Leukemias and Lymphomas for NEET PG — Complete Guide 2026

Version 1.0 — Published February 2026

Haematology-oncology questions are NEET PG staples — the child with pancytopenia, the CML patient in chronic phase, the young adult with mediastinal mass and cervical lymphadenopathy, the alcoholic with DIC and circulating promyelocytes. Recognising the cytogenetic signature (Philadelphia chromosome, t(15;17), t(8;14), t(14;18)) plus the named first-line therapy separates marks. This guide covers acute leukemia classification, CML/CLL, APL, Hodgkin and non-Hodgkin lymphoma, febrile neutropenia, and tumour lysis syndrome. Pair with the medicine subject hub, the anaemia classification guide, and the peripheral smear image-MCQ walkthrough for integrated revision.

Acute leukemias — ALL vs AML

Acute leukemia is defined by ≥20% blasts in bone marrow or peripheral blood (WHO) with differentiation arrest and clonal expansion — splitting into acute lymphoblastic (ALL) and acute myeloid (AML) by lineage.

Epidemiology and presentation:

Cytochemistry and immunophenotype (NEET PG-tested):

Cytogenetics and prognosis:

Management:

• ALL — induction (vincristine + steroid + anthracycline + asparaginase ± TKI if Ph+) → consolidation → CNS prophylaxis (intrathecal methotrexate ± cranial RT) → maintenance (6-MP + MTX × 2–3 years). Blinatumomab (CD19/CD3 BiTE), CAR-T (tisagenlecleucel for refractory paediatric B-ALL)
• AML (non-APL) — "7+3" induction (cytarabine 7 d + anthracycline 3 d) → consolidation (high-dose cytarabine ± allo-HSCT for intermediate/poor risk) → targeted agents (midostaurin for FLT3, ivosidenib for IDH1, enasidenib for IDH2, venetoclax + azacitidine in unfit older patients)
• Paediatric ALL cure ~85–90%; adult ALL cure ~40%; AML cure ~30–40% overall (higher with HSCT)

CML and CLL

Chronic myeloid leukemia (CML) and chronic lymphocytic leukemia (CLL) are chronic leukemias — differing in lineage, cytogenetics, and targeted therapy — and both are high-yield NEET PG vignettes.

Chronic myeloid leukemia (CML):

• Myeloproliferative neoplasm; BCR-ABL1 fusion from t(9;22) Philadelphia chromosome → constitutively active tyrosine kinase
• Incidence 1–2/100,000; median age 55–65
• Three phases — chronic (85%, asymptomatic or fatigue/splenomegaly), accelerated (10–19% blasts), blast crisis (>=20% blasts — behaves like acute leukemia)
• Labs — leukocytosis with full myeloid spectrum (neutrophils, myelocytes, metamyelocytes, promyelocytes, basophilia, eosinophilia); low leukocyte alkaline phosphatase (LAP) score (vs high in leukemoid reaction); splenomegaly
• Diagnosis — bone marrow hypercellular; cytogenetics t(9;22); FISH or RT-PCR for BCR-ABL1 (quantitative PCR for monitoring)
• Treatment:
  • First-line — imatinib 400 mg OD (generic, NEET PG favourite); dasatinib, nilotinib, bosutinib (first-line alternatives)
  • Ponatinib for T315I mutation
  • Asciminib — myristoyl pocket inhibitor for resistant disease
  • Monitoring — BCR-ABL1 IS (international scale) every 3 months; goals: CHR (3 mo), CCyR (6 mo), MMR <0.1% (12 mo), DMR <0.0032%
  • Allo-HSCT reserved for TKI-resistant / blast crisis
• Treatment-free remission possible in sustained DMR for >=2 years

Chronic lymphocytic leukemia (CLL):

• Indolent mature B-cell neoplasm; identical to small lymphocytic lymphoma (SLL) — nodal form
• Commonest adult leukemia in the West; median age 70; rare in East Asia
• Often asymptomatic lymphocytosis on routine check; fatigue, lymphadenopathy, splenomegaly, recurrent infections (hypogammaglobulinaemia), autoimmune complications (AIHA, ITP, PRCA)
• Diagnosis — absolute B-lymphocyte count ≥5,000/μL with typical immunophenotype
• Immunophenotype — CD5+, CD19+, CD20 (dim), CD23+, kappa or lambda light-chain restricted; CD5+ B-cell is the key
• Peripheral smear — mature small lymphocytes, smudge cells (basket cells)
• Cytogenetics / prognosis (FISH panel):

• Staging:

• Treatment:
  • Watch-and-wait for early asymptomatic disease (no survival benefit to early treatment)
  • First-line (symptomatic) — BTK inhibitors (ibrutinib, acalabrutinib, zanubrutinib) or venetoclax + obinutuzumab (fixed duration); chemoimmunotherapy (FCR, BR) less used except in young fit IGHV-mutated without TP53 abnormality
  • TP53-aberrant or del(17p) — targeted agents only (BTK/BCL2); do NOT use chemoimmunotherapy
  • Richter transformation (5–10%) — to DLBCL; poor prognosis; treat like aggressive NHL

Acute promyelocytic leukemia

Acute promyelocytic leukemia (APL) is a subtype of AML (formerly M3) with t(15;17)(q22;q12) creating the PML-RARA fusion — it is a haematological emergency because of catastrophic bleeding from DIC before treatment takes effect.

Why APL is special:

• Released granules contain tissue factor and annexin II → overwhelming DIC
• Intracranial haemorrhage is the leading cause of early death (before and during induction)
• Unique responsiveness to differentiation therapy (ATRA + arsenic trioxide) — chemotherapy may not be needed in low-risk disease

Presentation:

• Pancytopenia with bleeding (mucocutaneous, GI, CNS); DIC (prolonged PT, APTT, low fibrinogen, raised D-dimer, thrombocytopenia)
• Hypogranular variant (microgranular APL) — may look like M4/M5; high WBC count; confirms by molecular testing
• Often presents before overt leukocytosis

Diagnosis:

• Morphology — hypergranular promyelocytes with faggot cells (bundles of Auer rods)
• Cytogenetics / FISH / RT-PCR — t(15;17) PML-RARA
• Variant fusions — PLZF-RARA (t(11;17)) ATRA-resistant; NPM-RARA (t(5;17)) responsive; STAT5B-RARA

Emergency management:

1. Start ATRA immediately on clinical/morphological suspicion — before molecular confirmation. Dose 45 mg/m²/day PO divided BD
2. Support DIC — platelets to maintain >=30–50 × 10⁹/L; fibrinogen >=1.5 g/L with cryoprecipitate; FFP to maintain INR <1.5
3. Avoid invasive procedures (lumbar puncture, central line in subclavian/IJ) during active DIC
4. Regimen — low-risk (WBC <=10,000): ATRA + arsenic trioxide (ATO) chemo-free — cure >95%. High-risk (WBC >10,000): ATRA + ATO ± idarubicin or gemtuzumab ozogamicin
5. Differentiation syndrome (~25%) — fever, dyspnoea, weight gain, pulmonary infiltrates, pleural/pericardial effusion, hypotension. Treat with dexamethasone 10 mg IV BD; continue ATRA/ATO if mild, interrupt if severe
6. Monitor PML-RARA by RT-PCR after consolidation — goal: undetectable at completion

Hodgkin lymphoma

Hodgkin lymphoma (HL) is a B-cell lymphoma defined by Reed-Sternberg (RS) cells — binucleate or multinucleate giant cells with "owl-eye" nucleoli — in a minority of the tumour amid an inflammatory background.

Epidemiology:

• Bimodal age distribution — 20–30 years (peak) and >55 years
• EBV-associated in ~40% of classical HL (higher in developing countries)
• Male:female ~1.4:1

Subtypes:

Presentation:

• Painless lymphadenopathy — cervical (60–80%), mediastinal (50%), axillary
• Contiguous nodal spread (unlike NHL)
• B symptoms — fever >38 °C, drenching night sweats, weight loss >10% in 6 months
• Pel-Ebstein fever (cyclical) — historical
• Alcohol-induced pain in affected lymph nodes — classical but rare
• Pruritus

Investigations:

• Excisional lymph node biopsy (needle biopsy insufficient for HL)
• CT/PET-CT neck-chest-abdomen-pelvis for staging
• Bone marrow biopsy — only if PET-CT suggests involvement
• HIV, HBV, HCV serology; echo/MUGA (anthracycline baseline); PFT (bleomycin baseline)
• ESR and B symptoms are prognostic

Ann Arbor staging (Cotswolds modification, now Lugano 2014):

Suffixes — A (no B symptoms), B (B symptoms), X (bulk >10 cm), E (extranodal extension from nodal site), S (splenic).

Favourable vs unfavourable early-stage HL: bulky disease (>=10 cm or >1/3 mediastinal diameter), >=3 nodal areas, high ESR, B symptoms, and extranodal extension make early-stage HL unfavourable (German Hodgkin Study Group / EORTC criteria).

Treatment:

• Early-stage favourable — ABVD × 2 + involved-site RT (ISRT 20–30 Gy)
• Early-stage unfavourable — ABVD × 4 + ISRT
• Advanced-stage — ABVD × 6 or BEACOPP (more toxic, used selectively); PET-adapted therapy de-escalates or escalates
• Relapsed/refractory — brentuximab vedotin (anti-CD30-MMAE), checkpoint inhibitors (nivolumab, pembrolizumab), autologous HSCT
• NLPHL — rituximab; R-ABVD; sometimes observation
• ABVD drugs & toxicities — Adriamycin (doxorubicin) — cardiotoxic; Bleomycin — pulmonary fibrosis; Vinblastine — neuropathy; Dacarbazine — nausea

Survival:

• Stage I–II: 5-year OS >95%
• Stage III–IV: 5-year OS 80–90%

Long-term risks:

• Second malignancies (breast, lung, thyroid, leukemia — from RT and alkylators)
• Cardiovascular disease (anthracycline + mediastinal RT)
• Infertility (alkylators)
• Hypothyroidism (neck RT)

Non-Hodgkin lymphomas

Non-Hodgkin lymphomas (NHL) are a heterogeneous group of mature B-, T-, or NK-cell malignancies — classified by the WHO 5th edition (2022) — with DLBCL and follicular lymphoma together accounting for about half of cases.

High-yield subtypes:

Staging: Ann Arbor (as HL). PET-CT used for aggressive NHL; CT alone for indolent. FDG-avid entities are aggressive NHLs and HL.

IPI (International Prognostic Index) — aggressive NHL:

• Age >60
• Stage III/IV
• ECOG >=2
• LDH elevated
• >=2 extranodal sites Each scores 1; 0–1 low, 2 low-intermediate, 3 high-intermediate, 4–5 high. Revised IPI (R-IPI) and NCCN-IPI for DLBCL with rituximab era.

Novel agents in NHL:

• CAR-T cell therapy (axicabtagene ciloleucel, tisagenlecleucel, lisocabtagene) — refractory DLBCL, FL, MCL
• Bispecific antibodies — glofitamab, epcoritamab, mosunetuzumab (CD20 × CD3)
• BTK inhibitors — ibrutinib, acalabrutinib, zanubrutinib (MCL, MZL, WM, CLL)
• BCL2 inhibitor — venetoclax
• PI3K inhibitors — idelalisib (restricted)
• EZH2 inhibitor — tazemetostat (FL)

Febrile neutropenia and tumor lysis syndrome

Febrile neutropenia and tumor lysis syndrome are the two oncology emergencies NEET PG tests most often — both demand protocolised, time-critical management.

Febrile neutropenia (FN):

• Definition — single oral/core temperature ≥38.3 °C OR sustained ≥38.0 °C for ≥1 h, AND ANC <500/μL (or <1000 with expected fall <500 within 48 h)
• Risk — Gram-negative bacteraemia (Pseudomonas, E. coli, Klebsiella), Gram-positive (coag-neg staph from CVCs, Staph aureus, viridans strep); fungal (Candida, Aspergillus) in prolonged neutropenia

Initial assessment:

• Full history — chemotherapy date, neutrophil trajectory, prior infections, prophylaxis, indwelling lines, symptoms
• Examination — every site (ports, lines, skin, perineum, oral mucosa — avoid rectal exam in neutropenic patients)
• Cultures — 2 sets of blood cultures (peripheral + central line), urine culture, stool if diarrhoea, throat swab; chest X-ray
• CBC, U&E, LFT, CRP, lactate, ABG, coagulation

MASCC score (Multinational Association for Supportive Care in Cancer) — identifies low-risk FN eligible for oral outpatient therapy:

• Total score (max 26); ≥21 = low-risk
• Components — no hypotension, no COPD, solid tumour/no prior fungal infection, no dehydration, outpatient status, age <60, symptom burden

Empirical antibiotics (within 1 hour of presentation):

G-CSF (filgrastim): not routinely for FN treatment but used for prophylaxis in high-risk chemotherapy regimens (>20% FN risk) and secondary prophylaxis after prior FN.

Prophylaxis: fluoroquinolone for prolonged neutropenia (>7 days), anti-PCP (cotrimoxazole), antifungal (posaconazole in AML induction, allo-HSCT), antiviral (acyclovir in allogeneic HSCT).

Tumor lysis syndrome (TLS):

• Metabolic consequence of rapid tumour cell lysis; hyperuricaemia, hyperkalaemia, hyperphosphataemia, secondary hypocalcaemia, AKI
• Highest risk — Burkitt lymphoma, ALL (high WBC), high-grade lymphoma, bulky / high-proliferative index disease; less commonly CLL post-venetoclax (ramp-up), solid tumours (rare)

Cairo-Bishop criteria:

• Laboratory TLS — ≥2 abnormalities within 3 days before to 7 days after chemotherapy start:
  • Uric acid >8 mg/dL or 25% rise
  • Potassium >6 mEq/L or 25% rise
  • Phosphate >4.5 mg/dL (adult) or >6.5 (child) or 25% rise
  • Calcium <7 mg/dL or 25% fall
• Clinical TLS — lab TLS + one of AKI (creatinine >=1.5× ULN), seizure, cardiac arrhythmia, sudden death

Risk stratification and prevention:

Established TLS — management:

• Aggressive IV fluids (isotonic saline) — maintain urine output 2–3 mL/kg/h
• Rasburicase (recombinant urate oxidase) — converts urate to soluble allantoin; contraindicated in G6PD deficiency (risk of haemolysis and methaemoglobinaemia)
• Treat hyperkalaemia — calcium gluconate (cardiac protection), insulin-dextrose, salbutamol nebuliser, sodium bicarbonate, loop diuretic, binders (patiromer, SZC); dialysis if refractory
• Treat hyperphosphataemia — phosphate binders (sevelamer, aluminium hydroxide)
• Symptomatic hypocalcaemia — IV calcium (caution: Ca × PO4 product >=60 risks calcium phosphate crystal deposition — avoid routine calcium repletion)
• Renal replacement therapy if refractory AKI, severe acidosis, or life-threatening electrolytes

Sources and references

1. Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo, Fauci, Kasper, Hauser, Longo, Jameson, Eds., 2022) — Chapters on acute and chronic leukemias, Hodgkin and non-Hodgkin lymphoma, and oncology emergencies.
2. DeVita, Hellman, and Rosenberg's Cancer: Principles and Practice of Oncology, 12th Edition (DeVita, Rosenberg, Lawrence, Eds., 2022) — Detailed sections on leukemia and lymphoma subtypes.
3. Hoffman Hematology: Basic Principles and Practice, 8th Edition (Hoffman, Benz, Silberstein, Heslop, Weitz, Anastasi, Salama, Abutalib, Eds., 2022) — Haematopathology and classification.
4. WHO Classification of Tumours: Haematolymphoid Tumours, 5th Edition (WHO, 2022).
5. Alaggio R et al. The 5th edition of the World Health Organization Classification of Haematolymphoid Tumours: Lymphoid Neoplasms. Leukemia 2022; 36:1720-1748.
6. Freifeld AG et al. IDSA Clinical Practice Guideline for the Use of Antimicrobial Agents in Neutropenic Patients with Cancer. Clin Infect Dis 2011; 52:e56-e93.
7. Coiffier B et al. Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review. J Clin Oncol 2008; 26:2767-2778.

Frequently asked questions

How many haematology-oncology questions appear in NEET PG?

Leukemias and lymphomas contribute 4-6 questions per NEET PG paper across medicine, pathology, and oncology. Recurring themes include ALL vs AML cytochemistry (MPO positive in AML, PAS positive in ALL), CML Philadelphia chromosome and imatinib, APL t(15;17) and all-trans retinoic acid (ATRA), Reed-Sternberg cells in Hodgkin lymphoma, DLBCL as the commonest NHL, Burkitt starry-sky pattern with t(8;14), and empirical piperacillin-tazobactam or cefepime for febrile neutropenia.

How do you distinguish ALL from AML?

ALL and AML are both acute leukemias with more than 20 percent blasts in bone marrow, but they differ in age, morphology, and markers. ALL is commoner in children (peak 2-5 years) — blasts are smaller with scant cytoplasm, PAS-positive, MPO-negative, and immunophenotype CD19/CD10/TdT (B-ALL) or CD3/CD7/TdT (T-ALL). AML is commoner in adults (median 65 years) — blasts are larger with cytoplasmic Auer rods, MPO-positive (myeloid lineages), non-specific esterase positive (M4/M5 monocytic), and CD13/CD33/CD34/MPO immunophenotype. ALL is often cured in children (85 percent); AML has worse prognosis except APL.

What is the Philadelphia chromosome?

The Philadelphia chromosome is a reciprocal translocation t(9;22)(q34;q11) that creates the BCR-ABL1 fusion gene encoding a constitutively active tyrosine kinase. It is pathognomonic for chronic myeloid leukemia (CML) — found in more than 95 percent of cases. It is also found in about 25 percent of adult and 3 percent of paediatric B-cell ALL, where it signals a very high-risk disease. The target therapy is tyrosine kinase inhibitors — imatinib (first-generation), dasatinib, nilotinib, bosutinib, and ponatinib (for T315I mutations). Deep molecular response (BCR-ABL less than 0.0032 percent on PCR) is the treatment goal.

Why is APL a haematological emergency?

Acute promyelocytic leukemia (APL, AML-M3) is defined by t(15;17)(q22;q12) creating the PML-RARA fusion. It is a haematological emergency because the promyelocytic granules release tissue factor and annexin, causing severe disseminated intravascular coagulation (DIC) and fatal bleeding — especially intracranial haemorrhage — often before the diagnosis is confirmed. Start all-trans retinoic acid (ATRA) immediately on morphological suspicion, before waiting for molecular confirmation. Arsenic trioxide plus ATRA (chemotherapy-free for low-risk) achieves cure rates over 90 percent. Watch for differentiation syndrome (fever, oedema, pulmonary infiltrates, hypotension — treat with dexamethasone).

What is Hodgkin lymphoma and how is it staged?

Hodgkin lymphoma is a B-cell malignancy characterised by Reed-Sternberg cells (CD15+, CD30+, CD45-, PAX5+) in a background of inflammatory cells. Bimodal age distribution (20-30 years and greater than 55). Classic subtypes — nodular sclerosis (commonest, young women), mixed cellularity, lymphocyte-rich, lymphocyte-depleted; plus nodular lymphocyte-predominant HL (CD20+, LP cells). Ann Arbor staging — I (single nodal region), II (two or more regions same side of diaphragm), III (both sides of diaphragm), IV (extranodal). Suffix A (no B symptoms) or B (fever greater than 38 degrees, night sweats, weight loss greater than 10 percent). Treatment — ABVD chemotherapy (doxorubicin, bleomycin, vinblastine, dacarbazine) plus radiation for early stage; brentuximab vedotin and checkpoint inhibitors in relapsed/refractory disease.

What is the commonest non-Hodgkin lymphoma?

Diffuse large B-cell lymphoma (DLBCL) is the commonest non-Hodgkin lymphoma, accounting for about 30 percent of cases in adults. Median age is 65. Aggressive but potentially curable. Immunophenotype — CD20+, CD45+, and either germinal-centre B-cell-like (GCB) or activated B-cell (ABC) by gene expression. Double-hit lymphoma (MYC plus BCL2 or BCL6) is a high-risk variant. Treatment is R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) every 21 days for 6 cycles. Cure rate 60-70 percent. Polatuzumab-R-CHP (pola-R-CHP) is the newer first-line for high-risk DLBCL per POLARIX.

What is Burkitt lymphoma?

Burkitt lymphoma is an aggressive B-cell NHL with translocation t(8;14)(q24;q32) juxtaposing MYC to the IgH enhancer in greater than 80 percent of cases (or variants t(2;8), t(8;22)). Three forms — endemic (African, EBV-associated, jaw/facial mass in children), sporadic (abdominal, ileocaecal), immunodeficiency-associated (HIV-related). Histology shows starry-sky appearance (scattered tingible-body macrophages engulfing apoptotic debris). Ki-67 proliferation index approaches 100 percent — doubling time less than 24 hours, making it the fastest-growing human tumour. Treatment is intensive short-course chemotherapy (CODOX-M/IVAC, or DA-EPOCH-R); prophylactic tumour lysis precautions and CNS prophylaxis are essential.

How do you manage febrile neutropenia?

Febrile neutropenia is a single temperature greater than or equal to 38.3 degrees or sustained greater than 38.0 for at least 1 hour, with absolute neutrophil count (ANC) less than 500 cells/microL (or less than 1000 with expected fall less than 500). It is a medical emergency — risk of Gram-negative bacteraemia and sepsis. Initial management — cultures (two sets including central line), chest X-ray, urinalysis; start empirical IV broad-spectrum antipseudomonal beta-lactam (piperacillin-tazobactam 4.5 g every 6 h, or cefepime 2 g every 8 h, or meropenem in severe sepsis) within 1 hour. Add vancomycin for catheter-related, soft-tissue, mucositis, hypotension, pneumonia, or MRSA colonisation. MASCC score greater than or equal to 21 identifies low-risk patients who may receive oral therapy outpatient.

What is tumor lysis syndrome?

Tumor lysis syndrome (TLS) is a cluster of metabolic abnormalities from rapid malignant cell death — hyperuricaemia, hyperkalaemia, hyperphosphataemia, secondary hypocalcaemia, and acute kidney injury (urate or calcium-phosphate crystal nephropathy). Occurs most often in Burkitt lymphoma, ALL, high-grade lymphoma, and bulky disease after chemotherapy initiation. Cairo-Bishop criteria define laboratory and clinical TLS. Prevention — vigorous IV fluids (2-3 L/m^2/day), allopurinol for low/moderate-risk, rasburicase (recombinant urate oxidase) for high-risk. Treatment — continue hydration, control potassium (insulin-dextrose, calcium gluconate for cardiac protection), rasburicase, haemodialysis if refractory AKI or life-threatening biochemistry.

What are the named translocations in haematological malignancies?

Classic NEET PG translocations — CML and Ph+ ALL t(9;22) BCR-ABL1 (targeted by imatinib). APL t(15;17) PML-RARA (targeted by ATRA + arsenic). Burkitt t(8;14) MYC-IgH. Follicular lymphoma t(14;18) IGH-BCL2. Mantle cell lymphoma t(11;14) CCND1-IGH. MALT lymphoma t(11;18) API2-MALT1 (gastric, H. pylori resistant). Ewing sarcoma t(11;22) EWSR1-FLI1 (not haematological but tested). AML good-prognosis markers include t(8;21) RUNX1-RUNX1T1 and inv(16) CBFB-MYH11. Poor prognosis include monosomy 5, monosomy 7, complex karyotype, FLT3-ITD.

Want more high-yield medicine revision? Review the anaemia classification guide, walk the peripheral smear image-MCQ, and use the AI tutor to drill cytogenetics and treatment pairings on demand.

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Written by: NEETPGAI Editorial Team Reviewed by: Pending SME Review Last reviewed: February 2026

This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.