C.R. Reddy Cancer Center · Leela Mahal Road, Nellore
Dr. Haritha ChiramanaMD, DMSenior medical oncologist & hemato-oncologistNellore Patient guides Book a Consultation
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.
← Lung Cancer mini review

Lung Cancer: MCQ bank

114 clinical-vignette questions in three levels: 38 basics, 42 applied and innovative, and 34 challenging (83 NSCLC, 31 SCLC; 8 built on schematic X-ray, CT, mammogram 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.

LevelScore 0 / 0 answered
Topic

Level 1 · Basics

Core facts for NEET-PG and USMLE Step 1–2: histology, risk factors, presentation, staging and first-line principles.

Q1NSCLCLevel 1Presentation, traps & genetics

Which paraneoplastic syndrome is most characteristic of squamous cell carcinoma of the lung?

  1. AEctopic ACTH (Cushing) syndrome
  2. BAnti-Hu sensory neuronopathy
  3. CHypercalcaemia due to PTH-related peptide
  4. DLambert-Eaton myasthenic syndrome
  5. ESIADH
Show answer

Answer: C. Squamous carcinoma classically secretes PTHrP, causing hypercalcaemia. SIADH, ectopic ACTH, Lambert-Eaton and anti-Hu syndromes are typical of small cell carcinoma.

Review: section 02

Q2NSCLCLevel 1Presentation, traps & genetics

A 58-year-old smoker has right shoulder and arm pain, wasting of the small muscles of the hand and ptosis with miosis on the right. The most likely diagnosis is:

  1. ASyringomyelia
  2. BCarpal tunnel syndrome
  3. CFrozen shoulder
  4. DCervical spondylotic myelopathy
  5. ESuperior sulcus (Pancoast) tumour
Show answer

Answer: E. Shoulder/arm pain, C8–T1 weakness and Horner syndrome in a smoker point to an apical (Pancoast) tumour invading the brachial plexus and sympathetic chain. It is often mislabelled as frozen shoulder or spondylosis.

Review: section 02

Q3NSCLCLevel 1Presentation, traps & genetics

A 30-year-old woman who has never smoked has an EGFR-mutant lung adenocarcinoma. Her sister asks whether she should be tested for the EGFR mutation. The correct advice is:

  1. ARelatives should have BRCA testing
  2. BRelatives should have yearly CT from age 25
  3. CRelatives should take a preventive EGFR inhibitor
  4. DTumour EGFR mutations are acquired, so relatives do not need EGFR testing
  5. EAll first-degree relatives need germline EGFR testing
Show answer

Answer: D. Common EGFR mutations in tumours are somatic. Families can be reassured; germline testing is reserved for rare patterns such as germline T790M or a variant suggesting a hereditary syndrome on NGS.

Review: section 02

Q4NSCLCLevel 1Presentation, traps & genetics

Which statement about lung cancer in India is most accurate?

  1. AA substantial share of patients, especially women, have never smoked
  2. BSquamous carcinoma is now the commonest type
  3. CAlmost all patients are heavy smokers over 70
  4. DBiomass smoke has no association with lung cancer
  5. EMost cases are diagnosed at stage I
Show answer

Answer: A. Indian patients are younger than in Western series, adenocarcinoma is now commonest, most present at stage III–IV, and a substantial share are never-smokers, with biomass and second-hand smoke as contributors.

Review: section 02

Q5NSCLCLevel 1Presentation, traps & genetics

A smoker's chest X-ray shows right upper lobe collapse with a convex bulge at the hilum, forming a reversed S-shaped fissure. What does this “Golden S sign” indicate?

  1. APneumothorax
  2. BA central hilar mass obstructing the right upper lobe bronchus
  3. CPleural effusion
  4. DNormal variant
  5. EMiddle lobe pneumonia
Show answer

Answer: B. The concave collapsed lobe plus the convex central mass make a reversed S. In an adult smoker it strongly suggests a central bronchial carcinoma: CT and bronchoscopy follow.

Review: section 02

Q6NSCLCLevel 1Presentation, traps & genetics

Exposure to which pair shows a multiplicative (synergistic) effect on lung cancer risk?

  1. ACaffeine and smoking
  2. BAsbestos and cigarette smoking
  3. CAlcohol and radon
  4. DObesity and asbestos
  5. EMobile phones and smoking
Show answer

Answer: B. Asbestos and smoking each raise risk, but together the risk is far greater than the sum. Radon also interacts with smoking.

Review: section 02

Q7NSCLCLevel 1Presentation, traps & genetics

Hypertrophic pulmonary osteoarthropathy (clubbing, painful periostitis of long bones) is most associated with:

  1. ACarcinoid tumour
  2. BSmall cell lung cancer
  3. CNon-small cell lung cancer, particularly adenocarcinoma
  4. DTuberculosis only
  5. EMesothelioma only
Show answer

Answer: C. Hypertrophic osteoarthropathy is a classic paraneoplastic feature of NSCLC; it may improve after tumour resection.

Review: section 02

Q8NSCLCLevel 1Presentation, traps & genetics

The histological type of lung cancer most common in never-smokers is:

  1. AAdenocarcinoma
  2. BCarcinoid
  3. CSquamous cell carcinoma
  4. DLarge cell carcinoma
  5. ESmall cell carcinoma
Show answer

Answer: A. Adenocarcinoma predominates in never-smokers, who also have more EGFR, ALK and other targetable drivers.

Review: section 02

Q9NSCLCLevel 1ImagePresentation, traps & genetics

The schematic H&E drawing shows nests of polygonal cells with concentric pink structures. Which immunostain is expected to be positive?

Schematic drawing · not a patient image
  1. ASynaptophysin
  2. Bp40
  3. CCD20
  4. DNapsin A
  5. ETTF-1
Show answer

Answer: B. Keratin pearls and intercellular bridges mean squamous cell carcinoma, which stains with p40 (and CK5/6). TTF-1 and napsin A mark adenocarcinoma; synaptophysin marks neuroendocrine tumours.

Review: section 02

Q10NSCLCLevel 1Screening, workup & staging

Which population was shown to benefit from low-dose CT screening in randomised trials (NLST, NELSON)?

  1. AOlder current or former heavy smokers
  2. BAdults with asthma
  3. CNever-smoking women with biomass exposure
  4. DPatients with treated tuberculosis
  5. EAll adults over 40
Show answer

Answer: A. NLST and NELSON enrolled heavy smokers (USPSTF now: age 50–80, ≥20 pack-years, quit within 15 years) and showed fewer lung cancer deaths. Screening never-smokers is not recommended outside research.

Review: section 03

Q11NSCLCLevel 1Screening, workup & staging

A 6 mm solid incidental nodule is found on CT in a 45-year-old never-smoker with no risk factors. According to Fleischner 2017, the recommended action is:

  1. AImmediate PET-CT
  2. BCT at 6–12 months, then consider CT at 18–24 months
  3. CCT-guided biopsy
  4. DSurgical wedge resection
  5. ENo follow-up at all
Show answer

Answer: B. Solid nodules of 6–8 mm in low-risk patients get CT at 6–12 months, then consider 18–24 months. Nodules under 6 mm in low-risk patients need no routine follow-up; over 8 mm: CT at 3 months, PET-CT or biopsy.

Review: section 03

Q12NSCLCLevel 1Screening, workup & staging

Brain MRI is recommended routinely in all of the following EXCEPT:

  1. ASmall cell lung cancer of any stage
  2. BStage III NSCLC planned for curative treatment
  3. CAny lung cancer patient with headache or focal signs
  4. DAsymptomatic stage IA peripheral NSCLC
  5. EStage IV NSCLC
Show answer

Answer: D. Brain MRI is advised for stage II–IV NSCLC, all small cell, and any neurological symptom; it is optional in stage IB and not needed for asymptomatic stage IA.

Review: section 03

Q13NSCLCLevel 1Screening, workup & staging

Which node station is classically NOT reachable by cervical mediastinoscopy?

  1. AStation 7 (subcarinal)
  2. BStation 4R
  3. CStation 2R
  4. DStation 5 (aortopulmonary window)
  5. EStation 4L
Show answer

Answer: D. Cervical mediastinoscopy reaches stations 2, 4 and 7. Stations 5 and 6 need an anterior mediastinotomy or VATS; EUS reaches 8 and 9.

Review: section 03

Q14NSCLCLevel 1Biomarkers

Which patients with advanced NSCLC should have broad molecular testing?

  1. AOnly patients under 50
  2. BOnly patients who fail chemotherapy
  3. CAll non-squamous NSCLC, and squamous NSCLC in never- or light smokers
  4. DOnly women who have never smoked
  5. EOnly adenocarcinomas with brain metastases
Show answer

Answer: C. Testing every advanced non-squamous NSCLC (and squamous in never/light smokers, young patients or mixed histology) avoids missing drivers in smokers, men and older patients.

Review: section 04

Q15NSCLCLevel 1Biomarkers

The most frequent actionable driver in Indian lung adenocarcinoma is:

  1. ABRAF V600E
  2. BALK fusion
  3. CEGFR mutation
  4. DKRAS G12C
  5. ERET fusion
Show answer

Answer: C. EGFR mutations occur in roughly a quarter to a third of Indian adenocarcinomas; ALK fusions in about 5%; KRAS mutations are less frequent than in Western series.

Review: section 04

Q16NSCLCLevel 1Biomarkers

An EGFR exon 20 insertion is found in metastatic NSCLC. Which first-line treatment is supported by a phase 3 trial?

  1. ACrizotinib
  2. BAmivantamab plus carboplatin–pemetrexed
  3. COsimertinib monotherapy
  4. DErlotinib
  5. EGefitinib
Show answer

Answer: B. Exon 20 insertions are insensitive to earlier EGFR TKIs. PAPILLON showed amivantamab plus platinum–pemetrexed improved progression-free survival over chemotherapy.

Review: section 04

Q17NSCLCLevel 1ImageBiomarkers

The schematic H&E drawing shows malignant glands. Before treating this tumour as metastatic disease, which test is essential?

Schematic drawing · not a patient image
  1. ABone marrow biopsy
  2. BBronchial washings for TB only
  3. CSerum CEA only
  4. DSputum cytology
  5. EMolecular testing for actionable drivers (EGFR, ALK, ROS1 and others) plus PD-L1
Show answer

Answer: E. Gland-forming tumour = adenocarcinoma, the subtype with the most targetable drivers. Driver testing and PD-L1 determine first-line therapy.

Review: section 04

Q18NSCLCLevel 1Local therapy

A fit 60-year-old has a 1.6 cm peripheral solid adenocarcinoma, node-negative on staging. Which operation is supported by JCOG0802 as at least as good as lobectomy for overall survival?

  1. ASleeve lobectomy
  2. BAnatomical segmentectomy with nodal assessment
  3. CObservation
  4. DWedge resection without nodal assessment
  5. EPneumonectomy
Show answer

Answer: B. JCOG0802 found segmentectomy non-inferior (in fact better) for overall survival in peripheral tumours ≤2 cm, at the cost of more local recurrence. Nodal assessment remains essential.

Review: section 05

Q19NSCLCLevel 1Local therapy

An 80-year-old with severe COPD has biopsy-proven stage IA NSCLC and is not fit for surgery. The preferred treatment is:

  1. APneumonectomy after pulmonary rehabilitation
  2. BErlotinib
  3. CConventional radiotherapy over 6 weeks with chemotherapy
  4. DObservation only
  5. EStereotactic ablative radiotherapy (SBRT)
Show answer

Answer: E. SBRT achieves local control around 90% in a few sessions and is the standard for medically inoperable stage I NSCLC.

Review: section 05

Q20NSCLCLevel 1Systemic therapy

A 48-year-old never-smoker has metastatic adenocarcinoma with EGFR exon 19 deletion. Which first-line drug improved overall survival over gefitinib or erlotinib in FLAURA?

  1. ADocetaxel
  2. BBevacizumab
  3. COsimertinib
  4. DCrizotinib
  5. EPembrolizumab
Show answer

Answer: C. FLAURA showed osimertinib improved both progression-free and overall survival compared with first-generation EGFR TKIs, with good brain activity.

Review: section 06

Q21NSCLCLevel 1Systemic therapy

Which first-line treatment is preferred for metastatic ALK-positive NSCLC?

  1. ADocetaxel
  2. BAlectinib or lorlatinib
  3. CCrizotinib only after chemotherapy
  4. DPembrolizumab monotherapy
  5. EGefitinib
Show answer

Answer: B. Next-generation ALK inhibitors (alectinib, lorlatinib, brigatinib) beat crizotinib and control brain disease well. Immunotherapy is of little benefit in ALK-positive disease.

Review: section 06

Q22NSCLCLevel 1Systemic therapy

Metastatic non-squamous NSCLC with no driver and PD-L1 TPS 75%, ECOG 1. A standard first-line option is:

  1. ABest supportive care only
  2. BSingle-agent docetaxel
  3. CPembrolizumab monotherapy
  4. DGefitinib
  5. EAlectinib
Show answer

Answer: C. For PD-L1 ≥50% without a driver, immunotherapy alone (pembrolizumab, atezolizumab, cemiplimab) is standard; chemo-immunotherapy is an alternative for bulky or rapid disease. KEYNOTE-024 showed a long-term survival advantage over chemotherapy.

Review: section 06

Q23NSCLCLevel 1Systemic therapy

For squamous metastatic NSCLC without a driver, which chemotherapy partner is NOT appropriate with pembrolizumab?

  1. APemetrexed
  2. BCarboplatin–nab-paclitaxel
  3. CCisplatin–gemcitabine
  4. DCarboplatin–paclitaxel
  5. ECarboplatin–gemcitabine
Show answer

Answer: A. Pemetrexed is inactive in squamous histology and is used only for non-squamous NSCLC; KEYNOTE-407 used carboplatin with paclitaxel or nab-paclitaxel.

Review: section 06

Q24NSCLCLevel 1Systemic therapy

Unresectable stage III NSCLC without a driver responds to concurrent chemoradiation. PACIFIC supports:

  1. AErlotinib for 2 years
  2. BProphylactic cranial irradiation
  3. CPneumonectomy
  4. DObservation
  5. EDurvalumab for 12 months
Show answer

Answer: E. PACIFIC showed consolidation durvalumab after chemoradiation improved progression-free and overall survival (5-year survival about 43% vs 33%).

Review: section 06

Q25NSCLCLevel 1Systemic therapy

Early palliative care integrated with oncology care in metastatic NSCLC (Temel et al.) led to:

  1. AMore aggressive end-of-life chemotherapy
  2. BShorter survival
  3. CBetter quality of life and mood, and longer median survival
  4. DNo change in quality of life
  5. EHigher hospital costs without benefit
Show answer

Answer: C. Early palliative care improved quality of life and depression and, despite less aggressive end-of-life care, was associated with longer survival.

Review: section 06

Q26NSCLCLevel 1Systemic therapy

Pemetrexed, used in non-squamous NSCLC, works mainly by:

  1. AStabilising microtubules
  2. BCross-linking DNA
  3. CInhibiting topoisomerase I
  4. DInhibiting folate-dependent enzymes such as thymidylate synthase
  5. EBlocking EGFR
Show answer

Answer: D. Pemetrexed is a multitargeted antifolate (thymidylate synthase, DHFR, GARFT). Folic acid and vitamin B12 are given to reduce toxicity. It is inactive in squamous histology.

Review: section 06

Q27NSCLCLevel 1Survivorship

After curative resection of NSCLC, recommended surveillance imaging is:

  1. ACT chest every 6 months for 2–3 years, then yearly low-dose CT
  2. BPET-CT every 3 months for life
  3. CTumour markers every month
  4. DChest X-ray every month
  5. ENo imaging after 1 year
Show answer

Answer: A. NCCN and ESMO advise CT every 6 months for 2–3 years then yearly low-dose CT, mainly to detect relapse early and second primary lung cancers. Routine PET and markers are not recommended.

Review: section 08

Q28SCLCLevel 1At a glance

Approximately what proportion of patients with small cell lung cancer have extensive-stage disease at diagnosis?

  1. AAbout half are stage I
  2. BAbout two thirds
  3. CAlmost all
  4. DAbout one quarter
  5. EAbout 10%
Show answer

Answer: B. Around 60–70% present with extensive-stage disease because of the rapid doubling time and early dissemination.

Review: section 01

Q29SCLCLevel 1At a glance

Small cell lung cancer arises predominantly in:

  1. APatients with asbestosis, in the pleura
  2. BPatients with EGFR mutations as the primary driver
  3. CNever-smoking young women, in the periphery
  4. DChildren
  5. ECurrent or former heavy smokers, usually in central airways
Show answer

Answer: E. Almost all patients have a heavy smoking history; tumours are typically central with bulky nodes.

Review: section 01

Q30SCLCLevel 1Presentation, traps & genetics

Which microscopic description fits small cell carcinoma of the lung?

  1. ASmall round cells with scant cytoplasm, finely granular chromatin, absent nucleoli and nuclear moulding
  2. BGlandular structures with mucin
  3. CSpindle cells with storiform pattern
  4. DUniform cells in nests with low mitotic rate
  5. ELarge cells with prominent nucleoli and keratin pearls
Show answer

Answer: A. Small cell carcinoma shows “salt and pepper” chromatin, inconspicuous nucleoli, moulding, crush artefact and very high mitotic activity. Keratin pearls suggest squamous carcinoma; glands, adenocarcinoma; low-grade nests, carcinoid.

Review: section 02

Q31SCLCLevel 1Presentation, traps & genetics

Which immunohistochemical panel supports neuroendocrine differentiation in small cell carcinoma?

  1. ACalretinin and WT1
  2. Bp40 and CK5/6
  3. CSynaptophysin, chromogranin, CD56 (and INSM1)
  4. DCD20 and CD3
  5. EHMB-45 and S100
Show answer

Answer: C. Neuroendocrine markers support the diagnosis (which is mainly morphological). p40/CK5/6 indicate squamous carcinoma; calretinin/WT1 mesothelioma; CD markers lymphoma; HMB-45 melanoma.

Review: section 02

Q32SCLCLevel 1Presentation, traps & genetics

Which electrolyte disturbance is the classic paraneoplastic feature of small cell lung cancer?

  1. AHypophosphataemia from FGF23
  2. BHypercalcaemia from PTHrP
  3. CHyperkalaemia
  4. DHypermagnesaemia
  5. EHyponatraemia from SIADH
Show answer

Answer: E. About one in ten small cell cancers cause SIADH. PTHrP-mediated hypercalcaemia is typical of squamous carcinoma.

Review: section 02

Q33SCLCLevel 1Presentation, traps & genetics

Lambert-Eaton myasthenic syndrome associated with small cell lung cancer is caused by antibodies against:

  1. AMuscle-specific kinase
  2. BAquaporin-4
  3. CPotassium channels
  4. DP/Q-type voltage-gated calcium channels
  5. EAcetylcholine receptors
Show answer

Answer: D. Antibodies reduce presynaptic acetylcholine release; weakness improves briefly with repeated effort, unlike myasthenia gravis.

Review: section 02

Q34SCLCLevel 1Presentation, traps & genetics

Ectopic ACTH production by small cell lung cancer typically presents with:

  1. AHyperkalaemia
  2. BHypercalcaemia
  3. CWeight gain with striae over many years
  4. DHypokalaemic metabolic alkalosis, oedema and hyperglycaemia, often without classic Cushingoid features
  5. EHypoglycaemia
Show answer

Answer: D. Cortisol rises so rapidly that the classic habitus has no time to develop; hypokalaemia and alkalosis dominate. It worsens prognosis and infection risk.

Review: section 02

Q35SCLCLevel 1ImagePresentation, traps & genetics

A bronchoscopic biopsy from a central mass in a heavy smoker shows the appearance in the schematic H&E drawing. The most likely diagnosis is:

Schematic drawing · not a patient image
  1. AHamartoma
  2. BSmall cell carcinoma
  3. CCarcinoid tumour
  4. DAdenocarcinoma
  5. ESquamous cell carcinoma
Show answer

Answer: B. Sheets of small round blue cells with scant cytoplasm, nuclear moulding and crush (smeared) artefact are classic small cell carcinoma; neuroendocrine markers and a very high Ki-67 support it.

Review: section 02

Q36SCLCLevel 1Screening, workup & staging

Limited-stage small cell lung cancer is best defined as disease that:

  1. AIs confined to one hemithorax and regional nodes and can be encompassed in a tolerable radiotherapy field
  2. BHas only one distant metastasis
  3. CHas no lymph node involvement
  4. DCan be removed by pneumonectomy
  5. EIs under 3 cm in size
Show answer

Answer: A. The working definition is about radiotherapy feasibility. Extensive stage means disease beyond that field, including malignant effusion or distant metastases.

Review: section 03

Q37SCLCLevel 1Local therapy

The main purpose of prophylactic cranial irradiation (PCI) in small cell lung cancer is to:

  1. AReduce the incidence of symptomatic brain metastases in patients who responded to initial treatment
  2. BShrink the primary tumour
  3. CTreat existing large brain metastases
  4. DPrevent bone metastases
  5. EReplace chemotherapy
Show answer

Answer: A. PCI targets microscopic brain disease after a good response. In limited stage it reduced brain metastases and improved survival in older studies; MRI surveillance is an alternative, especially in extensive stage.

Review: section 05

Q38SCLCLevel 1Systemic therapy

The standard chemotherapy backbone for small cell lung cancer is:

  1. ASingle-agent paclitaxel
  2. BPlatinum (cisplatin or carboplatin) plus etoposide
  3. CPemetrexed plus carboplatin
  4. DGemcitabine plus docetaxel
  5. EImatinib
Show answer

Answer: B. Platinum–etoposide has been the backbone for decades; checkpoint inhibitors are added in extensive stage and durvalumab follows chemoradiation in limited stage.

Review: section 06

Level 2 · Applied & innovative

Clinical reasoning: calculations (pack-years, predicted lung function, NNT), CT and fluid findings, reading trial results, sequencing traps.

Q39NSCLCLevel 2Presentation, traps & genetics

A 52-year-old bidi smoker has received 3 months of antituberculous treatment for a right upper zone opacity. Sputum was never tested. He has lost more weight and now has haemoptysis. What is the most appropriate next step?

  1. AStart a course of broad-spectrum antibiotics only
  2. BSwitch to second-line TB drugs empirically
  3. CRepeat chest X-ray after 3 months
  4. DContinue antituberculous treatment for 6 more months
  5. EContrast CT chest and tissue diagnosis, with sputum NAAT
Show answer

Answer: E. TB must be proven microbiologically. Unproven TB that is not improving needs CT and tissue (bronchoscopy, EBUS or CT-guided biopsy); the same sample can be tested for TB. Empirical drug-resistant regimens without proof are inappropriate.

Review: section 02

Q40NSCLCLevel 2Presentation, traps & genetics

An EGFR-mutant adenocarcinoma responding to osimertinib for 18 months now progresses rapidly with liver metastases and a rising neuron-specific enolase. What is the most important next step?

  1. ADouble the dose of osimertinib
  2. BBiopsy a progressing lesion to look for small-cell transformation
  3. CAdd pembrolizumab to osimertinib
  4. DSwitch to gefitinib
  5. EStart whole-brain radiotherapy
Show answer

Answer: B. Rapid visceral progression with rising neuroendocrine markers suggests transformation to small cell carcinoma (a few percent of resistance), which needs platinum–etoposide. Immunotherapy added to an EGFR TKI raises pneumonitis risk and is ineffective.

Review: section 02

Q41NSCLCLevel 2ImagePresentation, traps & genetics

A 64-year-old smoker with 2 months of cough. Based on the schematic chest X-ray shown, what is the most likely diagnosis and next step?

RSchematic drawing · not a patient image
  1. ARight upper lobe pneumonia: antibiotics and repeat X-ray in 6 weeks only
  2. BRight pneumothorax: chest drain
  3. CPleural effusion: thoracentesis
  4. DNormal X-ray: reassure
  5. ERight upper lobe collapse from a central hilar mass (Golden S sign): contrast CT and bronchoscopy
Show answer

Answer: E. The collapsed right upper lobe pulls the horizontal fissure up (concave laterally) while a central mass makes it bulge medially, giving a reversed S. A central bronchial carcinoma must be excluded with CT and bronchoscopy.

Review: section 02

Q42NSCLCLevel 2ImagePresentation, traps & genetics

A 58-year-old bidi smoker has right shoulder pain radiating down the inner arm and a right Horner syndrome. The schematic X-ray is shown. Which is the best next imaging test to plan treatment?

RSchematic drawing · not a patient image
  1. AMRI of the thoracic inlet and brachial plexus, plus CT and PET-CT staging
  2. BCervical spine X-ray only
  3. CShoulder ultrasound
  4. DBarium swallow
  5. ERepeat chest X-ray in 3 months
Show answer

Answer: A. An apical mass with rib destruction, arm pain and Horner syndrome is a superior sulcus (Pancoast) tumour. MRI defines plexus, vertebral and vascular invasion; induction chemoradiation then surgery is the usual curative route when resectable.

Review: section 02

Q43NSCLCLevel 2Screening, workup & staging

A patient has a 4 cm right upper lobe mass, an enlarged subcarinal node and a right pleural effusion. Which first diagnostic procedure gives both diagnosis and the highest stage?

  1. AWedge resection of the mass
  2. BBronchial washings
  3. CSputum cytology
  4. DPleural fluid cytology with cell block
  5. ECT-guided biopsy of the lung mass
Show answer

Answer: D. A malignant effusion is M1a; proving it diagnoses and stages in one step and may provide a cell block for molecular testing. If negative twice, thoracoscopy follows. Biopsying the primary alone may leave the stage unresolved.

Review: section 03

Q44NSCLCLevel 2Screening, workup & staging

In an Indian patient with suspected lung cancer, PET-CT shows uptake in mediastinal nodes. Before denying surgery, the clinician should:

  1. ARepeat PET after 6 weeks of antibiotics
  2. BOrder tumour markers
  3. CStart chemoradiation immediately
  4. DConfirm nodal involvement by EBUS-TBNA
  5. EAccept the PET result as proof of N2 disease
Show answer

Answer: D. Granulomatous disease (TB, fungal) causes false-positive nodal uptake. Tissue confirmation (EBUS ± EUS, mediastinoscopy) is required before a patient is called unresectable.

Review: section 03

Q45NSCLCLevel 2Screening, workup & staging

Before right lower lobectomy (5 of 19 segments), a patient has FEV1 and DLCO of 70% predicted, giving predicted post-operative values of about 52%. Following the ACCP approach, the next step is:

  1. AProceed to surgery with no further testing
  2. BFormal cardiopulmonary exercise testing straight away
  3. CDeclare inoperable and refer for SBRT
  4. DA low-technology exercise test (stair climb or shuttle walk)
  5. EArterial blood gas analysis to decide
Show answer

Answer: D. Predicted post-operative value = measured × (1 − segments removed ÷ functioning segments). Both ≥60%: low risk. Either 30–60% (both ≥30%): stair climb (≥22 m) or shuttle walk (≥400 m); failure leads to cardiopulmonary exercise testing. Below 30%: exercise testing directly. Blood gases do not decide resectability.

Review: section 03

Q46NSCLCLevel 2Screening, workup & staging

A 56-year-old man smoked 15 cigarettes a day from age 18 to 54 and quit 2 years ago. Is he eligible for low-dose CT screening under the USPSTF 2021 criteria?

  1. ANo: he must be over 60
  2. BNo: he must have at least 30 pack-years
  3. COnly if he has symptoms
  4. DNo: former smokers are excluded
  5. EYes: about 27 pack-years, age 50–80, quit within 15 years
Show answer

Answer: E. Pack-years = packs per day × years: 0.75 × 36 ≈ 27. USPSTF 2021: age 50–80, ≥20 pack-years, current smoker or quit within 15 years. Screening stops after 15 years of abstinence.

Review: section 03

Q47NSCLCLevel 2Screening, workup & staging

CT shows a new 2.2 cm spiculated solid nodule with a pleural tag in the right upper lobe of a 64-year-old smoker; a CT 2 years ago was normal. The next step is:

  1. APET-CT and tissue diagnosis with staging, aiming at curative treatment
  2. BRepeat CT in 12 months
  3. CTumour markers
  4. DAntibiotics and repeat X-ray
  5. EReassure because it is under 3 cm
Show answer

Answer: A. A new, spiculated solid nodule over 8 mm in a smoker is highly suspicious. Fleischner guidance for nodules >8 mm is PET-CT or tissue sampling; this one needs full staging toward resection or SBRT.

Review: section 03

Q48NSCLCLevel 2Screening, workup & staging

Planned right pneumonectomy: preoperative DLCO is 60% predicted and perfusion scintigraphy shows the right lung receives 55% of total flow. The predicted post-operative DLCO is about:

  1. A45%: proceed without further tests
  2. B33%: stair climb only
  3. CCannot be calculated
  4. D60%: low risk
  5. E27%: cardiopulmonary exercise testing is needed
Show answer

Answer: E. ppo DLCO = 60 × (1 − 0.55) = 27%. Under 30% (ACCP) needs formal cardiopulmonary exercise testing; VO2 max below 10 mL/kg/min would favour non-surgical options.

Review: section 03

Q49NSCLCLevel 2Screening, workup & staging

A lymphocytic exudative pleural effusion in a 58-year-old smoker has an ADA of 18 U/L; one cytology sample is negative. The best next step is:

  1. ATalc pleurodesis immediately
  2. BDischarge with follow-up
  3. CRepeat cytology with a cell block and, if negative, thoracoscopic pleural biopsy
  4. DStart antituberculous treatment
  5. EClosed (blind) pleural biopsy only
Show answer

Answer: C. A low ADA makes TB less likely. Cytology yield rises with repeated sampling; thoracoscopy is the most sensitive test (80–99%). Blind closed biopsy has limited value for cancer.

Review: section 03

Q50NSCLCLevel 2Screening, workup & staging

A patient has a right upper lobe mass and a 2 cm hard node in the left supraclavicular fossa. Which first biopsy is best?

  1. ABronchoscopic biopsy of the primary
  2. BCT-guided biopsy of the lung mass
  3. CUltrasound-guided biopsy of the supraclavicular node
  4. DMediastinoscopy
  5. EWait for PET results before any biopsy
Show answer

Answer: C. Sample the site that proves the highest stage with the least risk: a positive supraclavicular node is N3 and confirms the diagnosis and stage in one step.

Review: section 03

Q51NSCLCLevel 2ImageScreening, workup & staging

An incidental CT (lung window, schematic) in a 62-year-old ex-smoker shows the lesion illustrated, new since a scan 3 years ago. Which feature most raises suspicion of malignancy?

RSchematic drawing · not a patient image
  1. ACentral popcorn calcification
  2. BSmooth margins with laminated calcification
  3. CFat density within the lesion
  4. DSpiculated margins with a pleural tag
  5. ESize stable for 2 years
Show answer

Answer: D. Spiculation, pleural tagging, upper-lobe location, growth and smoking history all favour cancer. Popcorn calcification and fat suggest hamartoma; central or laminated calcification and 2-year stability suggest benignity.

Review: section 03

Q52NSCLCLevel 2ImageScreening, workup & staging

The schematic CT shows a right pleural effusion with nodular pleural thickening in a patient with a known lung mass. How does this finding change stage if proven malignant?

RSchematic drawing · not a patient image
  1. AIt does not affect stage
  2. BIt makes the disease M1a (stage IVA), changing intent from cure to control
  3. CIt is N2 disease
  4. DIt makes the disease M1c2
  5. EIt is T3 disease
Show answer

Answer: B. Malignant pleural effusion or pleural nodules are M1a. Prove it (cytology, thoracoscopy) because a non-malignant effusion would leave curative options open.

Review: section 03

Q53NSCLCLevel 2Biomarkers

Which drug–target pairing is INCORRECT?

  1. ALorlatinib – ALK fusion
  2. BOsimertinib – EGFR exon 19 deletion
  3. CCapmatinib – MET exon 14 skipping
  4. DSelpercatinib – ROS1 fusion
  5. ESotorasib – KRAS G12C
Show answer

Answer: D. Selpercatinib targets RET fusions. ROS1 is treated with taletrectinib, repotrectinib, entrectinib or crizotinib.

Review: section 04

Q54NSCLCLevel 2Biomarkers

After 20 months on first-line osimertinib, re-biopsy of progressing disease shows the original EGFR exon 19 deletion plus a new EGFR C797S mutation. What does C797S do?

  1. AIt is a germline variant needing family testing
  2. BIt removes the cysteine to which osimertinib binds covalently, causing resistance
  3. CIt sensitises the tumour to immunotherapy
  4. DIt predicts benefit from rechallenge with osimertinib
  5. EIt indicates small-cell transformation
Show answer

Answer: B. Osimertinib binds irreversibly to cysteine 797; the C797S substitution prevents this. Next options are chemotherapy-based (± amivantamab) or trials.

Review: section 04

Q55NSCLCLevel 2Local therapy

In concurrent chemoradiation for stage III NSCLC, RTOG 0617 showed that escalating the radiation dose to 74 Gy compared with 60 Gy:

  1. AReduced pneumonitis
  2. BEliminated the need for chemotherapy
  3. CImproved overall survival
  4. DWorsened overall survival
  5. EWas equivalent with fewer side effects
Show answer

Answer: D. High-dose radiotherapy was harmful (worse survival, likely from cardiac and lung toxicity). About 60 Gy in 30 fractions remains standard.

Review: section 05

Q56NSCLCLevel 2Local therapy

A patient with EGFR-mutant NSCLC has three asymptomatic brain metastases under 1 cm. A reasonable initial approach is:

  1. AStart a brain-penetrant EGFR TKI and repeat MRI at 6–8 weeks
  2. BNeurosurgical resection of all three lesions
  3. CSteroids alone
  4. DImmediate whole-brain radiotherapy before any systemic therapy
  5. EChemotherapy with pembrolizumab
Show answer

Answer: A. Osimertinib (and ALK inhibitors for ALK-positive disease) has high intracranial activity. Small asymptomatic lesions can be watched closely on the TKI, reserving radiosurgery for non-response or symptoms.

Review: section 05

Q57NSCLCLevel 2Local therapy

A 66-year-old with idiopathic pulmonary fibrosis (FVC 72%, DLCO 55%) has a 1.8 cm peripheral adenocarcinoma, cT1b N0. Which statement is most appropriate?

  1. APneumonectomy is preferred to remove all fibrotic lung
  2. BLung-sparing (sublobar) surgery is favoured; radiotherapy and immunotherapy carry a higher risk of severe pneumonitis
  3. CObservation is mandatory because ILD makes cancer treatment futile
  4. DSBRT is clearly safer than surgery in ILD
  5. EPerioperative chemo-immunotherapy is standard because ILD patients were well represented in the trials
Show answer

Answer: B. ILD raises both lung cancer risk and treatment toxicity (acute exacerbation after surgery, radiation and immune pneumonitis). For stage I–II disease with adequate function, surgery with lung-sparing resection is favoured; SBRT has not been shown to be safer, and ILD patients were excluded from perioperative immunotherapy trials.

Review: section 05

Q58NSCLCLevel 2Local therapy

A patient with metastatic NSCLC and a KRAS G12C mutation has three asymptomatic brain metastases (largest 1.5 cm) without mass effect. The usual first step is:

  1. AWhole-brain radiotherapy is contraindicated
  2. BSotorasib alone with MRI in 6–8 weeks
  3. CRadiotherapy to the brain metastases, then systemic therapy
  4. DObservation of the brain lesions until symptoms develop
  5. EOsimertinib
Show answer

Answer: C. Brain-penetrant TKIs allow systemic therapy first for EGFR, ALK, RET and suitable ROS1 tumours. For MET exon 14, KRAS G12C and BRAF-driven disease, radiotherapy (usually radiosurgery for a few lesions) followed by systemic therapy is generally preferred.

Review: section 05

Q59NSCLCLevel 2Local therapy

JCOG0802 tested segmentectomy against lobectomy in a non-inferiority design. What does “non-inferiority” mean here?

  1. ANon-inferiority trials cannot affect practice
  2. BThe aim was to show segmentectomy is not unacceptably worse than lobectomy within a pre-set margin
  3. CThe trial showed the two operations are identical
  4. DThe aim was to prove segmentectomy is superior
  5. ELobectomy was found inferior
Show answer

Answer: B. Non-inferiority trials test whether a less invasive option keeps outcomes within a predefined margin. JCOG0802 met this and even showed better overall survival with segmentectomy, though local recurrence was higher.

Review: section 05

Q60NSCLCLevel 2Systemic therapy

An Indian patient with EGFR-mutant metastatic NSCLC cannot afford osimertinib. Which regimen improved overall survival over gefitinib alone in a randomised trial from Tata Memorial Centre?

  1. AAfatinib plus cetuximab
  2. BGefitinib at a double dose
  3. CGefitinib plus bevacizumab
  4. DGefitinib plus pemetrexed–carboplatin
  5. EErlotinib plus pembrolizumab
Show answer

Answer: D. Noronha et al. (J Clin Oncol 2020) showed gefitinib with pemetrexed–carboplatin improved progression-free and overall survival over gefitinib alone, offering an affordable option.

Review: section 06

Q61NSCLCLevel 2Systemic therapy

A patient completed adjuvant chemotherapy and atezolizumab for stage IIIA NSCLC (no driver) and relapses with liver metastases 4 months later. How should this relapse be treated?

  1. AOsimertinib
  2. BAs second-line disease: docetaxel ± ramucirumab or another non-cross-resistant option
  3. CObservation until symptomatic
  4. DAs first-line disease: repeat platinum doublet with a checkpoint inhibitor
  5. ERestart atezolizumab alone
Show answer

Answer: B. Relapse within about 6 months of adjuvant therapy suggests resistance and is managed as second-line disease. Relapse after more than 12 months is generally treated as first-line metastatic disease; 6–12 months is individualised.

Review: section 06

Q62NSCLCLevel 2Systemic therapy

In PACIFIC, 5-year overall survival was about 43% with durvalumab and 33% with placebo. Approximately how many patients must be treated for one additional patient to be alive at 5 years?

  1. A3
  2. B100
  3. C10
  4. D43
  5. E33
Show answer

Answer: C. Absolute difference 43 − 33 = 10 percentage points; number needed to treat = 1/0.10 = 10. Reading results in absolute terms helps weigh cost and toxicity.

Review: section 06

Q63NSCLCLevel 2Systemic therapy

A trial reports an overall-survival hazard ratio of 0.77 (95% CI 0.61–0.96). The best interpretation is:

  1. A23 patients must be treated to save one life
  2. B23% more patients were alive at 5 years
  3. CAt any time point, the risk of death was about 23% lower with the experimental treatment
  4. DMedian survival was 23% longer by definition
  5. EThe result is not statistically significant
Show answer

Answer: C. A hazard ratio describes relative risk of the event over time. It is not an absolute difference, and does not translate directly into a median gain. A confidence interval excluding 1 indicates significance.

Review: section 06

Q64NSCLCLevel 2Systemic therapy

A randomised trial of a new drug shows a large progression-free survival benefit, but overall survival is similar; most control patients crossed over to the new drug at progression. The most reasonable reading is:

  1. AThe control arm was inferior from the start
  2. BThe trial was negative and should be ignored
  3. CProgression-free survival is always the more important end point
  4. DCrossover may dilute an overall-survival difference; sequencing the drug later may give similar survival
  5. EThe drug is ineffective
Show answer

Answer: D. When control patients receive the drug at progression, overall survival compares early versus later use. The decision then weighs time without progression, toxicity, quality of life and cost.

Review: section 06

Q65NSCLCLevel 2Systemic therapy

A patient with PD-L1 85% NSCLC received one dose of pembrolizumab before NGS returned an EGFR exon 19 deletion. What is the best approach?

  1. AStop pembrolizumab and start EGFR-directed therapy, watching closely for pneumonitis
  2. BGive radiotherapy only
  3. CSwitch to nivolumab
  4. DContinue pembrolizumab alone
  5. EAdd osimertinib to pembrolizumab
Show answer

Answer: A. EGFR-mutant tumours gain little from immunotherapy, and osimertinib after recent PD-1 blockade raises the risk of severe pneumonitis. Never combine them; monitor carefully when switching.

Review: section 06

Q66NSCLCLevel 2Systemic therapy

On ipilimumab plus nivolumab, a patient develops fatigue, headache and hyponatraemia; morning cortisol and ACTH are both low, while TSH and free T4 are also low. The most likely diagnosis is:

  1. AImmune-related hypophysitis
  2. BPrimary adrenal insufficiency
  3. CHyperthyroidism
  4. DBrain metastases
  5. ESIADH from the tumour
Show answer

Answer: A. Low cortisol with low ACTH (and central hypothyroidism) points to pituitary failure, typical of CTLA-4 blockade. Replace glucocorticoid before thyroid hormone.

Review: section 06

Q67NSCLCLevel 2Survivorship

Eight months after chemoradiation and durvalumab, an Indian patient develops a new cavitating lesion in the opposite lung. The best next step is:

  1. ARestart durvalumab
  2. BStart second-line chemotherapy immediately
  3. CAssume radiation fibrosis
  4. DStart empirical antituberculous treatment without tests
  5. ESputum NAAT and tissue sampling before calling it progression
Show answer

Answer: E. TB reactivation can occur on immunotherapy or steroids, and cavities can be infective, metastatic or a new primary. Microbiology and tissue prevent wrong treatment.

Review: section 08

Q68SCLCLevel 2Presentation, traps & genetics

Which feature best distinguishes Lambert-Eaton myasthenic syndrome from myasthenia gravis?

  1. AThymoma on CT
  2. BResponse only to thymectomy
  3. CPtosis that worsens through the day
  4. DStrength and reflexes improve briefly after sustained exercise, with dry mouth
  5. EPositive acetylcholine-receptor antibodies
Show answer

Answer: D. LEMS causes proximal weakness, reduced reflexes that increase after effort (post-tetanic facilitation) and autonomic features. Ocular and bulbar onset with fatigability suggests myasthenia gravis.

Review: section 02

Q69SCLCLevel 2Presentation, traps & genetics

A lung tumour contains small cell carcinoma mixed with an adenocarcinoma component. How is it classified and treated?

  1. ALarge-cell neuroendocrine carcinoma
  2. BTwo separate primaries
  3. CCombined small cell carcinoma, treated as small cell lung cancer
  4. DAdenocarcinoma, treated with EGFR testing only
  5. ECarcinoid tumour
Show answer

Answer: C. The WHO classifies these as combined small cell carcinoma (naming the other component). Treatment follows small cell principles.

Review: section 02

Q70SCLCLevel 2Screening, workup & staging

Which patient with small cell lung cancer needs invasive mediastinal staging before treatment?

  1. AA patient with a malignant pleural effusion
  2. BA patient with liver metastases
  3. CA patient with a 2.5 cm peripheral tumour and no nodal disease on PET-CT, being considered for surgery
  4. DA patient with bulky mediastinal nodes on CT
  5. EA patient with brain metastases
Show answer

Answer: C. Only apparent T1–2 N0 disease is considered for surgery, so pathological nodal confirmation is essential. Obvious nodal or distant disease needs no further invasive staging.

Review: section 03

Q71SCLCLevel 2Biomarkers

An EGFR exon 19-deleted adenocarcinoma transforms into small cell carcinoma on osimertinib. Re-biopsy will most likely show:

  1. ASmall cell histology that retains the original EGFR mutation, often with TP53 and RB1 loss
  2. BA germline EGFR mutation
  3. CLoss of the EGFR mutation and a new KRAS mutation
  4. DSquamous transformation with PD-L1 100%
  5. EAn ALK fusion
Show answer

Answer: A. Transformed tumours keep the founding EGFR mutation; TP53 and RB1 loss increase the risk. Treatment switches to platinum–etoposide.

Review: section 04

Q72SCLCLevel 2Local therapy

A patient with limited-stage small cell lung cancer presents with superior vena cava obstruction. The standard treatment is:

  1. AStenting and best supportive care
  2. BSteroids alone
  3. CSurgery first
  4. DPalliative radiotherapy alone
  5. EConcurrent chemotherapy with definitive thoracic radiotherapy, with curative intent
Show answer

Answer: E. SVCO does not change the curative intent in limited stage. Chemotherapy works quickly; stenting is reserved for severe symptoms.

Review: section 05

Q73SCLCLevel 2Systemic therapy

A patient with SIADH from small cell lung cancer has sodium 118 mmol/L and mild confusion. Which statement is correct?

  1. ASIADH is unrelated to the tumour
  2. BGive large volumes of normal saline
  3. CCorrect sodium slowly and start chemotherapy promptly, which treats the SIADH
  4. DDelay chemotherapy until sodium is normal for a month
  5. ECorrect sodium to normal within 6 hours
Show answer

Answer: C. Over-rapid correction risks osmotic demyelination (limit about 8–10 mmol/L in 24 hours). Fluid restriction, hypertonic saline for symptoms and prompt chemotherapy (which removes the source) are key.

Review: section 06

Q74SCLCLevel 2Systemic therapy

A woman with extensive-stage small cell lung cancer has three small asymptomatic brain metastases. The usual approach is:

  1. AWhole-brain radiotherapy before any systemic therapy
  2. BStart chemo-immunotherapy, then treat remaining brain lesions with radiosurgery or whole-brain radiotherapy after induction
  3. CObservation only
  4. DThoracic radiotherapy first
  5. ENeurosurgery for all three lesions
Show answer

Answer: B. Asymptomatic brain metastases can be treated systemically first, with radiotherapy after induction. Symptomatic brain metastases are usually irradiated first.

Review: section 06

Q75SCLCLevel 2Systemic therapy

A 70-year-old with newly diagnosed extensive-stage small cell lung cancer is bed-bound (ECOG 3) because of liver metastases and breathlessness; before the illness he was fully active. What is the best plan?

  1. ABest supportive care only, because of ECOG 3
  2. BWait until performance status improves
  3. CRadiotherapy to the liver
  4. DOffer chemotherapy promptly, with careful supportive care, because responses are often rapid
  5. EImmunotherapy alone
Show answer

Answer: D. Poor performance status caused by the cancer itself often improves rapidly with chemotherapy. Comorbidity-driven poor status is different.

Review: section 06

Q76SCLCLevel 2Systemic therapy

After four cycles of chemo-immunotherapy for extensive-stage disease, a patient has a good response at distant sites but a residual 3 cm hilar mass. A reasonable addition is:

  1. AConsolidative thoracic radiotherapy
  2. BStopping maintenance immunotherapy
  3. CPneumonectomy
  4. DWhole-brain radiotherapy
  5. ESwitching to tarlatamab
Show answer

Answer: A. Consolidative thoracic radiotherapy for residual chest disease after a good response reduced chest relapse in the CREST trial; data with chemo-immunotherapy are limited but it is commonly used.

Review: section 06

Q77SCLCLevel 2Systemic therapy

During the first tarlatamab infusion, a patient develops fever 39 °C and hypotension responding to fluids. The most likely cause is:

  1. ASepsis from neutropenia
  2. BTumour lysis syndrome
  3. CAdrenal crisis from immunotherapy
  4. DAnaphylaxis to etoposide
  5. ECytokine release syndrome
Show answer

Answer: E. Tarlatamab, a DLL3 × CD3 T-cell engager, commonly causes cytokine release syndrome (mostly grade 1–2) during early doses; neurotoxicity (ICANS) is also monitored. Tocilizumab and steroids treat severe cases.

Review: section 06

Level 3 · Challenging

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

Q78NSCLCLevel 3Screening, workup & staging

A 14 mm part-solid nodule has persisted for 4 months with a 7 mm solid component. The best interpretation is:

  1. ABenign because it has not grown
  2. BA pure ground-glass nodule needing no follow-up
  3. CAlmost certainly infection; repeat in 2 years
  4. DA hamartoma
  5. EHighly suspicious for adenocarcinoma; plan tissue diagnosis or resection
Show answer

Answer: E. A persistent part-solid nodule with a solid component of 6 mm or more is highly suspicious (often invasive adenocarcinoma) even without growth, and should be managed with tissue or resection after multidisciplinary review.

Review: section 03

Q79NSCLCLevel 3Screening, workup & staging

Under the IASLC 9th edition TNM, a 2.5 cm tumour with metastasis to a single ipsilateral mediastinal node station and no distant spread is staged as:

  1. AT1c N2 M0, stage IIIA
  2. BT2a N2b M0, stage IIIB
  3. CT1c N2a M0, stage IIIA
  4. DT1c N2a M0, stage IIB
  5. ET1c N1 M0, stage IIB
Show answer

Answer: D. The 9th edition splits N2 into N2a (one station) and N2b (multiple). T1 N2a is stage IIB; T1 N2b is IIIA; T2 N2a is IIIA; T2 N2b is IIIB.

Review: section 03

Q80NSCLCLevel 3Screening, workup & staging

Which finding makes a lung cancer M1c2 under the 9th edition?

  1. AA single brain metastasis
  2. BMultiple metastases confined to the liver
  3. CMetastases in more than one extrathoracic organ system
  4. DA malignant pleural effusion
  5. EA separate nodule in the contralateral lung
Show answer

Answer: C. M1c is now split: M1c1 = multiple metastases in one organ system; M1c2 = metastases in several organ systems. A single extrathoracic metastasis is M1b; pleural effusion and contralateral nodules are M1a.

Review: section 03

Q81NSCLCLevel 3ImageScreening, workup & staging

A 55-year-old never-smoker has the 18 mm lesion shown on CT (schematic), persistent after 3 months, with a 7 mm solid component. What is the most likely pathology?

RSchematic drawing · not a patient image
  1. ASquamous carcinoma
  2. BSmall cell carcinoma
  3. CHamartoma
  4. DAdenocarcinoma (minimally invasive or invasive) arising from a ground-glass precursor
  5. EHealed tuberculous granuloma
Show answer

Answer: D. A persistent part-solid nodule is typically adenocarcinoma-spectrum: the ground-glass part reflects lepidic growth and the solid part often invasion. A solid component ≥6 mm is highly suspicious and needs surgical or tissue management.

Review: section 03

Q82NSCLCLevel 3Biomarkers

A plasma ctDNA NGS test in a never-smoker with metastatic adenocarcinoma shows no driver. The correct interpretation is:

  1. AThe tumour is squamous
  2. BPD-L1 testing is now unnecessary
  3. CA driver is not excluded; test tissue as well
  4. DRepeat plasma testing monthly
  5. ENo driver is present; start chemo-immunotherapy at once
Show answer

Answer: C. Plasma tests have high specificity but limited sensitivity (low shedding, especially with limited disease or brain-only spread). A negative result needs tissue confirmation; a positive result can be acted on.

Review: section 04

Q83NSCLCLevel 3Biomarkers

Single-gene EGFR PCR is negative in a never-smoker with metastatic adenocarcinoma. ALK IHC is negative. What should be done?

  1. ANGS with RNA for fusions (ROS1, RET, NTRK) and other drivers
  2. BRepeat EGFR PCR on the same block
  3. CConclude that there is no driver
  4. DStart EGFR TKI empirically
  5. EStart pembrolizumab monotherapy regardless of PD-L1
Show answer

Answer: A. PCR and IHC miss ROS1, RET, NTRK fusions, MET exon 14, BRAF, HER2 and uncommon EGFR variants. Never-smokers have a high chance of another driver; RNA-based NGS is the best way to find fusions.

Review: section 04

Q84NSCLCLevel 3Biomarkers

At progression on lorlatinib after alectinib, which test result would best guide the next step?

  1. ARe-biopsy or ctDNA for ALK resistance mutations and bypass pathways
  2. BRepeat ALK IHC on the diagnostic sample
  3. CPD-L1 on the original biopsy
  4. DGermline ALK testing
  5. ESerum CEA
Show answer

Answer: A. Resistance mechanisms (compound ALK mutations, MET amplification, histological change) guide subsequent therapy. Tumour markers and old samples do not reflect current biology.

Review: section 04

Q85NSCLCLevel 3Biomarkers

For first-line treatment of ROS1-positive metastatic NSCLC with brain metastases, which choice best reflects current evidence?

  1. ACrizotinib, because of superior brain penetration
  2. BTaletrectinib or repotrectinib
  3. COsimertinib
  4. DSelpercatinib
  5. EPembrolizumab monotherapy
Show answer

Answer: B. Next-generation ROS1 inhibitors (taletrectinib, repotrectinib) give high response rates, long progression-free survival and good brain activity; crizotinib penetrates the brain poorly.

Review: section 04

Q86NSCLCLevel 3Biomarkers

A patient with metastatic NSCLC and an activating HER2 (ERBB2) mutation progresses after chemo-immunotherapy. Which option has phase 2 evidence as an oral targeted therapy?

  1. ALapatinib
  2. BErlotinib
  3. CZongertinib
  4. DTrastuzumab alone
  5. EImatinib
Show answer

Answer: C. Zongertinib, a HER2-selective TKI, showed high response rates in previously treated HER2-mutant NSCLC (Beamion LUNG-1). Trastuzumab deruxtecan is another option (watch for ILD).

Review: section 04

Q87NSCLCLevel 3Local therapy

After complete (R0) resection of pN2 NSCLC and adjuvant chemotherapy, the Lung ART trial showed that postoperative radiotherapy:

  1. ADoubled overall survival
  2. BImproved disease-free survival only in squamous cancers
  3. CReduced brain metastases
  4. DWas required for all pN2 patients
  5. EDid not improve disease-free survival and increased cardiopulmonary deaths
Show answer

Answer: E. Lung ART showed no significant disease-free survival benefit and more cardiopulmonary toxicity, so PORT is not routine after R0 resection; it is used for positive margins.

Review: section 05

Q88NSCLCLevel 3Local therapy

On cardiopulmonary exercise testing before lobectomy, a patient's VO2 max is 9 mL/kg/min. The best interpretation is:

  1. ARepeat spirometry only
  2. BHigh risk: consider sublobar resection, SBRT or other non-surgical options
  3. CVO2 max is irrelevant to lung resection
  4. DLow risk: proceed with lobectomy
  5. EModerate risk: proceed with pneumonectomy
Show answer

Answer: B. VO2 max >20 mL/kg/min is low risk, 10–20 individualised, <10 high risk (mortality >10% after anatomical resection).

Review: section 05

Q89NSCLCLevel 3Systemic therapy

In FLAURA2, adding platinum–pemetrexed to first-line osimertinib in EGFR-mutant NSCLC:

  1. AWorsened overall survival
  2. BWas only tested in exon 20 insertions
  3. CReduced haematological toxicity
  4. DHad no effect on progression-free survival
  5. EImproved progression-free and, at final analysis, overall survival, with more toxicity
Show answer

Answer: E. FLAURA2 improved progression-free survival and the final analysis showed longer overall survival (median about 47.5 vs 37.6 months), at the cost of more haematological toxicity and clinic visits.

Review: section 06

Q90NSCLCLevel 3Systemic therapy

In KEYNOTE-042 (pembrolizumab vs chemotherapy for PD-L1 ≥1%), the overall survival benefit was:

  1. ALargest in PD-L1 1–49%
  2. BLimited to squamous tumours
  3. CSeen only in EGFR-positive patients
  4. DAbsent in all subgroups
  5. EDriven mainly by patients with PD-L1 ≥50%
Show answer

Answer: E. Exploratory analysis showed little benefit in the 1–49% group; the overall result reflected the ≥50% subgroup. Immunotherapy alone at 1–49% is reserved for those who cannot have chemotherapy.

Review: section 06

Q91NSCLCLevel 3Systemic therapy

After resection of stage II EGFR exon 19-deleted NSCLC and adjuvant chemotherapy, ADAURA showed that osimertinib for 3 years:

  1. AHad no effect
  2. BWas inferior to adjuvant pembrolizumab
  3. CWas only beneficial for stage IA
  4. DImproved disease-free and overall survival
  5. EImproved disease-free survival but worsened overall survival
Show answer

Answer: D. ADAURA showed a large disease-free survival benefit and a 5-year overall survival of 88% vs 78%, making EGFR testing of resected NSCLC mandatory.

Review: section 06

Q92NSCLCLevel 3Systemic therapy

A resectable stage IIIA (single-station N2) adenocarcinoma has no EGFR/ALK alteration. Which approach is supported by phase 3 trials such as KEYNOTE-671 and CheckMate 77T?

  1. ANeoadjuvant radiotherapy alone
  2. BNeoadjuvant chemo-immunotherapy, surgery, then adjuvant immunotherapy
  3. CObservation until symptoms
  4. DOsimertinib before surgery
  5. ESurgery alone
Show answer

Answer: B. Perioperative chemo-immunotherapy raised pathological complete response rates and event-free survival, and KEYNOTE-671 showed improved overall survival.

Review: section 06

Q93NSCLCLevel 3Systemic therapy

Why should durvalumab not be given after chemoradiation for EGFR-mutant stage III NSCLC?

  1. AIt is contraindicated in all women
  2. BDurvalumab is not approved for stage III disease
  3. CEGFR mutations predict durvalumab-induced haemorrhage
  4. DIt causes hypercalcaemia
  5. ELittle benefit, and osimertinib after immunotherapy raises pneumonitis risk; LAURA supports osimertinib instead
Show answer

Answer: E. Subgroup data show little benefit of PD-(L)1 blockade in EGFR-mutant disease and a higher risk of severe pneumonitis when osimertinib follows. LAURA showed osimertinib after chemoradiation markedly prolonged progression-free survival.

Review: section 06

Q94NSCLCLevel 3Systemic therapy

Which statement about KRAS G12C-mutant metastatic NSCLC is correct?

  1. AKRAS G12C predicts benefit from osimertinib
  2. BKRAS mutations are inherited
  3. CKRAS G12C tumours do not respond to immunotherapy
  4. DSotorasib doubled overall survival in CodeBreaK 200
  5. EChemo-immunotherapy is used first; sotorasib improved progression-free but not overall survival versus docetaxel
Show answer

Answer: E. KRAS G12C tumours (often in smokers) are treated with chemo-immunotherapy first. CodeBreaK 200 showed a modest progression-free survival gain over docetaxel without an overall survival difference.

Review: section 06

Q95NSCLCLevel 3Systemic therapy

A completely resected stage IIA (pT2b N1) RET fusion-positive adenocarcinoma has received adjuvant chemotherapy. Which next step has randomised evidence?

  1. AAdjuvant osimertinib
  2. BAdjuvant bevacizumab
  3. CAdjuvant alectinib
  4. DAdjuvant selpercatinib
  5. ENo further therapy is ever indicated
Show answer

Answer: D. LIBRETTO-432 showed adjuvant selpercatinib markedly improved event-free survival in resected stage IB–IIIA RET-positive NSCLC (small trial, short follow-up).

Review: section 06

Q96NSCLCLevel 3Systemic therapy

Resectable stage II EGFR exon 19-deleted NSCLC in a patient whose surgeon wants downstaging before lobectomy. Which induction option is supported by a phase 3 trial?

  1. ARadiotherapy alone
  2. BNivolumab plus chemotherapy (CheckMate 816)
  3. CAlectinib
  4. DDurvalumab alone
  5. EOsimertinib with or without chemotherapy (NeoADAURA)
Show answer

Answer: E. NeoADAURA showed improved major pathological response with neoadjuvant osimertinib ± chemotherapy. Immunotherapy trials largely excluded or showed little benefit in EGFR-mutant disease.

Review: section 06

Q97NSCLCLevel 3Systemic therapy

In PD-L1-negative (TPS <1%) metastatic NSCLC without a driver, which strategy is thought to add most beyond a single PD-1 inhibitor with chemotherapy?

  1. ABevacizumab alone
  2. BAdding CTLA-4 blockade (nivolumab + ipilimumab, or durvalumab + tremelimumab) with chemotherapy
  3. CPembrolizumab monotherapy
  4. DObservation
  5. EOsimertinib
Show answer

Answer: B. Exploratory data suggest dual PD-(L)1 + CTLA-4 blockade (with chemotherapy) performs relatively better in PD-L1-negative disease, at the cost of more immune toxicity.

Review: section 06

Q98NSCLCLevel 3Survivorship

The risk of a second primary lung cancer after resection of NSCLC is approximately:

  1. A1–2% per year, persisting long term
  2. BZero after 5 years
  3. C20% per year
  4. D0.01% per year
  5. EOnly in the first year
Show answer

Answer: A. Second primaries occur at about 1–2% per patient-year for many years, which is why annual low-dose CT continues beyond 5 years and smoking cessation remains vital.

Review: section 08

Q99SCLCLevel 3Presentation, traps & genetics

Which molecular finding is almost universal in small cell lung cancer?

  1. AALK fusion
  2. BInactivation of both TP53 and RB1
  3. CKRAS G12C mutation
  4. DBRAF V600E
  5. EEGFR exon 19 deletion
Show answer

Answer: B. Loss of TP53 and RB1 is near-universal. Targetable drivers are essentially absent in de novo small cell lung cancer.

Review: section 02

Q100SCLCLevel 3Biomarkers

Which statement about DLL3 in small cell lung cancer is correct?

  1. AIt is an inhibitory Notch ligand expressed on most small cell cancers and is the target of tarlatamab
  2. BIt predicts response to EGFR inhibitors
  3. CIt is a germline cancer-predisposition gene
  4. DIt is a driver mutation requiring NGS before treatment
  5. EIt is expressed mainly on normal lung epithelium
Show answer

Answer: A. DLL3 is aberrantly expressed on the surface of most small cell cancers; tarlatamab bridges DLL3 to CD3 on T cells. Testing is not required before treatment.

Review: section 04

Q101SCLCLevel 3Local therapy

In limited-stage small cell lung cancer, CONVERT compared twice-daily 45 Gy over 3 weeks with once-daily 66 Gy over 6.5 weeks and found:

  1. AOnce-daily was clearly superior
  2. BNeither improved on chemotherapy alone
  3. CNo significant difference in survival; both are acceptable
  4. DOnce-daily caused more oesophagitis
  5. ETwice-daily was clearly superior
Show answer

Answer: C. CONVERT did not show superiority of once-daily radiotherapy; survival and toxicity were similar, so both schedules are used, starting early with chemotherapy.

Review: section 05

Q102SCLCLevel 3Local therapy

In extensive-stage small cell lung cancer, the Japanese randomised trial of PCI versus MRI surveillance (Takahashi) found:

  1. APCI eliminated all brain metastases
  2. BA large survival benefit from PCI
  3. CNo overall-survival benefit from PCI when patients had regular brain MRI
  4. DPCI improved cognition
  5. EMRI surveillance worsened survival
Show answer

Answer: C. With MRI surveillance as the comparator, PCI did not improve survival. Either strategy is acceptable; the MAVERICK trial is testing this further.

Review: section 05

Q103SCLCLevel 3Local therapy

The landmark Turrisi (INT 0096) trial in limited-stage small cell lung cancer showed that twice-daily thoracic radiotherapy (45 Gy in 3 weeks) compared with once-daily 45 Gy over 5 weeks:

  1. AImproved 5-year survival, with more oesophagitis
  2. BWorsened survival
  3. CAllowed omission of chemotherapy
  4. DHad no effect on survival but reduced oesophagitis
  5. EReplaced the need for PCI
Show answer

Answer: A. Accelerated hyperfractionation improved 5-year survival (about 26% vs 16%) at the cost of more grade 3 oesophagitis. CONVERT later showed once-daily 66 Gy was not superior to twice-daily 45 Gy.

Review: section 05

Q104SCLCLevel 3Systemic therapy

In limited-stage small cell lung cancer without progression after chemoradiation, ADRIATIC showed that durvalumab:

  1. AHad no effect
  2. BWas harmful when given after PCI
  3. CImproved overall survival (median about 56 vs 33 months)
  4. DShould replace thoracic radiotherapy
  5. EOnly improved response rate
Show answer

Answer: C. ADRIATIC established consolidation durvalumab for up to 2 years after chemoradiation in limited-stage small cell lung cancer, with a large overall survival gain.

Review: section 06

Q105SCLCLevel 3Systemic therapy

Small cell lung cancer relapses 6 weeks after completing platinum–etoposide with atezolizumab. A preferred option supported by a phase 3 trial is:

  1. APlatinum–etoposide rechallenge
  2. BTarlatamab
  3. COsimertinib
  4. DPemetrexed
  5. EObservation
Show answer

Answer: B. Relapse within 6 months of first-line treatment indicates resistance; DeLLphi-304 showed tarlatamab, a DLL3/CD3 bispecific, improved overall survival over standard chemotherapy (lurbinectedin or topotecan are alternatives). After 6 months, tarlatamab or platinum rechallenge are both reasonable.

Review: section 06

Q106SCLCLevel 3Systemic therapy

A 62-year-old has a resected 2.4 cm small cell carcinoma, pT1c N0 after negative invasive mediastinal staging. What is recommended next?

  1. AAdjuvant platinum–etoposide chemotherapy, with PCI or MRI surveillance
  2. BDurvalumab alone
  3. CObservation only
  4. DThoracic radiotherapy alone
  5. EOsimertinib
Show answer

Answer: A. Resected node-negative small cell carcinoma still has high micrometastatic risk: adjuvant chemotherapy is given; nodal involvement would add radiotherapy.

Review: section 06

Q107SCLCLevel 3Systemic therapy

In extensive-stage disease, adding lurbinectedin to atezolizumab maintenance after induction (IMforte) is best suited to:

  1. APatients with symptomatic brain metastases
  2. BLimited-stage disease after chemoradiation
  3. CPatients with ECOG 3
  4. DPatients who progressed during induction
  5. EFit patients without brain metastases who responded to chemo-atezolizumab induction
Show answer

Answer: E. IMforte showed improved progression-free and overall survival in selected patients without progression after induction; patients with brain metastases were not the target population.

Review: section 06

Q108SCLCLevel 3Systemic therapy

In IMpower133 and CASPIAN, adding a PD-L1 antibody to platinum–etoposide in extensive-stage small cell lung cancer improved median overall survival by about:

  1. A12 months
  2. BNo difference
  3. C2–3 months, with a small group of long-term survivors
  4. D1 week
  5. E6 months but only in PD-L1-high tumours
Show answer

Answer: C. Median survival rose from about 10.3 months to 12.3–13.0 months. The modest median gain hides a durable tail; benefit did not depend on PD-L1.

Review: section 06

Level 2 · Applied & innovative

Clinical reasoning: calculations (pack-years, predicted lung function, NNT), CT and fluid findings, reading trial results, sequencing traps.

Q109NSCLCLevel 2Systemic therapy

A patient with ALK-positive NSCLC on lorlatinib has a serum cholesterol of 340 mg/dL and triglycerides of 480 mg/dL at 2 months. What is the best approach?

  1. AStart immunotherapy instead
  2. BIgnore: lipids do not matter in cancer
  3. CStart lipid-lowering therapy and continue lorlatinib with monitoring
  4. DStop lorlatinib permanently
  5. ESwitch to crizotinib immediately
Show answer

Answer: C. Hyperlipidaemia is the commonest lorlatinib effect and is managed with statins (± fibrates) while continuing the drug; mood, cognitive and weight changes are also watched.

Review: section 06

Q110NSCLCLevel 2Systemic therapy

On day 3 of brigatinib, a patient develops new breathlessness and hypoxia with bilateral ground-glass change. The most likely cause is:

  1. APulmonary embolism is the only possibility
  2. BRadiation pneumonitis
  3. CEarly-onset pulmonary events typical of brigatinib
  4. DALK-positive disease progression
  5. EExpected TKI response
Show answer

Answer: C. Brigatinib can cause early pulmonary toxicity in the first week, which is why treatment starts at a lower step-up dose. Hold the drug, exclude infection and embolism, and treat supportively.

Review: section 06

Q111NSCLCLevel 2Systemic therapy

A patient on dabrafenib plus trametinib for BRAF V600E NSCLC develops fever of 39 °C without a source. What is the correct first step?

  1. AHold the BRAF/MEK treatment, give antipyretics and restart when the fever settles
  2. BContinue treatment and start broad antibiotics only
  3. CSwitch to osimertinib
  4. DStop treatment permanently
  5. EAdd high-dose steroids and continue
Show answer

Answer: A. Pyrexia is a class effect of dabrafenib + trametinib: interrupt at the first fever, treat symptoms, exclude infection, and restart when settled; steroid prophylaxis can help recurrent episodes.

Review: section 06

Level 3 · Challenging

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

Q112NSCLCLevel 3Systemic therapy

A patient on capmatinib for MET exon 14 NSCLC has a rise in creatinine from 0.9 to 1.3 mg/dL with normal cystatin C and no symptoms. The best interpretation is:

  1. AAcute tubular necrosis needing dialysis
  2. BInhibition of renal creatinine transporters, not true loss of kidney function
  3. CDehydration from diarrhoea is certain
  4. DTumour lysis syndrome
  5. EImmune nephritis
Show answer

Answer: B. MET inhibitors block tubular creatinine secretion, raising serum creatinine without true GFR loss; a normal cystatin C supports this. Peripheral oedema is the commonest troublesome effect.

Review: section 06

Q113NSCLCLevel 3Systemic therapy

Six weeks after starting pembrolizumab, a 66-year-old has chest pain, ptosis, proximal weakness, troponin elevation and CK 4200 U/L. What is the most urgent action?

  1. AStart thyroxine
  2. BStop immunotherapy permanently and start high-dose IV steroids with cardiology input for immune myocarditis–myositis
  3. COrder a bone scan
  4. DGive oral steroids and continue immunotherapy
  5. EContinue pembrolizumab and repeat troponin in a week
Show answer

Answer: B. Myocarditis with myositis and myasthenia-like features is a rare but often fatal immune toxicity, usually in the first 1–3 months. Stop permanently, give high-dose IV steroids urgently, monitor in hospital and escalate immunosuppression if needed.

Review: section 06

Q114NSCLCLevel 3Systemic therapy

A patient with ALK-positive NSCLC on lorlatinib is diagnosed with pulmonary TB. Which treatment issue is most important?

  1. AStop lorlatinib permanently
  2. BRifampicin markedly lowers TKI levels and with lorlatinib can cause severe hepatotoxicity: plan a rifabutin-based or non-rifamycin regimen with the TB team
  3. CIsoniazid alone for 2 months is adequate
  4. DDouble the lorlatinib dose
  5. ENo interaction exists between TB drugs and TKIs
Show answer

Answer: B. Rifampicin is a strong CYP3A inducer. It reduces exposure to most TKIs, and the lorlatinib combination caused serious liver injury. Coordinate with the TB programme to use regimens without strong induction.

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.