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 (28 Diagnosis, 55 Treatment, 7 Survivorship; 3 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
In adults with acute lymphoblastic leukaemia (ALL), roughly how are B and T lineage cases divided?
AAbout 50% each
BAbout 75% B, 25% T
CAbout 25% B, 75% T
DOver 99% B
EAbout 90% T
Show answer
Answer: B. B-ALL is about three-quarters and T-ALL about a quarter of adult ALL. T-ALL peaks in adolescents and young adults, with a 2:1 male excess.
Answer: E. Three-quarters of B-ALL occurs before age 6; there is a second peak after 60. In children it is the commonest cancer, and more than 90% are cured.
A patient has a mediastinal mass of lymphoblasts and 8% marrow blasts. What is the diagnosis?
AAcute lymphoblastic leukaemia
BClassic Hodgkin lymphoma
CAcute myeloid leukaemia
DThymic carcinoma
ELymphoblastic lymphoma
Show answer
Answer: E. Leukaemia and lymphoblastic lymphoma are the same disease: ≥20% marrow blasts = ALL (with or without a mass); a mass with <20% marrow blasts = LBL. It is treated on the ALL protocol of that lineage.
This schematic blood film shows many small-to-medium blasts with scant, granule-free cytoplasm. Which test decides whether they are lymphoid or myeloid?
AFlow cytometry (immunophenotype)
BKaryotype alone
CSerum LDH
DAntigen-receptor gene rearrangement
EMorphology alone
Show answer
Answer: A. Immunophenotype decides lineage. Antigen-receptor gene rearrangements are not lineage-specific, and morphology cannot reliably separate lymphoblasts from myeloblasts.
Which pair of findings is typical of lymphoblasts?
ASurface immunoglobulin and MYC rearrangement
BTdT positive, myeloperoxidase negative
CAuer rods and CD117
DTdT negative, myeloperoxidase positive
EBoth TdT and myeloperoxidase positive
Show answer
Answer: B. Lymphoblasts are TdT-positive and MPO-negative. Myeloperoxidase or Auer rods point to AML; surface immunoglobulin with MYC rearrangement (TdT-negative) points to Burkitt.
Answer: D. B lineage: CD19, cytoplasmic CD79a and CD22. T lineage: cytoplasmic or surface CD3 with CD7. CD20 is present on more than 10–20% of blasts in about 40% of B-ALL.
Answer: B. T-ALL is defined by CD3 (cytoplasmic or surface) with CD7. It more often has a mediastinal mass, a high white count, CNS and testicular involvement.
A 19-year-old man has cough, breathlessness when lying flat and a swollen face. This is his schematic chest X-ray. What is the key safety step?
AStart a full course of anti-tuberculosis treatment
BBronchoscopy under general anaesthesia today
CCT-guided biopsy with the patient lying flat
DAssess airway, SVC and pericardium before sedation
EArrange mediastinoscopy before any imaging
Show answer
Answer: D. An anterior mediastinal mass (T-ALL/T-LBL in 50–75% of T-ALL) can obstruct the airway, SVC or cause tamponade. Image first, and take the diagnosis from the least invasive source: blood, marrow or pleural fluid.
Which constitutional condition is associated with a higher risk of ALL?
ACystic fibrosis
BDown syndrome
CTurner syndrome
DHaemophilia A
EMarfan syndrome
Show answer
Answer: B. Associations include ionising radiation, Down syndrome and other constitutional disorders, rare familial variants (PAX5, ETV6, TP53) and common inherited polymorphisms.
When is the diagnostic lumbar puncture usually done in ALL?
ABefore any blood test is done, on the day of admission
BAt the end of maintenance, to confirm cure
COnly at relapse, never at the time of diagnosis
DOnly if the patient develops a headache during treatment
EOnce blood blasts have cleared, with the first intrathecal
Show answer
Answer: E. Every patient needs a lumbar puncture, generally once blood blasts have cleared, with platelets and clotting corrected. Neurological signs need urgent imaging and LP.
ABlasts with ≥5 WBC/µL in the fluid, or a cranial nerve palsy
BA raised CSF protein alone, without any lymphoblasts
CLymphoblasts with fewer than 5 WBC/µL in the spinal fluid
DAny headache during induction, whatever the fluid shows
ENo lymphoblasts at all in the spinal fluid sample
Show answer
Answer: A. CNS-1: no blasts; CNS-2: blasts with <5 WBC/µL; CNS-3: blasts with ≥5 WBC/µL or a cranial nerve palsy. CNS-3 needs more frequent intrathecal therapy until the fluid clears.
A 22-year-old man is about to start ALL treatment. Which is offered before treatment?
AFertility counselling and sperm banking
BTestosterone injections
CNothing, as induction always causes sterility
DOrchidectomy
EVasectomy
Show answer
Answer: A. Fertility counselling and sperm banking are offered; induction does not usually cause sterility in younger patients. Echo, ECG, viral serology, pregnancy test and HLA typing are also done.
Answer: D. A TKI is essential but not enough on its own: it is paired with a steroid or chemotherapy and continued through every phase, and for at least a year after transplant.
After induction, MRD is 10⁻³ (0.1%) in a fit 35-year-old with Ph-negative B-ALL. What next?
AMaintenance tablets only
BRepeat induction with the same drugs only
CBlinatumomab, then allogeneic transplant
DCranial radiotherapy alone
EStop treatment and watch
Show answer
Answer: C. MRD ≥10⁻⁴ after induction is high risk: one or two cycles of blinatumomab (78% became MRD-negative in BLAST) and then allogeneic HCT if eligible.
Inotuzumab ozogamicin is an antibody-drug conjugate against which antigen?
ACD19
BCD30
CCD20
DCD33
ECD22
Show answer
Answer: E. CD22 is present on more than 90% of B-ALL. Inotuzumab carries a risk of hepatic veno-occlusive disease, especially just before a transplant.
How long does ALL maintenance usually last, and what does it contain?
A≥2 years: daily 6-MP, weekly methotrexate
BNone: maintenance is not needed after consolidation
COne month of high-dose steroids, then nothing
DSix months of weekly injections in hospital
ELifelong daily TKI tablets for every patient
Show answer
Answer: A. Maintenance is low-intensity treatment at home for at least 2 years, often with vincristine–steroid pulses. Outcomes are better when counts are kept suppressed.
Answer: B. ALL with WBC ≥100,000/µL or LDH ≥2× the upper limit is high risk (fluids plus rasburicase); all other ALL is intermediate risk (fluids plus allopurinol).
Which complication is especially linked with asparaginase?
AVenous thrombosis
BPeripheral neuropathy with foot drop
CPulmonary fibrosis on lung function
DHearing loss at high frequencies
EPleural effusion from capillary leak
Show answer
Answer: A. Asparaginase lowers antithrombin, protein C/S and fibrinogen: thrombosis occurs in 14% of adults. It also causes allergy, pancreatitis and liver problems.
Which late effect is particularly linked with dexamethasone in adolescents?
APulmonary fibrosis
BOsteonecrosis
CCataract only in infants
DHearing loss
EKidney stones
Show answer
Answer: B. Other late effects: neuropathy (vincristine), cognitive and endocrine effects (especially after cranial RT), cardiomyopathy (anthracyclines), infertility, obesity, abnormal glucose metabolism and second cancers.
These schematic flow cytometry plots are from marrow blasts. What is the diagnosis?
AT-lymphoblastic leukaemia
BBurkitt leukaemia
CB-lymphoblastic leukaemia
DAcute myeloid leukaemia
EChronic lymphocytic leukaemia
Show answer
Answer: C. The blasts are CD19+ CD10+ and TdT+ MPO−: B-lymphoblasts. Burkitt cells are TdT-negative with surface immunoglobulin; AML blasts are MPO-positive; T-ALL lacks CD19.
Blasts are CD19+, cytoplasmic CD79a+, MPO− and also express CD13 and CD33. What is the diagnosis?
AMixed-phenotype leukaemia by definition
BB-ALL
CAML, because CD13 and CD33 are present
DCML in chronic phase
ET-ALL with aberrant B markers
Show answer
Answer: B. Myeloid markers (CD13, CD33) do not exclude B-ALL; myeloperoxidase does. Mixed-phenotype leukaemia and CML in lymphoid blast phase are differentials.
Answer: C. Thymomas contain keratin-positive epithelium and polyclonal thymocytes of all stages. Indolent T-lymphoblastic proliferation is also TdT-positive but non-clonal.
Which MRD method can detect one leukaemic cell among a million?
AFlow cytometry with 6–8 colours
BKaryotype
CNGS of Ig/TCR rearrangements
DRoutine microscopy
EExpert microscopy
Show answer
Answer: C. Microscopy sees about 1 in 20, expert microscopy 1 in 100, flow 1 in 10,000, RQ-PCR 1 in 100,000 and NGS 1 in 1,000,000. "MRD-negative" needs an assay that reaches 10⁻⁴.
AIt is a favourable subtype with excellent results
BIt always carries the BCR::ABL1 fusion gene
CIt occurs only in young children, never in adults
DBCR::ABL1-like expression without the fusion
EIt is a subtype of T-ALL defined by NOTCH1
Show answer
Answer: D. Most cases carry kinase-activating changes (ABL-class, JAK2, CRLF2). It is up to one-third of adult B-ALL, high risk, and commoner in people of Hispanic ancestry; trials of ABL/JAK inhibitors are under way.
Which feature makes Ph-negative B-ALL high risk under the modified Hoelzer criteria?
AWhite count 45,000/µL
BCD10-positive (common) phenotype
CWhite count 20,000/µL
DAge 30
ERemission reached by week 3
Show answer
Answer: A. High risk (any one): age over 60, WBC >30,000/µL (B) or >100,000/µL (T), t(4;11) or t(1;19), Ph-like signature, pro-B (CD10-negative) blasts, more than 4 weeks to remission, MRD ≥10⁻⁴ after induction.
A 68-year-old with Ph-positive ALL is not fit for intensive chemotherapy. Which approach fits?
AA TKI with a steroid or gentle chemotherapy
BHyper-CVAD without a TKI, at reduced intensity
CRituximab alone, given weekly for a month
DSupportive care only, as cure is not possible
EAllogeneic transplant at once, before any TKI
Show answer
Answer: A. In older patients, dasatinib with low-intensity chemotherapy gave CR 96% and 5-year survival 36%. Chemotherapy-free dasatinib with a steroid, then blinatumomab, is also possible.
In Ph-positive ALL on dasatinib, BCR::ABL1 MRD starts to rise. What is done?
AStop all TKIs and watch the counts closely
BAdd rituximab to the dasatinib and continue
CContinue the same TKI
DGive cranial radiotherapy as the next step
EMutation test and a TKI switch
Show answer
Answer: E. Relapses on dasatinib often carry T315I, which ponatinib covers. Falling MRD in a fit patient leads to transplant; rising MRD needs a mutation test and a switch.
A patient with Ph-positive ALL has a history of pleural effusions and heart failure. Which TKI is best avoided?
APonatinib
BImatinib
CNone, all are equivalent
DDasatinib
EAny TKI must be avoided
Show answer
Answer: D. Dasatinib is favoured for its CNS penetration but avoided with effusions, bleeding or heart failure. Imatinib is generic and cheaper but slower; ponatinib covers T315I at the cost of arterial events.
Why is inotuzumab given, if possible, not immediately before an allogeneic transplant?
AIt causes severe graft-versus-host disease
BIt causes severe neuropathy after transplant
CIt destroys the donor T cells in the graft
DHigher risk of liver veno-occlusive disease
EIt prevents the donor cells from engrafting
Show answer
Answer: D. In INO-VATE, VOD occurred in 9% vs 1%, and in 10 of 48 transplanted patients. Plan the sequence with the transplant team; ursodeoxycholic acid prophylaxis and defibrotide for severe VOD.
T-ALL relapses in a 30-year-old. Which approach fits?
ABlinatumomab, then transplant if in remission
BNelarabine-based chemotherapy, then transplant
CA TKI alone, continued for at least two years
DInotuzumab, then transplant if in remission
ERituximab with chemotherapy, then maintenance
Show answer
Answer: B. Inotuzumab and blinatumomab target B-cell antigens (CD22, CD19), so they do not work in T-ALL. After relapse, survival in adult T-ALL is poor without transplant.
Which approach is suggested for an older, unfit adult with T-ALL?
ABlinatumomab alone
BMini-hyper-CVD with venetoclax
CRituximab-based chemotherapy
DInotuzumab with dexamethasone
ESupportive care is the only option
Show answer
Answer: B. This is expert opinion; inotuzumab does not work without CD22. For frail patients, vincristine with prednisone or POMP can control the disease for a time.
Which preparation is needed before high-dose methotrexate?
AWithhold leucovorin until day 7, then start it
BRestrict fluids to protect the kidneys from overload
CGive a PPI and an NSAID for comfort during it
DLeave effusions in place and drain them afterwards
EHydrate, alkalinise, drain effusions, stop PPIs
Show answer
Answer: E. Effusions act as a reservoir and delay clearance. Levels are monitored, leucovorin rescue given, and glucarpidase used within 48–60 hours when levels stay high with kidney injury.
A cerebral sinus thrombosis develops during asparaginase treatment. What is done?
AHold asparaginase; LMW heparin; consider resuming later
BStop all ALL treatment permanently and observe
CContinue asparaginase unchanged and add daily aspirin
DGive fresh frozen plasma only, with no anticoagulant
EStart thrombolysis in every case, whatever the bleeding risk
Show answer
Answer: A. VTE is treated with LMW heparin (anti-Xa monitoring) for at least 6 months; asparaginase is held for cerebral sinus thrombosis, large PE, proximal DVT or arterial clots.
In remission, a single follow-up MRD test is low-level positive. What is correct?
AIt means the laboratory test must be faulty
BMRD results are never useful once induction is over
CNot relapse by itself; act if persistent or rising
DIt needs an immediate transplant without any repeat
EIt always means relapse: start salvage therapy today
Show answer
Answer: C. MRD levels fluctuate; reappearance should be confirmed on a second sample. Persistent or rising MRD triggers a donor search and closer monitoring.
DNB, DM and USMLE Step 3 level: landmark trials, newer targeted drugs and difficult decisions.
Q61TreatmentLevel 3Systemic therapy
In CALGB 10403 (295 patients aged 17–39 on a paediatric regimen), what was 3-year survival?
A50%
B30%
C15%
D73%
E95%
Show answer
Answer: D. Treatment deaths were 3%; a quarter had raised liver enzymes and 5% thromboses. It showed that adult oncologists can safely deliver a paediatric regimen.
In UKALL XII/ECOG 2993, what did sibling-donor transplant do in standard-risk ALL?
ANo survival change and no extra non-relapse deaths
BFewer non-relapse deaths and fewer relapses as well
CWorse survival because of more relapses after transplant
D5-year survival 62% vs 52%; more non-relapse deaths
E5-year survival 90% vs 20%, with no extra deaths
Show answer
Answer: D. In high-risk disease, fewer relapses (37% vs 63%) were offset by non-relapse mortality (36% vs 14%). A meta-analysis confined the survival gain to patients under 35.
Which statement about CD19 CAR-T products for ALL is correct?
AObecabtagene: much less severe CRS and ICANS
BBrexucabtagene is approved only for young children
CCAR-T products for ALL target CD22 alone
DTisagenlecleucel is approved only for adults over 65
ENexCAR19 is approved only in the United States
Show answer
Answer: A. Tisagenlecleucel is used up to 25 years (ELIANA), brexucabtagene in adults (ZUMA-3). NexCAR19 received CDSCO approval on 13 October 2023 for relapsed B-cell lymphoma and leukaemia. Trials differ, so products should not be ranked.
Which statement about adult T-ALL biology is correct?
AETP-ALL is the commonest type of adult T-ALL
BCDKN2A deletion is never found in T-ALL
CTP53 mutation predicts an excellent response
DNOTCH1/FBXW7 without RAS/PTEN: longer survival
ET-ALL is driven mainly by the BCR::ABL1 fusion
Show answer
Answer: D. About half of adults have this favourable profile (Trinquand 2013). ETP-ALL (5–10%) depends on BCL-2, which is why venetoclax is studied; TP53 mutation (10–15%) predicts resistance.
For CNS relapse of ALL, which radiotherapy is described?
ACranial RT 24 Gy with ≥6 intrathecal treatments
BNo RT; intrathecal therapy only, twice a week
CWhole-body RT 2 Gy, then maintenance tablets
DCraniospinal RT 54 Gy, with no intrathecal therapy
ECranial RT 12 Gy alone, with no intrathecal therapy
Show answer
Answer: A. For CNS-3 at diagnosis, cranial RT (typically 18 Gy) can be added in later phases. Some Indian centres still give prophylactic cranial RT (12 Gy) to adults on BFM-type protocols, accepting the late effects.
In one Indian series, how did treatment delays affect relapse-free survival in ALL?
AIt fell from 95% to 90%
BIt rose from 43% to 69%
CThere was no effect
DIt fell to 0%
EIt fell from 69% to 43%
Show answer
Answer: E. Abandonment (11–15%) and interruptions are major causes of failure; a written plan for the 2–3 years of treatment and social support help (Ganesan 2021).
At KGMU Lucknow (Shukla 2025), what proportion of 75 ALL patients on BFM-95 did not complete induction?
A75.0%
B50.0%
C0%
D1.0%
E10.6%
Show answer
Answer: E. Abandonment, resistant infections, cost and limited transplant access shape every decision in Indian ALL care (Ganesan 2021); plan support at diagnosis.
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.