Table 2 Summary of patients from the literature who have data for multiple TKI-refractory lesions with SCLC transformation.

From: Small cell lung cancer transformation and T790M mutation: complimentary roles in acquired resistance to kinase inhibitors in lung cancer

Case

Author

Age1

Sex

Mut.2

TKI3

Details of the patient

Ref.

1

Zakowski, et al.

45

F

19 del

erlotinib → gefitinib

Examined lesions from five organ sites all showed SCLC with no mutations in exons 18–24 of EGFR or exon 2 of KRAS.

6

2

Morinaga, et al.

46

F

19 del

gefitinib

Resected brain tumour and biopsied lung lesion both showed SCLC.

7

3

Sequist, et al.

67

F

L858R

erlotinib

Metastatic lesions in the lung, thoracic lymph nodes, liver and nodules along the diaphragm all showed SCLC without T790M or MET amp. Brain metastasis retained adenocarcinoma without T790M or MET amp.

3

4

Niederst, et al.

56

F

L858R

erlotinib

Metastatic lesions in the lung and liver showed SCLC transformation with PIK3CA E545K mutation (without T790M), while the diaphragm tumour showed adenocarcinoma with T790M (without PIK3CA mutation).

3,15

5

Fallet, et al.

44

F

19 del

erlotinib

Tumour stenosis of the upper-right lobe bronchus showed SCLC without T790M, while bronchial aspirate showed adenocarcinoma with T790M.

9

6

Present case

76

F

19 del

gefitinib

Most metastatic lesions (7/9) had the SCLC component. TKI-refractory lesions with adenocarcinoma histology, but not SCLC, only harboured T790M.

—

  1. 1Age at initial diagnosis of lung cancer.
  2. 2Type of EGFR-activating mutation (19 del: exon 19 deletion; or L858R point mutation).
  3. 3Type of EGFR tyrosine kinase inhibitor(s).
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