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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.
← Chronic Myeloid Leukaemia mini review

Chronic Myeloid Leukaemia: MCQ bank

90 clinical-vignette questions in three levels: 30 basics, 30 applied and innovative, and 30 challenging (23 Diagnosis, 60 Treatment, 7 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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Topic

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

Which genetic change defines chronic myeloid leukaemia (CML)?

  1. AJAK2 V617F point mutation
  2. Bt(9;22) making BCR::ABL1
  3. Ct(15;17) making PML::RARA
  4. Dt(8;21) making RUNX1::RUNX1T1
  5. Et(14;18) joining IGH to BCL2
Show answer

Answer: B. The Philadelphia chromosome, t(9;22)(q34;q11.2), joins BCR to ABL1. One fusion gene drives the disease, and it is the target of every tyrosine kinase inhibitor (TKI).

Review: section 01

Q2DiagnosisLevel 1At a glance

What does the BCR::ABL1 fusion gene produce?

  1. AA transcription factor that blocks maturation
  2. BA growth factor receptor without a kinase
  3. CAn anti-apoptotic protein of the BCL2 family
  4. DA truncated tumour suppressor protein
  5. EA tyrosine kinase that is always switched on
Show answer

Answer: E. The fusion makes a constitutively active ABL1 tyrosine kinase. TKIs block this kinase; asciminib binds a different site (the myristoyl pocket) from the others (the ATP site).

Review: section 01

Q3DiagnosisLevel 1Presentation, traps & genetics

Which is the only established risk factor for CML?

  1. ABenzene exposure
  2. BTobacco smoking
  3. CA parent with CML
  4. DEpstein-Barr virus infection
  5. EIonising radiation
Show answer

Answer: E. Ionising radiation is the only known risk factor. There is no familial tendency, and CML is not passed on to children.

Review: section 02

Q4DiagnosisLevel 1ImagePresentation, traps & genetics

This schematic blood film is from a 45-year-old with a white count of 150,000/µL and a large spleen. Which description fits it best?

Schematic drawing · not a patient image
  1. AGranulocytes at every stage, with basophils
  2. BLymphocytes with hair-like cytoplasmic projections
  3. CNeutrophils with toxic granules and Döhle bodies
  4. DSmall mature lymphocytes and smudge cells
  5. EUniform blasts containing Auer rods
Show answer

Answer: A. Chronic-phase CML shows every stage from myeloblast to neutrophil, more myelocytes than metamyelocytes, basophilia (always) and often eosinophilia, with blasts usually under 2%.

Review: section 02

Q5DiagnosisLevel 1Presentation, traps & genetics

About what proportion of people with CML have no symptoms when it is found?

  1. ANearly all
  2. BUp to half
  3. CAbout 9 in 10
  4. DFewer than 1 in 20
  5. EAbout 1 in 10
Show answer

Answer: B. Up to half are diagnosed from a routine blood count. When present, symptoms include fatigue (34%), weight loss (20%), sweats and abdominal fullness (15% each).

Review: section 02

Q6DiagnosisLevel 1Presentation, traps & genetics

Which physical sign is most typical of chronic-phase CML?

  1. AGum hypertrophy
  2. BGeneralised lymphadenopathy
  3. CSkin nodules
  4. DSplenomegaly
  5. EJaundice
Show answer

Answer: D. The spleen is palpable in about half to three-quarters of patients, causing early satiety or left-sided pain. Nodes, skin or soft-tissue masses suggest a later phase.

Review: section 02

Q7DiagnosisLevel 1Presentation, traps & genetics

A 30-year-old with pneumonia has a white count of 45,000/µL. Which finding favours a leukemoid reaction over CML?

  1. ABasophilia on the film
  2. BToxic granules and Döhle bodies in neutrophils
  3. CMore myelocytes than metamyelocytes
  4. DA spleen palpable 8 cm below the costal margin
  5. EA platelet count of 700,000/µL
Show answer

Answer: B. Toxic granulation and Döhle bodies point to infection or inflammation; leukemoid reactions are rarely as high as CML and are BCR::ABL1 negative. Basophilia, a myelocyte bulge and a big spleen favour CML.

Review: section 02

Q8DiagnosisLevel 1ImageScreening, workup & staging

This schematic shows chromosomes 9 and 22 from a marrow karyotype. What is the shortened chromosome marked by the arrow called?

Marrow karyotype, chromosomes 9 and 22 (schematic)9der(9)22der(22)ABL1BCRSchematic drawing · not a patient image
  1. AA derivative chromosome 7
  2. BAn isochromosome 17q
  3. CA ring chromosome 22
  4. DThe Philadelphia chromosome
  5. EA double-minute chromosome
Show answer

Answer: D. The reciprocal translocation moves ABL1 from chromosome 9 to chromosome 22, leaving a short der(22): the Philadelphia (Ph) chromosome. More than 90% of patients show it on banding.

Review: section 03

Q9DiagnosisLevel 1Screening, workup & staging

Which test confirms the diagnosis of CML in a blood sample?

  1. AFlow cytometry for CD34
  2. BSerum vitamin B12 level
  3. CBCR::ABL1 by RT-PCR (or FISH)
  4. DLeucocyte alkaline phosphatase score
  5. EJAK2 V617F mutation testing
Show answer

Answer: C. CML is confirmed by t(9;22) on banding or FISH and/or BCR::ABL1 by RT-PCR, in blood or marrow. The transcript type and a baseline on the International Scale should be recorded.

Review: section 03

Q10DiagnosisLevel 1Screening, workup & staging

BCR::ABL1 is positive in the blood. Why is a bone marrow examination still advised at diagnosis?

  1. ATo exclude tuberculosis of the bone marrow
  2. BTo define the phase and find extra chromosomes
  3. CTo measure iron stores before starting treatment
  4. DTo obtain the platelet count needed for ELTS
  5. ETo confirm that BCR::ABL1 is really present
Show answer

Answer: B. Blood PCR confirms CML, but marrow morphology (blasts) and karyotype (extra chromosomes) decide the phase and the risk. A marrow is omitted only when the result would not change treatment.

Review: section 03

Q11DiagnosisLevel 1Screening, workup & staging

Which four items make up the ELTS score?

  1. AWhite count, basophils, eosinophils, sex
  2. BKaryotype, transcript type, JAK2, age
  3. CAge, haemoglobin, LDH, albumin
  4. DSpleen, liver, lymph nodes, B symptoms
  5. EAge, spleen size, blood blasts, platelets
Show answer

Answer: E. The EUTOS long-term survival (ELTS) score uses age, spleen size in cm, blood blasts and platelets. It was built on TKI-treated patients and best predicts death from CML; ELN 2025 prefers it to Sokal, Euro and EUTOS.

Review: section 03

Q12DiagnosisLevel 1Screening, workup & staging

Why should the spleen be measured and samples sent before hydroxyurea is started?

  1. AHydroxyurea causes splenic rupture
  2. BThe spleen grows during hydroxyurea
  3. CThe ELTS score is valid only on untreated values
  4. DHydroxyurea prevents a later TKI from working
  5. EHydroxyurea makes BCR::ABL1 undetectable
Show answer

Answer: C. ELTS needs untreated spleen size, blasts and platelets. Hydroxyurea itself does not affect later milestones, but the risk score is lost if values are recorded after it.

Review: section 03

Q13DiagnosisLevel 1Biomarkers

What is a major molecular response (MMR) in CML?

  1. ABCR::ABL1 of 1% or less on the International Scale
  2. BA normal white count and a spleen that is not palpable
  3. CNo Philadelphia-positive marrow metaphases
  4. DBCR::ABL1 of 10% or less on the International Scale
  5. EBCR::ABL1 of 0.1% or less on the International Scale
Show answer

Answer: E. MMR (MR3) is BCR::ABL1 ≤0.1% IS; MR4 is ≤0.01%, MR4.5 ≤0.0032% and MR5 ≤0.001%. Deep molecular response means MR4 or deeper.

Review: section 04

Q14DiagnosisLevel 1Biomarkers

Which set of findings defines a complete haematological response?

  1. AWBC <10,000/µL, platelets <450,000/µL, no immature cells, basophils <5%, spleen impalpable
  2. BBCR::ABL1 below 10% on the International Scale at 3 months of treatment
  3. CNormal haemoglobin and no symptoms, whatever the size of the spleen or the platelet count
  4. DNo Philadelphia-positive metaphases among 20 or more marrow cells counted
  5. EWBC <20,000/µL with any platelet count, blasts under 5% and a spleen of any size
Show answer

Answer: A. Complete haematological response is the first goal of treatment. No Ph-positive metaphases is a complete cytogenetic response; ≤10% at 3 months is a molecular milestone.

Review: section 04

Q15TreatmentLevel 1Systemic therapy

Which statement about the first TKI in chronic-phase CML is correct?

  1. AImatinib, a 2G TKI or asciminib give similar long-term survival
  2. BImatinib is no longer recommended for any patient
  3. CPonatinib is the preferred first TKI for most patients
  4. DSecond-generation TKIs add about 10% to overall survival
  5. EInterferon should be added to every first-line TKI
Show answer

Answer: A. 2G TKIs and asciminib give faster and deeper responses and fewer transformations than imatinib, but no overall survival gain. Comorbidity, risk score, goals and cost decide the choice.

Review: section 06

Q16TreatmentLevel 1Systemic therapy

Which TKI binds the myristoyl pocket of ABL1 rather than the ATP-binding site?

  1. ADasatinib
  2. BImatinib
  3. CBosutinib
  4. DNilotinib
  5. EAsciminib
Show answer

Answer: E. Asciminib is an allosteric (STAMP) inhibitor. Because it binds a different site, it works against many ATP-site mutations, including T315I, but myristoyl-pocket mutations resist it.

Review: section 06

Q17TreatmentLevel 1Systemic therapy

Pleural effusion is a characteristic side effect of which TKI?

  1. ANilotinib
  2. BAsciminib
  3. CBosutinib
  4. DImatinib
  5. EDasatinib
Show answer

Answer: E. Dasatinib causes pleural and pericardial effusions and, rarely, pulmonary arterial hypertension. It also impairs platelet function and can prolong the QTc.

Review: section 06

Q18TreatmentLevel 1Systemic therapy

For which patient is nilotinib generally best avoided?

  1. AA 45-year-old with lactose intolerance
  2. BA 50-year-old with Crohn disease
  3. CA 30-year-old with a past pleural effusion
  4. DA 58-year-old with diabetes and a past stroke
  5. EA 25-year-old with no other illness
Show answer

Answer: D. Nilotinib causes arterial occlusive disease, raised glucose and cholesterol, QTc prolongation and pancreatitis. It is avoided with diabetes, high cardiovascular risk or a previous vascular event. A past effusion argues against dasatinib; bowel disease against bosutinib.

Review: section 06

Q19TreatmentLevel 1Systemic therapy

Which side effect is most typical of bosutinib, mainly in the first weeks?

  1. APleural effusion
  2. BGynaecomastia
  3. CDiarrhoea
  4. DPeriorbital oedema
  5. EPeripheral arterial occlusion
Show answer

Answer: C. Bosutinib commonly causes early diarrhoea and raised liver enzymes; some start low and escalate. It is avoided with bowel, liver or kidney disease.

Review: section 06

Q20TreatmentLevel 1Systemic therapy

How often should BCR::ABL1 (IS) be measured on a TKI until MMR is reached?

  1. AAt least every 3 months
  2. BOnly at 12 months
  3. COnce a year
  4. DOnly when the blood count changes
  5. EEvery week
Show answer

Answer: A. PCR is done at least every 3 months until MMR is achieved and confirmed, then every 3–6 months (UpToDate) or 4–6 months (ELN 2025); more often if values fluctuate or rise.

Review: section 06

Q21TreatmentLevel 1Systemic therapy

Which set of results is "favourable" under ELN 2025 at 3, 6 and 12 months?

  1. A≤1%, ≤0.1% and ≤0.01%
  2. BUndetectable at every time point
  3. C≤50%, ≤10% and ≤1%
  4. D≤10%, ≤10% and ≤10%
  5. E≤10%, ≤1% and ≤0.1%
Show answer

Answer: E. Favourable milestones are BCR::ABL1 ≤10% at 3 months, ≤1% at 6 months and ≤0.1% (MMR) at 12 months. ELN 2025 renamed optimal/warning/failure as favourable/warning/unfavourable.

Review: section 06

Q22TreatmentLevel 1Systemic therapy

BCR::ABL1 is rising on imatinib. What is the first thing to check?

  1. AMissed tablets and interacting drugs
  2. BA whole-body PET-CT scan
  3. CHLA typing of brothers and sisters
  4. DA kinase-domain mutation by NGS
  5. EA repeat bone marrow biopsy and karyotype
Show answer

Answer: A. "Resistance" is often missed tablets. Ask kindly and specifically about adherence and new medicines before ordering mutation tests or switching.

Review: section 06

Q23TreatmentLevel 1Systemic therapy

A kinase-domain mutation test shows T315I. Which TKIs can still work?

  1. ADasatinib or nilotinib
  2. BPonatinib or asciminib
  3. CImatinib at a higher dose
  4. DAny second-generation TKI
  5. EBosutinib or nilotinib
Show answer

Answer: B. T315I resists imatinib, dasatinib, nilotinib and bosutinib. Ponatinib or asciminib are used, with a parallel donor search.

Review: section 06

Q24TreatmentLevel 1Systemic therapy

Among carefully selected patients who stop their TKI, about what proportion stay in treatment-free remission?

  1. AAbout 20%
  2. B40–50%
  3. CAbout 75%
  4. DNearly all
  5. EUnder 5%
Show answer

Answer: B. About 40–50% of eligible patients stay off treatment. Most who relapse lose MMR in the first 6–8 months and regain their response when the TKI is restarted.

Review: section 06

Q25TreatmentLevel 1Systemic therapy

A woman with chronic-phase CML becomes pregnant and her counts rise in the first trimester. Which treatment can be used at any stage of pregnancy?

  1. AInterferon
  2. BImatinib
  3. CNilotinib
  4. DHydroxyurea
  5. EDasatinib
Show answer

Answer: A. All TKIs are potentially teratogenic until organogenesis is complete (around week 16). Interferon, including pegylated forms, can be used at any time; imatinib or nilotinib only after week 16; dasatinib is avoided throughout.

Review: section 06

Q26SurvivorshipLevel 1Systemic therapy

A man taking imatinib wants to father a child. What is the advice?

  1. ASwitch to interferon until conception
  2. BStop the TKI for 3 months before trying
  3. CContinue the TKI while trying to conceive
  4. DStore sperm and avoid natural conception
  5. EStop the TKI and use hydroxyurea instead
Show answer

Answer: C. There is no convincing effect of TKIs on male fertility or on their children: in 428 pregnancies of partners of men on TKIs, 93.5% were live births with 2.5% congenital abnormalities.

Review: section 06

Q27TreatmentLevel 1Systemic therapy

How is myeloid blast phase of CML treated?

  1. AInterferon plus low-dose cytarabine
  2. BRadiotherapy to the spleen and marrow
  3. CA TKI with AML-type induction, then transplant
  4. DHydroxyurea and blood transfusions only
  5. EA TKI alone, continued for life
Show answer

Answer: C. Myeloid blast phase is treated like AML (intensive induction or, in older patients, a hypomethylating agent ± venetoclax) with a TKI, followed by allogeneic transplant where possible.

Review: section 06

Q28SurvivorshipLevel 1Survivorship

In Indian studies, up to what share of patients with CML do not take their TKI regularly?

  1. AAbout 1 in 20
  2. BUp to one-third
  3. CAbout three-quarters
  4. DUnder 1 in 50
  5. EAlmost all
Show answer

Answer: B. Non-adherence affects up to one-third of Indian patients and shortens event-free survival. Adherence is treatment: ask at every visit, involve the family and link to assistance programmes.

Review: section 08

Q29SurvivorshipLevel 1Survivorship

With TKI treatment, what is the life expectancy of most patients diagnosed in chronic phase?

  1. AShorter than with interferon
  2. BNormal only after a transplant
  3. CClose to the general population
  4. DAbout 10 years at most
  5. EAbout 3 to 5 years from diagnosis
Show answer

Answer: C. Life expectancy now approaches that of the general population (Bower 2016), although ELN 2025 notes small residual losses in Swedish data.

Review: section 08

Q30DiagnosisLevel 1Presentation, traps & genetics

How does the age at diagnosis in Indian hospital series compare with Western registries?

  1. AThe same (median 66 years)
  2. BMostly children under 15
  3. CAbout a decade younger (median 32–42 years)
  4. DAbout a decade older (median 75 years)
  5. EOnly people over 80
Show answer

Answer: C. Indian hospital series report median ages of 32–42, with more symptoms, bigger spleens and more high-risk scores, compared with 55 in Europe and 66 in the US. The Mumbai population registry shows the usual peak at 55–74, so referral patterns explain part of the gap.

Review: section 02

Level 2 · Applied & innovative

Clinical reasoning: calculations (pack-years, risk scores, NNT), imaging and laboratory findings, reading trial results, sequencing traps.

Q31DiagnosisLevel 2Presentation, traps & genetics

Which finding at diagnosis should make you think of MDS or an advanced phase rather than typical chronic-phase CML?

  1. ABasophilia on the film
  2. BA platelet count of 700,000/µL
  3. CA low platelet count
  4. DEosinophilia on the film
  5. EA white count of 300,000/µL
Show answer

Answer: C. Low platelets are uncommon in chronic phase. High platelets (over 600,000/µL in 15–30%), basophilia, eosinophilia and very high white counts are typical of chronic phase.

Review: section 02

Q32DiagnosisLevel 2Screening, workup & staging

A 40-year-old has a white count of 120,000/µL with myelocytes and basophils and a 10 cm spleen. Routine quantitative PCR for p210 and p190 is negative. What next?

  1. AStart imatinib without further tests
  2. BFISH for BCR::ABL1 with a marrow karyotype
  3. CDiagnose a leukemoid reaction and give antibiotics
  4. DRepeat the same PCR in 3 months
  5. ETreat as polycythaemia vera with hydroxyurea
Show answer

Answer: B. Routine kits detect only p210 and p190; p230 and rare transcripts, and some cryptic fusions, need FISH or a personalised assay. With high suspicion and a negative karyotype, FISH is mandatory.

Review: section 03

Q33DiagnosisLevel 2Screening, workup & staging

A man treated for chronic-phase CML for 3 years now has lymphoblasts on his blood film. What should you assume, and do?

  1. AReactive lymphocytosis after infection: no action
  2. BLymphoid blast phase: flow cytometry and lumbar puncture
  3. CA second cancer (CLL): watch and wait without tests
  4. DAn imatinib side effect: reduce the dose of imatinib
  5. EA viral reaction: repeat the blood film in 2 weeks
Show answer

Answer: B. Lymphoblasts in a patient with CML mean lymphoid blast phase until proved otherwise. Lineage by flow cytometry decides treatment (a Ph+ ALL-type regimen with a TKI), and a lumbar puncture is needed.

Review: section 03

Q34DiagnosisLevel 2Screening, workup & staging

A marrow at diagnosis shows 14% blasts. How do ICC 2022 and WHO 2022 classify it?

  1. ABoth systems: chronic phase without any risk features
  2. BBoth systems: blast phase, treated like acute leukaemia
  3. CICC: accelerated; WHO: chronic with a high-risk feature
  4. DICC: blast phase; WHO: accelerated phase
  5. EBoth systems: accelerated phase, with no other label
Show answer

Answer: C. ICC keeps three phases (accelerated 10–19% blasts, basophils ≥20%, high-risk extra chromosomes). WHO 2022 has only chronic and blast phase and lists blasts 10–19% as a high-risk feature. Both agree such patients need a more potent TKI and closer monitoring.

Review: section 03

Q35DiagnosisLevel 2Screening, workup & staging

What blast percentage defines blast phase in ICC 2022 and WHO 2022, and how did the older ELN criteria differ?

  1. A30% or more in all systems
  2. B5% or more; the older ELN criteria used 10% or more
  3. C50% or more; the older ELN criteria used 30% or more
  4. D20% or more; the older ELN criteria used 30% or more
  5. E10% or more; the older ELN criteria used 20% or more
Show answer

Answer: D. Both modern systems use ≥20% blasts (or extramedullary blast proliferation, or bona fide lymphoblasts). Most trials used the older ELN cut-off of ≥30%, so read trial phase definitions carefully.

Review: section 03

Q36DiagnosisLevel 2Biomarkers

A patient's BCR::ABL1 was 0.08% (IS) in laboratory A. A cheaper laboratory B now reports 0.3%. What is the correct step?

  1. ADouble the TKI dose and recheck in a year
  2. BOrder a kinase-domain mutation test straight away
  3. CArrange a bone marrow biopsy and karyotype
  4. DDeclare loss of MMR and switch to another TKI
  5. ERepeat in the original IS laboratory before acting
Show answer

Answer: E. Results are comparable only on the International Scale in a standardised laboratory: one laboratory, one scale. Never switch on one result; repeat near a threshold within 1–2 months.

Review: section 04

Q37TreatmentLevel 2Systemic therapy

A 60-year-old with diabetes, a past myocardial infarction and a high ELTS score has chronic-phase CML. Which first-line choice fits best?

  1. ANilotinib, because the ELTS score is high
  2. BImatinib with interferon added from the start
  3. CDasatinib, bosutinib or asciminib, not nilotinib
  4. DInterferon alone, to avoid TKI toxicity
  5. EPonatinib, because the risk score is high
Show answer

Answer: C. High ELTS favours a 2G TKI or asciminib; comorbidity then decides. Nilotinib is avoided with diabetes or vascular disease. Interferon added to a TKI is not recommended, and ponatinib is not a first-line drug.

Review: section 06

Q38TreatmentLevel 2Systemic therapy

Which TKI is best avoided in a patient with chronic lung disease and a previous pleural effusion?

  1. ADasatinib
  2. BImatinib
  3. CAsciminib
  4. DBosutinib
  5. ENilotinib
Show answer

Answer: A. Dasatinib causes effusions and pulmonary arterial hypertension, so lung disease, effusions and bleeding disorders argue against it.

Review: section 06

Q39TreatmentLevel 2Systemic therapy

A patient on dasatinib is started on omeprazole for dyspepsia. What is the concern?

  1. AOmeprazole causes pleural effusion
  2. BDasatinib levels rise to toxic levels
  3. CThe PCR result becomes falsely low
  4. DLess dasatinib is absorbed
  5. EThere is no interaction
Show answer

Answer: D. Acid-suppressing drugs reduce absorption of dasatinib and nilotinib (a dasatinib formulation that tolerates them exists in some markets). Check every new prescription, including azoles, macrolides and QT-prolonging drugs.

Review: section 06

Q40TreatmentLevel 2Systemic therapy

When should an ECG be done after starting nilotinib or dasatinib?

  1. AAt baseline and 1–2 weeks after starting
  2. BOnly before stopping treatment
  3. COnce a year
  4. DOnly if the patient has palpitations
  5. EIt is not needed with these TKIs
Show answer

Answer: A. An ECG for the QTc is done at baseline, 1–2 weeks after starting nilotinib or dasatinib, after dose changes and when new QT-prolonging drugs are added; potassium and magnesium are corrected.

Review: section 06

Q41TreatmentLevel 2ImageSystemic therapy

This schematic chart shows one patient's BCR::ABL1 (IS) on first-line imatinib. How does ELN 2025 classify the 6-month result?

BCR::ABL1 (IS), first-line imatinib (schematic)100%10%1%0.1%0.01%0.001%0 mo3 mo6 mo12 mo60%8%4%duemonths on treatment · log scaleSchematic drawing · not a patient image
  1. ATreatment-free remission can be tried
  2. BFavourable: no change needed
  3. CUnfavourable: a switch is preferred
  4. DWarning: a switch may be needed
  5. EMajor molecular response
Show answer

Answer: D. At 6 months, ≤1% is favourable, >1–10% is warning and >10% is unfavourable. A warning result calls for a repeat, questions about missed doses and interacting drugs, and a decision based on the trend and the patient's goals.

Review: section 06

Q42TreatmentLevel 2Systemic therapy

Two weeks after starting imatinib, the platelet count has fallen mildly and the patient is well. What is appropriate?

  1. AContinue: early cytopenias reflect the leukaemia clearing
  2. BStop imatinib permanently and switch to another TKI
  3. CBegin a work-up for urgent allogeneic transplant
  4. DStart an erythropoietin-stimulating agent at once
  5. ESwitch to ponatinib because of primary resistance
Show answer

Answer: A. Mild early cytopenias are mostly the leukaemia clearing; continue. Severe ones need a hold or dose reduction. Erythropoietin-stimulating agents are avoided (thrombosis, no benefit).

Review: section 06

Q43TreatmentLevel 2Systemic therapy

BCR::ABL1 has risen on two tests and the patient takes every tablet with no interacting drugs. What comes next?

  1. AAdding interferon to the same TKI and continuing
  2. BStopping all treatment and watching the counts
  3. CA drug holiday of 3 months, then repeat the PCR
  4. DIncreasing hydroxyurea alongside the same TKI
  5. EMarrow (blasts, karyotype) and a mutation test
Show answer

Answer: E. After confirming the rise and checking adherence and interactions, look for progression (blasts, extra chromosomes) and kinase-domain mutations, then switch TKI. Mutation testing is not done at diagnosis in chronic phase.

Review: section 06

Q44TreatmentLevel 2Systemic therapy

A patient loses response on dasatinib (first line). No mutation is found. Which next step fits current guidance?

  1. ASwitch back to imatinib
  2. BSwitch to nilotinib
  3. CBosutinib, as it always works after dasatinib
  4. DPonatinib or asciminib, and start a donor search
  5. EContinue dasatinib and recheck in a year
Show answer

Answer: D. After a 2G TKI fails, another 2G TKI rarely works; ponatinib or asciminib are preferred. ELN 2025 advises a donor search from resistance to the first 2G TKI.

Review: section 06

Q45TreatmentLevel 2Systemic therapy

F317L is found in a patient losing response on dasatinib. Which TKI is NOT expected to work against this mutation?

  1. APonatinib
  2. BDasatinib
  3. CAsciminib
  4. DBosutinib
  5. ENilotinib
Show answer

Answer: B. In the ELN 2025 mutation table, F317L/V/I/C resists dasatinib; nilotinib, bosutinib, ponatinib and asciminib remain options. These are in-vitro data, read with the patient's history.

Review: section 06

Q46TreatmentLevel 2Systemic therapy

V299L is found in a patient on bosutinib. Which of these is a suitable next TKI?

  1. ANilotinib
  2. BImatinib at a higher dose
  3. CDasatinib
  4. DBosutinib at the same dose
  5. EImatinib
Show answer

Answer: A. V299L resists dasatinib and bosutinib; nilotinib, ponatinib and asciminib are listed as options. Most kinase-domain mutations resist imatinib.

Review: section 06

Q47TreatmentLevel 2Systemic therapy

Four months after stopping a TKI in deep remission, a patient loses MMR. What is the correct response?

  1. AWait for a second positive result 3 months later
  2. BStart ponatinib
  3. CArrange an urgent allogeneic transplant
  4. DRestart the TKI; no mutation test is needed
  5. EOrder a mutation test before restarting
Show answer

Answer: D. Loss of MMR after stopping is the trigger to restart (one result is enough under ELN 2025). Mutation testing is not needed: 90–95% regain their response on the same TKI.

Review: section 06

Q48TreatmentLevel 2Systemic therapy

After stopping a TKI, when do most molecular relapses occur?

  1. AAfter 5 years off treatment
  2. BEvenly spread over 10 years
  3. CIn the second year off treatment
  4. DIn the first week after stopping
  5. EWithin the first 6–8 months
Show answer

Answer: E. More than 80% of molecular relapses occur in the first 6–8 months, so PCR is done every 6–8 weeks early on, then every 2 months, then every 3–6 months for life. Late loss of MMR occurs in up to 14% after 2 years.

Review: section 06

Q49TreatmentLevel 2Systemic therapy

A 29-year-old woman has been in MR4 for 3 years on imatinib (6 years in total) and wants a pregnancy. What does ELN 2025 advise?

  1. AContinue imatinib throughout the whole pregnancy
  2. BAdvise against pregnancy at any time in the future
  3. CStop the TKI as for TFR, then plan the pregnancy
  4. DSwitch to nilotinib and try to conceive straight away
  5. ESwitch to dasatinib before trying to conceive
Show answer

Answer: C. With MR4 or deeper, women stop as for TFR with close monitoring. Pregnancy should be raised at diagnosis with every woman of child-bearing age; planned pregnancies take time.

Review: section 06

Q50TreatmentLevel 2Systemic therapy

A woman in MMR (but not MR4) with regular cycles and good access to testing wants a pregnancy. Which option does ELN 2025 accept?

  1. ASwitch to ponatinib before trying to conceive
  2. BContinue the TKI until the first positive test
  3. CUndergo allogeneic transplant before conceiving
  4. DContinue the TKI throughout the whole pregnancy
  5. EStop the TKI only after the baby is delivered
Show answer

Answer: B. With MMR, women may stop and watch, or (with regular cycles and access to tests) continue until the first positive pregnancy test, then stop. Without MMR the response should be deepened first.

Review: section 06

Q51TreatmentLevel 2Systemic therapy

CML is diagnosed at 10 weeks of pregnancy: white count 60,000/µL, low ELTS, no extra chromosomes, no symptoms. What is reasonable?

  1. AStart dasatinib now, as it is the most potent TKI
  2. BWatchful waiting; leukapheresis or interferon if needed
  3. CTermination of the pregnancy in every case
  4. DStart imatinib now, before the counts rise further
  5. EHydroxyurea throughout the rest of the pregnancy
Show answer

Answer: B. With WBC <100,000/µL, low or intermediate ELTS and no extra chromosomes, watchful waiting is reasonable; leukapheresis and/or interferon for symptoms or high counts; aspirin and/or LMW heparin for high platelets. No TKI before week 16.

Review: section 06

Q52TreatmentLevel 2Systemic therapy

Which TKI should be avoided throughout pregnancy, even after week 16?

  1. ANone: all are allowed after week 16
  2. BNilotinib
  3. CImatinib
  4. DInterferon (not a TKI)
  5. EDasatinib
Show answer

Answer: E. Imatinib and nilotinib cross the placenta poorly and can be used after week 16 if control is lost. Dasatinib reached 75% of maternal levels in the one case measured and is avoided throughout.

Review: section 06

Q53TreatmentLevel 2Systemic therapy

A mother on imatinib after delivery asks about breastfeeding. What is the advice?

  1. ABreastfeed only on alternate days
  2. BBreastfeeding is safe on imatinib only
  3. CSwitch to dasatinib to breastfeed
  4. DNo TKI while breastfeeding
  5. EBreastfeeding is safe on any TKI
Show answer

Answer: D. ELN 2025 advises no TKI while breastfeeding. The choice between breastfeeding and restarting treatment is planned in advance with the mother.

Review: section 06

Q54TreatmentLevel 2Systemic therapy

A fit 40-year-old with CML presents in myeloid blast phase with no prior TKI. What is the best plan?

  1. ATKI with intensive AML induction, then transplant
  2. BHydroxyurea and palliative care from the start
  3. CImatinib alone, continued for the rest of life
  4. DIntensive AML chemotherapy without any TKI
  5. ETreatment-free remission once induction ends
Show answer

Answer: A. In 104 patients, 5-year OS was 30% with a TKI plus intensive chemotherapy, 28% with a TKI plus a hypomethylating agent, 13% with a TKI alone and 0% with chemotherapy alone. Imatinib is avoided in blast phase; transplant follows.

Review: section 06

Q55TreatmentLevel 2Systemic therapy

In lymphoid blast phase of CML, which combination is used?

  1. AInterferon and hydroxyurea, continued indefinitely
  2. BTKI + Ph+ ALL regimen, lumbar puncture, then transplant
  3. CA TKI alone, without any chemotherapy or transplant
  4. DAML-type induction chemotherapy without a TKI
  5. ERadiotherapy to the spleen and the whole marrow
Show answer

Answer: B. Lymphoid blast phase (about one-third of blast phases) is treated like Ph+ ALL (hyper-CVAD best studied; blinatumomab or inotuzumab with a TKI emerging), with CNS assessment and allogeneic transplant.

Review: section 06

Q56TreatmentLevel 2Local therapy

In which situation is a lumbar puncture indicated in CML?

  1. ALymphoid blast phase or neurological signs
  2. BEvery patient at diagnosis
  3. CBefore every bone marrow biopsy
  4. DEvery patient before stopping a TKI
  5. ENeurologically well patients in myeloid blast phase
Show answer

Answer: A. A lumbar puncture is done in lymphoid blast phase or with neurological signs, not in neurologically well patients with myeloid blast phase. Dasatinib, bosutinib, nilotinib and ponatinib cross the blood-brain barrier.

Review: section 05

Q57TreatmentLevel 2Systemic therapy

A patient presents de novo in accelerated phase. Which statement is correct?

  1. AImatinib is the preferred TKI in this phase
  2. BTransplant is needed before any TKI is given
  3. CNo TKI is effective once accelerated phase is reached
  4. DA 2G TKI is preferred to imatinib; no TFR attempts
  5. ETFR can be tried after 2 years of deep response
Show answer

Answer: D. De novo accelerated phase is treated with a 2G TKI (or ponatinib, or upfront transplant), continued indefinitely; there are no TFR data. BCR::ABL1 <10% at 3 months predicts better survival.

Review: section 06

Q58TreatmentLevel 2ImageSystemic therapy

This schematic chest X-ray is from a 55-year-old on dasatinib for 2 years with new breathlessness. What is the most appropriate approach?

RSchematic drawing · not a patient image
  1. ASwitch to imatinib at once without any further assessment
  2. BAssess the effusion, exclude other causes, hold or reduce dasatinib
  3. CContinue dasatinib unchanged and add a diuretic only
  4. DStop all TKIs permanently and watch the counts
  5. EStart anti-tuberculosis treatment empirically for 6 months
Show answer

Answer: B. Effusions on dasatinib need a chest X-ray and exclusion of infection, heart failure, kidney disease and progression. Some need thoracentesis, a drain or pleurodesis, with interruption or dose reduction; persistent problems mean a switch.

Review: section 06

Q59SurvivorshipLevel 2Survivorship

Which ongoing checks matter most for a patient on long-term nilotinib?

  1. APulmonary function every 3 months
  2. BBone marrow every 6 months
  3. CBlood pressure, glucose and lipids
  4. DThyroid scans every year
  5. EHearing and vision
Show answer

Answer: C. Cardiovascular risk is highest with ponatinib and nilotinib. Blood pressure, glucose, lipids and symptoms of vascular disease are checked at visits; age, hypertension, diabetes, lipids and smoking add risk whatever the TKI.

Review: section 08

Q60SurvivorshipLevel 2Survivorship

A 12-year-old on imatinib for 18 months has slowed growth. Which statement is correct?

  1. AAlways temporary, with full catch-up within 6 months
  2. BA recognised TKI effect: watch height, puberty, thyroid and bone
  3. CUnrelated to the TKI, so no action or follow-up is needed
  4. DA sign that the CML has progressed to blast phase
  5. EA reason to stop imatinib at once and permanently
Show answer

Answer: B. In the German CML-PAED II study, median height fell by 0.35 SD at 12 months and 0.76 SD at 24 months. Children need growth, puberty, thyroid and bone surveillance and endocrinology input.

Review: section 08

Level 3 · Challenging

DNB, DM and USMLE Step 3 level: landmark trials, newer targeted drugs and difficult decisions.

Q61TreatmentLevel 3Systemic therapy

In IRIS, what was the 18-month progression-free survival with imatinib versus interferon plus cytarabine?

  1. A92% vs 97%
  2. B80% vs 60%
  3. C75% vs 70%
  4. D97% vs 92%
  5. E99% vs 50%
Show answer

Answer: D. IRIS (1106 patients) established imatinib, with better quality of life. 10-year OS was 84%, with most of the control arm crossing over.

Review: section 06

Q62TreatmentLevel 3Systemic therapy

In ENESTnd, how many progressions to accelerated or blast phase occurred on imatinib compared with the two nilotinib arms?

  1. ANone in any arm
  2. B12 vs 33 and 40
  3. C9 vs 12 and 33
  4. D100 vs 50 and 25
  5. E33 vs 12 and 9
Show answer

Answer: E. Nilotinib reduced progression but caused more cardiovascular events, with no overall survival gain.

Review: section 06

Q63TreatmentLevel 3Systemic therapy

In a meta-analysis of 8 trials (2974 patients) comparing 2G TKIs with imatinib, what was the rate of progression?

  1. A10% vs 20%, with a survival gain
  2. BNo difference in progression
  3. C0.8% vs 3.0%, with no survival difference
  4. D0.8% vs 3.0%, with a 10% survival gain
  5. E3.0% vs 0.8%, favouring imatinib
Show answer

Answer: C. Second-generation TKIs gave faster, deeper responses and fewer transformations (Yun 2016), but overall survival was the same.

Review: section 06

Q64TreatmentLevel 3Systemic therapy

In ASC4FIRST, what was the MMR rate at 96 weeks with asciminib versus investigator-chosen TKIs?

  1. A96% vs 52%
  2. B37.6% vs 15.8%
  3. C52.0% vs 74.1%
  4. D74.1% vs 52.0%
  5. E44% vs 23%
Show answer

Answer: D. Asciminib also gave event-free survival of 85.6% vs 70.6% and fewer discontinuations; overall survival is not yet reported. FDA approved it first line; EMA only after ≥2 TKIs.

Review: section 06

Q65TreatmentLevel 3Systemic therapy

In ASCEMBL (patients after 2 or more TKIs), what was the MMR rate at 96 weeks?

  1. ANo difference
  2. B60% with asciminib vs 40% with ponatinib
  3. C37.6% with asciminib vs 15.8% with bosutinib
  4. D15.8% with asciminib vs 37.6% with bosutinib
  5. E74.1% with asciminib vs 52.0% with bosutinib
Show answer

Answer: C. Asciminib also caused fewer discontinuations for side effects than bosutinib.

Review: section 06

Q66TreatmentLevel 3Systemic therapy

In PACE (chronic phase after dasatinib or nilotinib, or with T315I), which pair of results is correct for ponatinib?

  1. A5-year OS 73%, arterial occlusive events 31%
  2. BMMR 90%, arterial occlusive events 1%
  3. C5-year OS 31%, arterial occlusive events 73%
  4. D5-year OS 50%, no vascular events
  5. ENo responses in T315I
Show answer

Answer: A. PACE gave a major cytogenetic response in 60% and MMR in 40%, but vascular events in 31%. OPTIC then tested response-based dose reduction.

Review: section 06

Q67TreatmentLevel 3Systemic therapy

What was the key design idea of OPTIC?

  1. ACompare ponatinib with allogeneic transplant in T315I
  2. BUse ponatinib first line in low-risk chronic phase
  3. CStop ponatinib after 12 months in major molecular response
  4. DStart ponatinib higher, reduce once BCR::ABL1 <1%
  5. ECombine ponatinib with pegylated interferon
Show answer

Answer: D. Response-based reduction balanced efficacy (44%, 29% and 23% below 1% at 12 months by starting dose) against arterial events (10%, 5% and 3%).

Review: section 06

Q68TreatmentLevel 3Systemic therapy

In a registry comparison of patients with T315I, what was 48-month survival with ponatinib versus allogeneic transplant?

  1. A30% vs 80%
  2. B73% vs 56%
  3. C20% vs 20%
  4. D95% vs 40%
  5. E56% vs 73%
Show answer

Answer: B. Nicolini 2017 favoured ponatinib in chronic phase with T315I. Omacetaxine is no longer manufactured; olverembatinib is approved only in China.

Review: section 06

Q69TreatmentLevel 3Systemic therapy

In EURO-SKI (755 patients), what proportion kept MMR 6 and 12 months after stopping a TKI?

  1. A90% and 85%
  2. B46% and 61%
  3. C100% and 95%
  4. D20% and 10%
  5. E61% and 46%
Show answer

Answer: E. LAST reported 77% at 6 and 71% at 12 months, with less fatigue, depression, diarrhoea and sleep disturbance. Similar results followed nilotinib (ENESTfreedom) and dasatinib (DASFREE).

Review: section 06

Q70TreatmentLevel 3Systemic therapy

In DESTINY, what was the treatment-free remission rate after halving the dose for 12 months before stopping, in patients with MR4 or deeper?

  1. A25%
  2. B10%
  3. C95%
  4. D45%
  5. E72%
Show answer

Answer: E. De-escalation before stopping also lets a patient who relapses restart at the reduced dose. Overall, 40–50% of eligible patients stay off treatment.

Review: section 06

Q71TreatmentLevel 3Systemic therapy

Which statement about late outcomes after stopping a TKI is correct?

  1. ALate MMR loss in up to 14%; sudden blast phase ≤0.1%
  2. BRelapse never happens after 12 months off treatment
  3. COnce MMR is lost, a second response is unusual
  4. DBlast phase occurs in about 10% of those who stop
  5. EMost relapses happen more than 5 years after stopping
Show answer

Answer: A. Monitoring is the safety net: >80% of relapses come in the first 6–8 months, late loss can occur (Rousselot 2020), and 90–95% regain their response on restarting. A withdrawal syndrome (aches) affects 20–30%.

Review: section 06

Q72TreatmentLevel 3Systemic therapy

In CML Study IV (Lauseker 2023), what was 10-year survival in patients still above 10% BCR::ABL1 at 12 months?

  1. AUnder 5%
  2. BAbout 20%
  3. CAbout 55%
  4. DAbout 80%
  5. EAbout 95%
Show answer

Answer: C. Patients who missed the 3-, 6- or 12-month milestones still had about 80% 10-year survival, but only 55% if BCR::ABL1 was still >10% at 12 months. This is why ELN 2025 bases switching on the trend, adherence, comorbidity and goals.

Review: section 06

Q73TreatmentLevel 3Systemic therapy

Without an early molecular response on imatinib, what did switching to dasatinib achieve in DASCERN?

  1. ANo difference in major molecular response
  2. BMore progressions to blast phase on dasatinib
  3. CTreatment-free remission in most patients
  4. DDeeper responses (MMR 77% vs 44%), same survival
  5. EA large overall survival gain over imatinib
Show answer

Answer: D. Fit or younger patients seeking TFR may switch for a deeper response; older or comorbid patients may continue with close monitoring.

Review: section 06

Q74SurvivorshipLevel 3Survivorship

In Marin 2010, what proportion of patients with 90% adherence or more reached MMR at 6 years, compared with those below 90%?

  1. A28% vs 95%
  2. B100% vs 80%
  3. C60% vs 55%
  4. D50% vs 45%
  5. E95% vs 28%
Show answer

Answer: E. No patient with ≤80% adherence reached MMR. Adherence is part of treatment, and in India non-adherence (Ganesan 2011) shortens event-free survival.

Review: section 08

Q75DiagnosisLevel 3Screening, workup & staging

In CML Study IV (Saussele 2015), how did 8-year overall survival change across Charlson comorbidity groups?

  1. AIt was the same in all groups
  2. BFrom 80% to 75%
  3. CFrom 94% (Charlson 2) to 46% (7 or more)
  4. DFrom 99% to 95%
  5. EFrom 46% to 94% (rising with comorbidity)
Show answer

Answer: C. Comorbidity now predicts survival more than CML itself for many patients, because most now die of other causes. ELTS best predicts death from CML.

Review: section 03

Q76TreatmentLevel 3Systemic therapy

In 104 patients with myeloid blast phase (Saxena 2021), what was 5-year overall survival with a TKI plus intensive chemotherapy?

  1. A0%
  2. B50%
  3. C60%
  4. D30%
  5. E80%
Show answer

Answer: D. 5-year OS was 30% with TKI + intensive chemotherapy, 28% with TKI + a hypomethylating agent, 13% with a TKI alone and 0% with chemotherapy alone. MATCHPOINT (ponatinib + FLAG-IDA) bridged two-thirds back to chronic phase.

Review: section 06

Q77TreatmentLevel 3Systemic therapy

In lymphoid blast phase treated with hyper-CVAD plus a TKI (Strati 2014), what was median overall survival with and without allogeneic transplant?

  1. A9 months vs 93 months
  2. BNot reached in either group
  3. C93 months vs 9 months
  4. D60 months vs 48 months
  5. E24 months in both groups
Show answer

Answer: C. Transplant after remission is the main route to long-term survival in blast phase. Lymphoid blast phase makes up about one-third of blast phases.

Review: section 06

Q78TreatmentLevel 3Systemic therapy

Among imatinib-exposed pregnancies with known outcome (Pye 2008), about what proportion had fetal abnormalities?

  1. AAbout 50%
  2. BAbout 1%
  3. CAbout 10%
  4. DNone
  5. EAbout 30%
Show answer

Answer: C. Of 180 exposed pregnancies, half with known outcome were normal and about 10% had abnormalities. Risk is assumed from implantation (about 15 days after fertilisation) until about week 16, which is why women stop TKIs.

Review: section 06

Q79TreatmentLevel 3Systemic therapy

In the ELN registry of 87 women diagnosed with CML during pregnancy (Chelysheva 2024), what happened?

  1. A76% had a normal childbirth, no excess malformations
  2. BMost women progressed to blast phase in pregnancy
  3. CNearly all women received dasatinib in pregnancy
  4. DMalformations occurred in about half of the babies
  5. EMost pregnancies had to be terminated for safety
Show answer

Answer: A. Treatment was mostly interferon and, after week 16, imatinib. In advanced phase, treatment cannot wait, and termination should be discussed with the woman and her family.

Review: section 06

Q80TreatmentLevel 3Systemic therapy

In a Japanese series of 70 pregnancies (Kondo 2025), when did planned pregnancies occur compared with unplanned ones?

  1. AA median 4.1 vs 10.6 years after diagnosis
  2. BBoth within the first year
  3. COnly after allogeneic transplant
  4. DA median 10.6 vs 4.1 years after diagnosis
  5. EA median 1 vs 10 years after diagnosis
Show answer

Answer: D. Planned pregnancies (during TFR or on interferon) take time, which is why parenting is discussed from diagnosis.

Review: section 06

Q81DiagnosisLevel 3Biomarkers

Which transcripts are expected to resist asciminib?

  1. AThose lacking ABL1 exon 2 (e13a3, e14a3)
  2. BAny p190 (e1a2) transcript, whatever the phase
  3. CThe rare p230 (e19a2) transcript in every case
  4. DThe common e13a2 and e14a2 transcripts
  5. EAny transcript carrying the T315I mutation
Show answer

Answer: A. Rare transcripts without ABL1 exon 2 are expected to resist asciminib (ELN 2025). The transcript type also decides how to monitor; e14a2 is associated with more successful TFR.

Review: section 04

Q82TreatmentLevel 3Systemic therapy

Which statement about compound kinase-domain mutations is correct?

  1. AThey respond best to imatinib at a standard dose
  2. BThey always respond to bosutinib as second line
  3. CSanger sequencing detects them better than NGS
  4. DThey are found routinely at diagnosis in chronic phase
  5. ESome with T315I resist both ponatinib and asciminib
Show answer

Answer: E. Compound mutations (two in the same molecule) resist most TKIs. NGS finds emerging clones earlier than Sanger sequencing and identifies compound mutations; transplant should be considered.

Review: section 06

Q83TreatmentLevel 3Systemic therapy

Under the ELN 2025 mutation table, which TKI is NOT recommended for E255K/V?

  1. ADasatinib
  2. BNilotinib
  3. CPonatinib
  4. DAsciminib
  5. ENone: all four are recommended
Show answer

Answer: B. ELN lists dasatinib, ponatinib and asciminib for E255K/V; nilotinib and bosutinib are not recommended. The UpToDate in-vitro table also lists bosutinib, so read the laboratory report with both tables.

Review: section 06

Q84TreatmentLevel 3Systemic therapy

F359V is found in a patient losing response on nilotinib. Which option does the ELN 2025 table recommend?

  1. AContinuing nilotinib
  2. BStopping all TKIs
  3. CAsciminib
  4. DDasatinib
  5. EImatinib at a higher dose
Show answer

Answer: D. For F359V/I/C, ELN lists dasatinib and ponatinib; nilotinib, bosutinib and asciminib are not recommended. (UpToDate also lists bosutinib for F359V.)

Review: section 06

Q85TreatmentLevel 3Systemic therapy

A myristoyl-pocket mutation (for example A337V) is found on asciminib. Which statement is correct?

  1. AATP-site TKIs may still work
  2. BOnly imatinib remains active
  3. CA higher asciminib dose overcomes it
  4. DIt always means blast phase
  5. ENo TKI can work any longer
Show answer

Answer: A. Myristoyl-pocket mutations resist asciminib but not the ATP-site TKIs, which bind elsewhere on the kinase.

Review: section 06

Q86TreatmentLevel 3Local therapy

Which statement on allogeneic transplant in CML reflects ELN 2025?

  1. AReduced-intensity conditioning is preferred for every patient
  2. BMyeloablative conditioning is preferred where possible
  3. CDonor search should wait until ponatinib has failed
  4. DTKIs must never be given again after transplant
  5. ETransplant of resistant blast phase is advised outside trials
Show answer

Answer: B. Reduced intensity is used for older or less fit patients. A donor search starts at resistance to the first 2G TKI, and transplant referral at resistance to ponatinib and/or asciminib. TKIs and donor lymphocytes treat molecular relapse after transplant.

Review: section 05

Q87TreatmentLevel 3Systemic therapy

In de novo accelerated phase treated with dasatinib or nilotinib (Ohanian 2014), what was the complete cytogenetic response rate in 21 patients?

  1. AAbout 90%
  2. BAbout 10%
  3. CNone
  4. DAbout 50%
  5. EAbout 30%
Show answer

Answer: A. A 2G TKI is preferred to imatinib in de novo accelerated phase, continued indefinitely. In transformed accelerated phase, dasatinib after imatinib gave complete haematological responses in 50% and complete cytogenetic responses in 32%.

Review: section 06

Q88SurvivorshipLevel 3Survivorship

In the international registry of 535 children (Millot 2026), what was 3-year PFS by ELTS group (low, intermediate, high)?

  1. A99% in all groups
  2. B72.0%, 91.7% and 97.1%
  3. C50%, 40% and 30%
  4. D80%, 60% and 20%
  5. E97.1%, 91.7% and 72.0%
Show answer

Answer: E. 3-year OS was 97.4%. Children have bulky disease, more lymphoid blast crises and slower growth on imatinib, and stopping succeeds less often (28.6% in STOP IMAPED at 6 months).

Review: section 08

Q89TreatmentLevel 3At a glance

What did the Tata Memorial series (Parikh 2013; 972 patients, median age 36) show?

  1. AInterferon gave better results than imatinib
  2. BGeneric imatinib gave much worse responses
  3. COS was only 40% at 5 years on imatinib
  4. DMost patients presented in blast phase
  5. EOS 86% at 51 months; generic = innovator
Show answer

Answer: E. Generic imatinib and assistance programmes (GIPAP, Max Foundation) made CML treatable for most Indian patients. ELN 2025 puts generic imatinib at as little as US$200–500 a year.

Review: section 01

Q90TreatmentLevel 3Systemic therapy

In heavily pretreated patients (Hughes 2019), what proportion reached MMR at 12 months on asciminib?

  1. A90% overall and 80% of those with T315I
  2. B10% overall and none with T315I
  3. C74% overall and 52% with T315I
  4. D48% overall and 28% of those with T315I
  5. E28% overall and 48% of those with T315I
Show answer

Answer: D. Responses included some patients after ponatinib. For T315I, asciminib is given at a higher dose than for other mutations.

Review: section 06

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.