For health professionals. This section uses clinical terms and is general education for doctors, nurses and students, not advice for an individual patient. Patients and families: please read our patient guides instead, Cancer Myth Busters · Understanding your cancer report · Living through cancer treatment, or speak with your own doctor.
90 clinical-vignette questions in three levels: 30 basics, 30 applied and innovative, and 30 challenging (30 Diagnosis, 55 Treatment, 5 Survivorship; 4 built on schematic imaging, endoscopy or histology drawings). Practise question by question with instant marking, or take a timed mock test with a result summary by topic, level and section. You can also print the page as a booklet.
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Timed mock test. Random questions, about 80 seconds each (30 questions in 40 minutes). Answers stay hidden until you submit or time runs out; then you get a score by topic, level and section.
Level 1 · Basics
Core facts for NEET-PG and USMLE Step 1–2: histology, risk factors, presentation, staging and first-line principles.
Q1DiagnosisLevel 1At a glance
About what share of acute leukaemias in adults is acute myeloid leukaemia (AML)?
AAbout 50%
BAbout 80%
CAbout 20%
DUnder 10%
ENearly 100%
Show answer
Answer: B. AML is the commonest acute leukaemia of adults; median age at diagnosis is 65–68 in Western registries. In children under 10 it is under 10% of acute leukaemias, where ALL dominates.
Which statement about the white count at diagnosis of AML is correct?
AIt is always above 100,000/µL at diagnosis
BIt is normal only in APL, never in other AML
CA count under 5,000/µL rules out AML
DIt is the test that makes the diagnosis
EA normal or low count does not exclude AML
Show answer
Answer: E. A quarter to two-fifths of patients have fewer than 5,000 white cells (median about 15,000/µL). The smear, not the count, makes the diagnosis: blasts are seen in nearly all patients.
This schematic blood film is from a 55-year-old with fever and bruises. What is the pink rod-shaped inclusion marked by the arrow?
AA Döhle body
BA Howell-Jolly body
CToxic granulation
DA Russell body
EAn Auer rod
Show answer
Answer: E. Auer rods are fused azurophilic granules in myeloblasts. They are pathognomonic of myeloid lineage; bundles of them ("faggot cells") are typical of APL.
For most AML without a defining genetic lesion, what marrow or blood blast count is needed for the diagnosis?
A30% or more
B20% or more
C50% or more
D5% or more
E10% or more
Show answer
Answer: B. Most AML needs ≥20% blasts (also BCR::ABL1-positive AML). Defining lesions (APL, CBF fusions, KMT2A and others) need ≥10%, and NPM1-mutated AML any count under WHO. Myeloid sarcoma counts as AML at any marrow count.
This schematic drawing shows the gums of a 48-year-old with a new acute leukaemia. Which AML type does it suggest?
AAML with t(8;21)
BAcute promyelocytic leukaemia
CPure erythroid leukaemia
DMonocytic AML
EChronic myeloid leukaemia in chronic phase
Show answer
Answer: D. Gum hypertrophy and violaceous skin nodules (leukaemia cutis) suggest monocytic AML. Patients are often sent to the dentist first: a blood count with a smear is the right test.
Answer: B. Known risks are previous chemotherapy (alkylating agents, topoisomerase II inhibitors) or radiotherapy, an earlier MDS or MPN, benzene, smoking and obesity. Most AML arises from clonal haematopoiesis that gathers further mutations.
A mass biopsied from the orbit shows sheets of myeloid blasts; the marrow has 6% blasts. How is this classified?
AA lymphoma until proved otherwise
BMDS, because marrow blasts are under 20%
CA small round cell tumour of the orbit
DAML (myeloid sarcoma), whatever the marrow
EA benign reactive inflammatory lesion
Show answer
Answer: D. Myeloid sarcoma counts as AML at any marrow blast count and is treated as AML. It needs myeloid immunostains, because it is easily called a small round cell tumour or lymphoma.
A 26-year-old has gum bleeding, a low fibrinogen and many granular cells on the smear. When should ATRA be started?
AAfter the bleeding has stopped
BAfter the bone marrow report
CAt once, the same day, on suspicion of APL
DOnly if the white count is above 10,000/µL
EOnly after PML::RARA is confirmed
Show answer
Answer: C. Bleeding with low fibrinogen and granular cells is APL until proved otherwise. ATRA is started on suspicion; confirmation by PCR or FISH comes later.
A fit 45-year-old has AML with a FLT3 mutation. What is added to 7+3 induction?
AImatinib or dasatinib
BRituximab or obinutuzumab
CMidostaurin or quizartinib
DATRA or arsenic trioxide
EVenetoclax or azacitidine
Show answer
Answer: C. Midostaurin (ITD or TKD) or quizartinib (ITD) is added to induction and continued in consolidation and maintenance. Every fit FLT3-mutated patient should get one.
Which drug is added to induction for CD33-positive core-binding-factor AML?
AMidostaurin
BBlinatumomab
CArsenic trioxide
DIvosidenib
EGemtuzumab ozogamicin
Show answer
Answer: E. Gemtuzumab ozogamicin targets CD33, which nearly all CBF AML express. It gives fewer relapses and better 5-year survival, with the largest benefit in CBF AML (Hills 2014).
What is the standard first treatment for an older adult with AML who is unfit for intensive chemotherapy but not frail?
AVenetoclax with azacitidine
BImatinib
CSupportive care only, with no drugs
DATRA with arsenic trioxide
E7+3 induction
Show answer
Answer: A. In VIALE-A, venetoclax with azacitidine improved survival over azacitidine alone. IDH1-mutated AML can be treated with ivosidenib plus azacitidine.
What is the preferred induction for low- or intermediate-risk APL (white count 10,000/µL or less)?
AATRA with arsenic trioxide
B7+3 without ATRA
CAllogeneic transplant
DATRA alone
EVenetoclax with azacitidine
Show answer
Answer: A. ATRA plus arsenic trioxide gave 72-month event-free survival of about 97% in APL0406. Where arsenic is not available, ATRA with an anthracycline is used.
A patient on induction has a temperature of 38.6°C and neutrophils of 200/µL. What is the first step?
AParacetamol now and review on the morning round
BWait 24 hours for the blood culture results before antibiotics
CGranulocyte transfusion before any antibiotic
DStart an antifungal only, with no antibiotic
ECultures, then an antipseudomonal beta-lactam within 60 min
Show answer
Answer: E. Neutropenic fever is an emergency: cultures, then an antipseudomonal beta-lactam within 60 minutes. Local resistance patterns guide the choice.
A breathless patient has a white count of 200,000/µL and haemoglobin of 6 g/dL. What should be avoided if possible?
AStarting induction
BIntravenous fluids
CPlatelet transfusion if bleeding
DHydroxyurea
EA rapid red cell transfusion
Show answer
Answer: E. Red cells raise blood viscosity and can precipitate leukostasis. Cytoreduce first (induction, or hydroxyurea if induction is delayed) and transfuse slowly only if essential.
For a patient at high risk of tumour lysis, which drug is given with intravenous fluids, after checking for G6PD deficiency?
AFurosemide
BSodium bicarbonate
CAllopurinol alone
DRasburicase
ECalcium gluconate
Show answer
Answer: D. High risk (in AML, WBC ≥100,000/µL): fluids plus rasburicase, which is avoided in G6PD deficiency. Intermediate risk: fluids plus allopurinol.
A fit 40-year-old with adverse-risk AML reaches first complete remission. What is the usual next step?
AAllogeneic transplant in first remission
BTwo years of ATRA maintenance
COral azacitidine maintenance alone
DAutologous stem cell transplant
ENo further treatment, with close follow-up
Show answer
Answer: A. Adverse risk: allogeneic HCT in CR1. Favourable risk: consolidation, with transplant only for persistent or rising MRD. Intermediate risk: decided on MRD, donor and transplant risk.
A patient on ATRA for APL develops fever, breathlessness and weight gain. Which drug is started at once?
AHeparin
BDexamethasone
CFurosemide alone
DErythropoietin
EVancomycin alone
Show answer
Answer: B. Differentiation syndrome is treated with dexamethasone as soon as it is suspected ("dexamethasone first, questions later"), with cultures, antibiotics, oxygen and diuretics as needed.
Which is a recognised late effect of AML treatment?
ALoss of hearing from daunorubicin
BHeart damage from anthracyclines
CDiabetes from 7+3
DLiver cirrhosis from ATRA
EChronic kidney stones from cytarabine
Show answer
Answer: B. Late effects include anthracycline heart damage, infertility, chronic graft-versus-host disease and infections after transplant, second cancers, fatigue and the financial toll of treatment.
In English data (2001–2006), what was the main factor by which 5-year survival from AML fell?
AAge at diagnosis
BBlood group
CHeight
DPlace of birth
ESex
Show answer
Answer: A. 5-year survival was about 50% under 40, 33% at 40–59, 13% at 60–69 and 3% at 70–79. Results are better with favourable genetics and modern targeted and transplant care.
Where is a bone marrow sample taken in suspected AML?
AAnterior tibia, as in adults generally
BSternum, for both aspirate and biopsy
CPosterior iliac crest
DA vertebral body, under CT guidance
EThe femoral head, under anaesthesia
Show answer
Answer: C. A unilateral aspirate (500-cell count) and biopsy are taken from the posterior iliac crest; the sternum is acceptable for aspiration only. Warn the laboratory: fresh samples are needed for flow, karyotype, FISH and molecular tests.
When is a lumbar puncture done in an adult with newly diagnosed AML?
AIn APL, on the first day
BOnly after transplant
COnly for neurological symptoms
DBefore every cycle of chemotherapy
EIn every patient at diagnosis
Show answer
Answer: C. There is no routine CNS prophylaxis in adult AML. Image first if there are focal signs; correct platelets and clotting; in APL defer the LP until the coagulopathy is corrected.
In the Vellore series of 380 patients with non-APL AML, why did most not start standard treatment?
AAdvanced age
BLack of money
CLack of a diagnosis
DRefusal of transfusion
EPreference for herbal medicine
Show answer
Answer: B. Only 29% started standard treatment, and 81% of the rest did not for lack of money. Median age was 40, symptoms had lasted a median of 4 weeks, and patients travelled a median of 580 km.
Which tests are sent at once in every suspected case of AML to look for DIC?
ASerum protein electrophoresis
BHbA1c and a lipid profile
CPT, aPTT, fibrinogen and D-dimer
DTroponin and creatine kinase
ESerum ferritin and transferrin
Show answer
Answer: C. DIC is common in APL and in monocytic AML with a high count. Results guide platelet and cryoprecipitate support and raise the suspicion of APL; recheck often in APL.
A marrow shows 12% blasts with t(8;21) RUNX1::RUNX1T1. What is the diagnosis?
AMDS/AML
BMDS with excess blasts
CAML
DCML in blast phase
EA reactive marrow after infection
Show answer
Answer: C. With a defining lesion (APL, CBF fusions, KMT2A, DEK::NUP214, MECOM, CEBPA), ≥10% blasts are enough for AML. t(8;21) occurs in 1–7% of adults (median age 25–30) and is favourable.
A marrow has 8% blasts and an NPM1 mutation. How does the WHO 5th edition classify it?
AClonal haematopoiesis only
BAML with mutated NPM1
CMDS with low blasts
DA normal marrow for age
EMDS/AML (ICC term)
Show answer
Answer: B. WHO accepts NPM1-mutated AML at any blast count; ICC 2022 asks for ≥10%. NPM1 without FLT3-ITD is favourable, and NPM1 transcripts can be followed by PCR.
A patient with a white count of 250,000/µL has a potassium of 7.2 mmol/L but a normal ECG. What should you do first?
AIgnore it, as high counts never affect potassium
BGive insulin-dextrose and calcium at once
CRecheck potassium on a heparinised plasma sample
DGive a potassium binder and stop fluids
EStart urgent haemodialysis
Show answer
Answer: C. Potassium leaks from cells in a clotted sample (pseudohyperkalaemia). A huge count also lowers glucose and oxygen in the tube; send the blood gas on ice.
This schematic blood film is from a 28-year-old with gum bleeding and a fibrinogen of 90 mg/dL. What is the immediate step?
AInsert a central line for induction today
BStart heparin for the clotting disorder
CLumbar puncture to look for CNS disease first
DStart ATRA now, before PML::RARA is confirmed
EWait for FISH results before any treatment
Show answer
Answer: D. Abnormal promyelocytes with dense granules and bundles of Auer rods mean APL until proved otherwise. ATRA is started on suspicion; lines, lumbar puncture and heparin are avoided during induction.
Answer: E. Platelets and cryoprecipitate keep these targets; no heparin; antifibrinolytics only in selected patients. In Lucknow, 34% got less support than planned because of shortages.
APL is confirmed in a 32-year-old with a white count of 14,000/µL. Which induction fits?
AATRA + arsenic alone, exactly as for low risk
B7+3 alone, with ATRA kept for relapse only
CHigh-risk treatment: ATRA with an anthracycline
DVenetoclax with azacitidine as first induction
EArsenic alone, without ATRA, until counts fall
Show answer
Answer: C. A white count >10,000/µL is high risk: ATRA with an anthracycline, or ATRA plus arsenic with hydroxyurea or an anthracycline for a rising count.
On day 9 of ATRA and arsenic for APL, a patient has fever, breathlessness, a 6 kg weight gain and this schematic chest X-ray. What is the best plan?
ADexamethasone now; usually continue the drugs
BStop ATRA and arsenic permanently today
CIncrease ATRA to speed up differentiation
DTreat as pneumonia with antibiotics alone
EDiuretics only, and review again tomorrow
Show answer
Answer: A. Differentiation syndrome (≥3 features: fever, hypoxia, weight gain >5 kg, lung opacities or effusions, hypotension, kidney injury) needs dexamethasone at once. Pause ATRA or arsenic only if severe or not better in 24–48 hours.
A fit 66-year-old develops AML 5 years after chemotherapy for breast cancer (intermediate-risk genetics). Which induction is preferred?
AATRA with arsenic
B7+3 with gemtuzumab
CLow-dose cytarabine
DCPX-351
EImatinib with 7+3
Show answer
Answer: D. For therapy-related or myelodysplasia-related AML with favourable or intermediate genetics, CPX-351 gave 5-year OS of 18% vs 8% with 7+3 in patients aged 60–75, with more patients reaching transplant.
A 30-year-old with AML has a RUNX1 variant at about half the reads on NGS, and an aunt had leukaemia. A sibling is the planned donor. What must be done first?
ACheck if the variant is germline; test the sibling
BCancel transplant and give chemotherapy only
CIgnore it, since RUNX1 variants are never inherited
DProceed with the sibling as donor without tests
EUse the patient's own stem cells (autologous)
Show answer
Answer: A. Familial disorders underlie 10–20% of AML/MDS in young adults. Clues: relatives with blood cancers, long-standing cytopenias, a germline-type variant (DDX41, RUNX1, GATA2, biallelic CEBPA). A sibling carrying it should not be the donor.
A 35-year-old with NPM1-mutated AML (no FLT3-ITD) is in remission with negative MRD. What is suggested?
AOral azacitidine only, without consolidation
BAllogeneic transplant in first remission for all
CNo further treatment after induction
DConsolidation; transplant only if MRD persists or rises
EATRA maintenance for two years after induction
Show answer
Answer: D. Favourable risk: consolidation (intermediate-dose cytarabine suggested over high-dose for most). Transplant is kept for persistent or rising MRD.
Who should be offered oral azacitidine maintenance after consolidation, as in QUAZAR?
AOnly patients after allogeneic transplant
BOnly patients with APL after arsenic
CAll patients with favourable-risk AML
DChildren with high-risk AML after induction
EAge 55 or more, intermediate or adverse risk
Show answer
Answer: E. QUAZAR showed longer survival (median OS 25 vs 15 months). FLT3-mutated AML gets an FLT3 inhibitor after chemotherapy or after transplant instead.
A 72-year-old with ECOG 1, Charlson 1 and normal heart, lung, liver and kidney function has AML. Which is correct?
ASupportive care is the only reasonable option
BAge over 70 means lower-intensity therapy only
CShe is frail by definition at this age
DShe can be treated as fit for intensive therapy
ETransplant is impossible at any age above 70
Show answer
Answer: D. Fitness (ECOG, Charlson or HCT-CI, organ function, cognition, wishes), not age alone, decides intensive versus lower-intensity therapy. Transplant eligibility also depends on organ function, not age.
A patient on venetoclax with azacitidine is started on posaconazole prophylaxis. What follows?
AVenetoclax dose is adjusted (azoles raise levels)
BVenetoclax is replaced by 7+3 induction
CPosaconazole must never be given with it
DAzacitidine is stopped while on posaconazole
ENo change is needed to either drug
Show answer
Answer: A. Azole antifungals raise venetoclax levels, so its dose is adjusted. The marrow is checked early in cycle 1 because responses are fast and counts may need time off venetoclax.
AML relapses 10 months after consolidation; FLT3-ITD is now present. Which drug improved survival over salvage chemotherapy?
AImatinib
BATRA
CMidostaurin
DIvosidenib
EGilteritinib
Show answer
Answer: E. In ADMIRAL, gilteritinib gave median OS 9.3 vs 5.6 months. Genetics are repeated at relapse because clones evolve; the transplant team is involved at once.
Relapsed AML has an NPM1 mutation. Which class of drug is now FDA-approved for it?
ABCR::ABL1 inhibitors
BBTK inhibitors
CMenin inhibitors
DJAK2 inhibitors
EAnti-CD20 antibodies
Show answer
Answer: C. Menin inhibitors are approved for NPM1-mutated AML and KMT2A-rearranged acute leukaemia. They cause differentiation syndrome and QT prolongation; Indian availability is to be confirmed.
Why must the genetic tests be repeated when AML relapses?
ARelapse is always a new, unrelated leukaemia
BClones evolve, so the target may have changed
CLaboratories require it for billing
DThe first results expire after 6 months
EGenetics never change, but staging does
Show answer
Answer: B. Relapse may come from the dominant clone gaining mutations or from a minor clone that survived treatment. A FLT3, IDH or NPM1 result at relapse can open a targeted option.
A patient with AML develops a new facial nerve palsy; CSF shows blasts. What is the right approach?
AHigh-dose systemic chemotherapy during cranial RT
BWait for nerve recovery before any CNS treatment
CIntrathecal therapy alone, with RT only if it fails
DCraniospinal RT as the first and only choice
EPrompt cranial radiotherapy with intrathecal therapy
Show answer
Answer: E. Cranial nerve palsies need RT (for example 18–25 Gy to the brain, field down to C2), started as soon as CNS involvement is suspected, because recovery falls with delay. Cranial RT spares the marrow; avoid high-dose systemic chemotherapy around it.
A myeloid sarcoma compresses the spinal cord. Which management is right?
AHydroxyurea alone, with RT kept for later relapse
BObservation until the marrow relapses, then chemotherapy
CSurgery alone, with no systemic therapy afterwards
DSteroids, urgent MRI, RT and/or decompression, plus systemic therapy
ESystemic therapy alone, with no RT or surgery at any stage of care
Show answer
Answer: D. Myeloid sarcoma is AML: systemic treatment is the main therapy. Add RT (about 20 Gy is generally enough) for compression of a vital structure or persistence after recovery from induction.
On day 5 of neutropenic fever a stable patient is still febrile on piperacillin-tazobactam with negative cultures. What next?
AAdd an antifungal (4–7 days of unexplained fever)
BAdd vancomycin routinely to the regimen
CChange to meropenem because of the fever alone
DStop all antibiotics while cultures are negative
EGive a granulocyte transfusion today
Show answer
Answer: A. Do not change antibiotics for fever alone in a stable patient. Vancomycin is for line, skin or soft-tissue infection, pneumonia or instability.
Which antifungal prophylaxis is used during AML induction?
AOral nystatin only, throughout induction
BFluconazole, or a mould-active azole in second induction
CNone until fever appears, then amphotericin for everyone
DAmphotericin for every patient from day 1
EAn echinocandin, but only after transplant
Show answer
Answer: B. Fluoroquinolone prophylaxis covers expected ANC <500/µL for >7 days; aciclovir for HSV-seropositive patients. In an Indian centre, fungal pneumonia was still diagnosed in 55% during induction.
AML is diagnosed at 9 weeks of pregnancy. What does the module advise?
ADelay all treatment until delivery
BStart ATRA only
CLow-dose cytarabine throughout pregnancy
DTermination of pregnancy, then treatment
ELeukapheresis until term
Show answer
Answer: D. In the first trimester, termination followed by treatment is advised. Later in pregnancy, urgent induction is discussed against temporary measures such as leukapheresis.
A man in remission from NPM1-mutated AML has a rising NPM1 transcript level in blood on two tests. What next?
ARepeat the test in 2 years
BA marrow examination and plans for relapse
CReassurance: blood MRD has no meaning
DStop follow-up, as he is in remission
EStart ATRA maintenance at once
Show answer
Answer: B. Some experts follow MRD in blood (NPM1, CBF fusions). A falling count or rising MRD needs a marrow, because NPM1 transcripts by PCR predict relapse.
In hyperleukocytosis where induction must be delayed, which measure lowers the white count?
AHigh-dose steroids for three days
BRed cell transfusion to dilute the blood
CHydroxyurea
DPlasma exchange, repeated daily
ELeukapheresis alone, without any drug
Show answer
Answer: C. Fit patients start induction at once. Leukapheresis has no proven benefit on its own and is used with hydroxyurea only for symptomatic leukostasis when induction cannot start.
Which advice suits a person living after AML treatment?
AReport fever only if it lasts a week
BStay active and social, with sensible precautions
CAvoid all other people for five years after treatment
DSkip all vaccines after a transplant
ENever exercise again after treatment
Show answer
Answer: B. Encourage activity and normal contact (sensible precautions while counts are low), follow the transplant team's vaccination schedule, and report fever, bleeding and new tiredness promptly.
In VIALE-A, what were median overall survival and complete remission with venetoclax plus azacitidine versus azacitidine alone?
AOS 10 vs 15 months; CR 18% vs 37%
BOS 32 vs 15 months; CR 70% vs 40%
COS 24 vs 8 months; CR 50% vs 10%
DOS 15 vs 10 months; CR 37% vs 18%
ENo survival difference
Show answer
Answer: D. Venetoclax combinations are standard for unfit adults. In VIALE-C, venetoclax was added to low-dose cytarabine for those unsuitable for an HMA.
In the Short 2020 meta-analysis, what was 5-year overall survival with negative versus positive MRD?
A34% vs 68%
B50% vs 45%
C18% vs 8%
D90% vs 10%
E68% vs 34%
Show answer
Answer: E. MRD negativity roughly doubled 5-year survival across ages, subtypes and methods. NPM1 and CBF fusions are followed by PCR; other AML by multiparameter flow.
What did the Hills 2014 meta-analysis show for gemtuzumab ozogamicin with induction?
ABenefit only in adverse-risk AML, none in CBF AML
BBenefit only in APL, with no gain in other AML
CMore relapses and deaths with gemtuzumab added
DNo survival benefit in any genetic risk group
EFewer relapses and better survival, most in CBF AML
Show answer
Answer: E. Benefit was seen in favourable and intermediate cytogenetics and was largest in core-binding-factor AML, which is nearly always CD33-positive.
In 102 patients with APL at SGPGIMS Lucknow (2014–2024), which finding is correct?
AInduction mortality about 1%, as in clinical trials
BAll deaths were caused by differentiation syndrome
CInduction mortality 24.5%; support limited by shortages
DNo patient received ATRA during induction
EMedian age 65, with most patients at low risk
Show answer
Answer: C. Median age was 33, 47% were high risk, and it took a median of 18 days from symptoms to diagnosis. Deaths were mostly from bleeding and infection.
How do early deaths in APL compare between clinical trials with early ATRA and population registries?
AAbout 1% in both
BAbout 29% in trials vs 3.7% in population registries
CAbout 3.7% in trials vs up to 29% in registries
DAbout 50% in both
ERegistries report fewer deaths than trials do
Show answer
Answer: C. The gap between trials and real life reflects delays in starting ATRA and in blood product support. ATRA on suspicion is the single most important step.
What did Ganzel 2021 find about CNS involvement at diagnosis of adult AML?
AFound in about 1–3%; it does not by itself worsen outcome
BIt always requires craniospinal RT
CIt doubles the risk of death
DFound in about half of patients
EIt is an indication for routine prophylaxis in all adults
Show answer
Answer: A. MRI and lumbar puncture are done only for neurological symptoms. Leptomeningeal AML without deficits is treated with intrathecal therapy; deficits need RT.
Why can IDH inhibitors cause differentiation syndrome?
AThey destroy CD33-positive blasts very fast
BThey lift the block caused by 2-hydroxyglutarate
CThey inhibit FLT3 signalling in the blasts
DThey release potassium from leukaemic cells
EThey deplete fibrinogen and trigger DIC
Show answer
Answer: B. IDH1/2 mutations (about 20%) make the oncometabolite 2-hydroxyglutarate. Ivosidenib, olutasidenib and enasidenib release the block, so blasts mature, as with ATRA in APL.
About how often does differentiation syndrome occur with different drugs?
AOnly with ATRA in APL, and never with other drugs
BOnly after allogeneic transplant, whatever the drug
CAbout 3% (APL), up to 20% (IDH/menin), about 25% (FLT3)
DAbout 25% (APL), up to 20% (IDH/menin), about 3% (FLT3)
EAbout 80% with every drug that causes differentiation
Show answer
Answer: D. Routine steroid prophylaxis is not suggested. Mimics include sepsis, heart failure, pulmonary embolism, alveolar haemorrhage and drug reactions.
After an ATO-containing regimen and molecular remission in APL, how often does relapse occur, and what is done?
A5–10% (20–30% if high risk); ATRA + arsenic, then auto-HCT
BAbout 1%; ATRA maintenance is then given for life
CAbout 80%; palliative care is the usual approach
DNever; no further PCR follow-up is ever needed
EAbout 50%; allogeneic transplant in every relapsed case
Show answer
Answer: A. No maintenance is needed after an ATO-containing regimen with molecular remission; without ATO, intermittent ATRA maintenance is used. Gemtuzumab treats molecular relapse where available.
What is the evidence for leukapheresis in hyperleukocytosis (Oberoi 2014)?
AIt prevents tumour lysis
BIt halves early mortality
CIt replaces induction chemotherapy
DIt is mandatory above 50,000/µL
ENo proven benefit on its own
Show answer
Answer: E. Leukapheresis is used with hydroxyurea only for symptomatic leukostasis when induction cannot start at once. Hyperleukocytosis occurs in 10–20% of new AML.
In what proportion of AML/MDS in young adults may an inherited predisposition be the cause?
AUnder 1%
BAbout 50%
CAll cases
D10–20%
EAbout 80%
Show answer
Answer: D. It is 5–10% in older adults. It matters when a sibling is the planned donor, so germline-type variants (DDX41, RUNX1, GATA2, biallelic CEBPA) need follow-up.
Prepared and reviewed by Dr. Haritha Chiramana for teaching. Facts compiled from current guidelines, primary trials and evidence summaries, written in our own words; drawings are original schematics, not patient images; no doses are included.