|LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 3 | Page : 384-385
Small-cell lung cancer with epidermal growth factor receptor mutation: Case report and review of literature
N Asai1, Y Ohkuni1, M Matsuda2, N Kaneko1
1 Department of Pulmonology, Kameda Medical Center, Chiba, Japan
2 Department of Oncology, Kameda Medical Center, Chiba, Japan
|Date of Web Publication||10-Dec-2014|
Dr. N Asai
Department of Pulmonology, Kameda Medical Center, Chiba
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Asai N, Ohkuni Y, Matsuda M, Kaneko N. Small-cell lung cancer with epidermal growth factor receptor mutation: Case report and review of literature. Indian J Cancer 2014;51:384-5
|How to cite this URL:|
Asai N, Ohkuni Y, Matsuda M, Kaneko N. Small-cell lung cancer with epidermal growth factor receptor mutation: Case report and review of literature. Indian J Cancer [serial online] 2014 [cited 2019 Oct 22];51:384-5. Available from: http://www.indianjcancer.com/text.asp?2014/51/3/384/146753
This is a case report and a review of epidermal growth factor receptor (EGFR) mutated small cell lung cancer (SCLC). In 2005, Araki, et al. published the first report of cases of EGFR mutated SCLC case.  Since then, five case reports, ,, a total of 14 patients with EGFR mutated SCLC have been demonstrated, including our case which we report here.
A 68-year old woman without smoking history was referred to our department due to an abnormal shadow [Figure 1]. Transbronchial lung biopsy (TBLB) was performed and SCLC was pathologically confirmed [Figure 2]. In terms of immunostaining, synaptophysin, thyroid transcription factor-1 (TTF-1), chromogranin A and cluster of differentiation (CD) 56 were positive and cytokeratin (CK) 5/6 was negative. EGFR mutation was detected because serum-carcinoembryonic antigen (CEA) was significantly high and exon 19 was confirmed. She was diagnosed as SCLC with EGFR mutation. While first-line chemotherapy with combination of carboplatin and etoposide and second-line chemotherapy with aumurubicin (AMR) were initially effective, she relapsed. With PS of 2, then, gefitinib was administered as third-line chemotherapy resulting in progressive disease. She is now receiving topotecan as fourth-line chemotherapy.
|Figure 1: Chest radiography shows a lobulated lesion in the right upper lung field (a) Chest CT shows a well-defined nodule with a little trabeculation on the right upper lobe (b) with pretracheal lymph node swelling (c)|
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|Figure 2: Microscopic findings of TBLB specimens reveal cancer cells showing high N/C ratio H and E, stain) (a) Immunohistochemical staining images of the tumor cells were positive for thyroid transcription factor-1 (b) and cluster of differentiation 56 (c) Cytokeratin 5/6 was negative (d)|
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Generally, there is a definite relationship between cigarette smoking and the development of SCLC. The proportion of women with SCLC has increased from 28% in 1973 to 50% in 2002.  In contrast, 9 (64.3%) were females and 10 (71.4%) of the 14 patients with EGFR mutated SCLC in this study never smoked. The epidemiology of EGFR mutated SCLC might be different from conventional SCLC.
It is well known that EGFR-TKI achieves a high response rate for mutated adenocarcinoma.  Four of the seven patients (57.1%) with EGFR mutated SCLC who received EGFR-TKI showed partial response as shown in [Table 1]. EGFR-TKI might be as effective for patients with EGFR mutated SCLC as adenocarcinoma with EGFR mutations.
|Table 1: Characteristics of patients with EGFR mutated SCLC and the outcomes|
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In terms of the EGFR mutation type, both exon 19 and 21 are thought to be very sensitive for EGFR-TKI.  Two of the four patients (50%) with exon 19 had PR, two of the four patients (50%) showed PD. Ando, et al. documented that poor PS could be related to antitumor response.  PS 2, which is relatively good and could be a predictive factor in our case as well. Another prognostic factor for EGFR-TKI could be exited and more cases should be investigated.
Tatematsu, et al. reported that five of the 122 SCLC patients during seven years were confirmed with EGFR mutations. Combined type of SCLC and adenocacinoma were found in three of the five patients. Two of the three were found in resected tumors and the remaining one was confirmed by transbronchial lung biopsy (TBLB).  Our case might have been a combined type as well since TBLB specimens are not large enough to fully examine the lesion pathologically.
| » Conclusion|| |
EGFR mutations should be examined in female patients who never smoked and who are showing a high CEA. The standard treatment for EGFR mutated SCLC is still unknown. More cases should be estimated and examined.
| » References|| |
Araki J, Okamoto I, Suto R, Ichikawa Y, Sasaki J. Efficacy of the tyrosine kinase inhibitor gefitinib in a patient with metastatic small cell lung cancer. Lung Cancer 2005;48:141-4.
Tatematsu A, Shimizu J, Murakami Y, Horio Y, Nakamura S, Hida T, et al.
Epidermal growth factor receptor mutations in small cell lung cancer. Clin Cancer Res 2008;14:6092-96.
Govindan R, Page N, Morgensztern D, Read W, Tierney R, Vlahiotis A, et al.
Changing epidemiology of small-cell lung cancer in the United States over the last 30 years: Analysis of the surveillance, epidemiologic, and end results database. J Clin Oncol 2006;24:4539-44.
Mok TS, Wu YL, Thongprasert S, Yang CH, Chu DT, Saijo N, et al.
Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. N Engl J Med 2009;361:947-57.
Ando M, Okamoto I, Yamamoto N, Takeda K, Tamura K, Seto T, et al.
Predictive factors for interstitial lung disease, antitumor response, and survival in non-small-cell lung cancer patients treated with gefitinib. J Clin Oncol 2006;24:2549-56.
[Figure 1], [Figure 2]
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