoadjuvant); capecitabine post-surgery	No hormone/HER2 target
BRCA mutation	PARP inhibitors (olaparib, talazoparib)	Germline BRCA1/2 mutated HER2−
CDK4/6 inhibitors	Palbociclib, ribociclib + aromatase inhibitor	Advanced ER+/HER2−

Key points:

Adjuvant endocrine therapy should be started after completion of chemotherapy.

Women with high clinical but low genomic risk (70-gene signature) gain little from adjuvant chemotherapy.

Tamoxifen is preferred in premenopausal women and men; aromatase inhibitors should NOT be used as monotherapy in premenopausal women.

Radiation: After breast-conserving surgery; also for node-positive disease.

Metastatic breast cancer: Treated as a chronic disease with sequential systemic therapy — endocrine therapy preferred for ER+ (unless visceral crisis), anti-HER2 therapy for HER2+, chemotherapy for TNBC.

— Goldman-Cecil Medicine, p. 2082–2085

4.2 Leukaemia Management

Pre-treatment Considerations (All Leukaemias)

Before starting chemotherapy:

Tumour lysis syndrome (TLS) prophylaxis: Aggressive IV hydration + allopurinol 100–600 mg/day
If very high WBC → rasburicase IV (converts uric acid to allantoin)
Urinary alkalinisation is NOT recommended (risk of xanthine/calcium phosphate precipitation)
Granulocytopenic fever: obtain blood cultures, start empiric broad-spectrum antibiotics
Leukostasis (WBC >100,000/µL → AML early death rate 20%): proceed to induction ASAP

4.2a Acute Lymphoblastic Leukaemia (ALL)

Treatment phases:

Induction (weeks 1–4)
Post-remission / Consolidation
CNS prophylaxis
Maintenance (up to 2–3 years)

Induction Regimen:

Core agents: Vincristine + Prednisone + L-Asparaginase + Daunorubicin (3–4 weeks)
Complete remission achieved in: 90% of children; 80–90% of adults

Post-remission Therapy:

Adults 18–59 with Philadelphia chromosome-positive (Ph+) ALL → add imatinib or dasatinib (BCR-ABL TKI)
High-risk adults → allogeneic stem cell transplantation (SCT) in first remission
Blinatumomab (bispecific CD3/CD19 T-cell engager) and inotuzumab ozogamicin (anti-CD22 antibody-drug conjugate) for relapsed/refractory ALL

CNS Prophylaxis: Intrathecal (IT) methotrexate ± cytarabine; cranial radiation now largely replaced by IT chemo.

Outcomes:

Paediatric ALL: 5-year survival ~90%
Adults (18–40 years): 65–75%; Adults >60: <20%

4.2b Acute Myeloid Leukaemia (AML)

Induction (Fit Adults) — "7+3" Regimen:

Cytarabine 100–200 mg/m²/day × 7 days (continuous infusion)
Daunorubicin 60–90 mg/m²/day × 3 days (or Idarubicin 10–12 mg/m²/day × 3 days)
Complete remission in 60–80% of patients
Profound myelosuppression always follows

Targeted Additions (based on mutations):

FLT3-mutated AML → add midostaurin 50 mg twice daily (days 8–21) during induction and consolidation → improved disease-free survival
IDH1-mutated AML → ivosidenib → extends median OS from 8 to 24 months
Favourable-risk AML → add gemtuzumab ozogamicin (anti-CD33 antibody-drug conjugate) on days 1, 4, 7
AML unfit for intensive chemo → Venetoclax (BCL-2 inhibitor) + azacitidine or decitabine (hypomethylating agents)

Post-remission Therapy:

Favourable risk (CBF AML): high-dose cytarabine (HiDAC) consolidation
Intermediate/Poor risk: allogeneic SCT in first remission (preferred if donor available)

4.2c Acute Promyelocytic Leukaemia (APL) — M3 AML

A special subtype with t(15;17) → PML-RARA fusion → differentiation block.

Treatment (Table 168-3):

Regimen A (preferred — no anthracycline):

Induction: ATRA 45 mg/m²/day orally (divided doses) + Arsenic trioxide (ATO) 0.15 mg/kg/day IV until morphologic remission
Consolidation: ATO 0.15 mg/kg/day × 5 days/week for 4 weeks, every 8 weeks × 4 cycles + ATRA 45 mg/m²/day × 2 weeks every 4 weeks × 7 cycles

Regimen B (with anthracycline):

Induction: ATRA 45 mg/m²/day + Idarubicin 12 mg/m² on days 2, 4, 6, 8
Consolidation: ATRA + Idarubicin, then ATRA + Mitoxantrone, then ATRA + Idarubicin

Critical complication: Differentiation syndrome (DS) — fever, fluid retention, respiratory distress due to rapid differentiation of promyelocytes. Treat with dexamethasone immediately. ATRA and ATO should not be stopped unless severe.

Outcomes: APL has the best prognosis of all AML subtypes — cure rates >90% with ATRA-ATO regimen.

4.2d Chronic Myeloid Leukaemia (CML)

Pathology: t(9;22) Philadelphia chromosome → BCR-ABL fusion gene → constitutive tyrosine kinase activity
Treatment: Tyrosine kinase inhibitors (TKIs) — Imatinib (1st gen), Dasatinib / Nilotinib (2nd gen), Ponatinib (3rd gen, for T315I mutation)
Goal: cytogenetic and molecular remission; most patients do NOT need SCT in chronic phase

4.2e Chronic Lymphocytic Leukaemia (CLL)

Asymptomatic, low-stage: Watch and wait
Treatment when indicated: Venetoclax + obinutuzumab (anti-CD20) or ibrutinib (BTK inhibitor) as 1st-line; FCR (fludarabine + cyclophosphamide + rituximab) for fit patients with IGHV-mutated disease

Quick Reference Summary Table

Topic	Key Points
Chemo principles	Cure → Control → Palliation; Adjuvant/Neoadjuvant; Combination preferred; Cell cycle specific vs. nonspecific
Alkylating agents	DNA crosslinking; non-cell cycle specific; cisplatin → nephrotoxicity; cyclophosphamide → hemorrhagic cystitis (mesna)
Antimetabolites	S-phase specific; MTX → leucovorin rescue; 6-MP + allopurinol → reduce dose 50–75%; 5-FU → hand-foot syndrome
Antibiotics	Doxorubicin → irreversible cardiotoxicity (dexrazoxane); Bleomycin → pulmonary fibrosis
Plant derivatives	Vincristine → neuropathy; Taxanes → neutropenia; stabilise vs. destabilise microtubules
Hormonal	Tamoxifen → endometrial cancer risk; AIs → postmenopausal only; LHRH agonists → initial flare
CINV	Acute (5-HT₃), Delayed (NK-1); prophylaxis: 5-HT₃ + NK-1 + dexamethasone for high-risk
Breast cancer	ER+ → endocrine therapy; HER2+ → trastuzumab; TNBC → pembrolizumab + chemo; BRCA → PARP inhibitor
ALL	Vincristine + Pred + L-Asp + Daunorubicin; Ph+ → imatinib; 90% CR in children
AML	"7+3" = cytarabine + daunorubicin; FLT3 → midostaurin; IDH1 → ivosidenib
APL (M3)	ATRA + Arsenic trioxide; >90% cure; watch for differentiation syndrome
CML	BCR-ABL → imatinib/dasatinib/nilotinib

*Sources: Lippincott Illustrated Reviews: Pharmacology (9781975170561); Goldman-Cecil Medicine (9780323930345)*This is a comprehensive synopsis covering all four topics. Here is a quick orientation:

What's covered:

Basic Principles — Goals of therapy (cure/control/palliation), types of chemotherapy (adjuvant/neoadjuvant/maintenance), combination regimen rationale, cell cycle specificity, drug resistance mechanisms.
Drug Classification & MOA — All major classes: alkylating agents, antimetabolites, antibiotics, vinca alkaloids, taxanes, topoisomerase inhibitors, hormonal agents, and targeted biologics — each with MOA, key indications, and signature ADRs. A system-by-system ADR table is included.
CINV — Types (acute/delayed/anticipatory), the CTZ–vomiting centre pathway, emetogenic potential of drugs, and the full antiemetic protocol by emetogenic risk level.
Breast Cancer — Molecular subtypes (Luminal A/B, HER2, TNBC), staging, surgical options, and the complete systemic therapy algorithm (endocrine, anti-HER2, immunotherapy, PARP inhibitors, CDK4/6 inhibitors). Leukaemia covers ALL (induction protocol, CNS prophylaxis, outcomes), AML ("7+3" regimen, targeted additions), APL (ATRA + arsenic trioxide, differentiation syndrome), CML (BCR-ABL/TKIs), and CLL.

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