Serum ProGRP and NSE levels predicting small cell lung cancer transformation in a patient with ALK rearrangement‑positive non‑small cell lung cancer: A case report

Oya,Yuko; Yoshida,Tatsuya; Uemura,Takehiro; Murakami,Yoshiko; Inaba,Yoshitaka; Hida,Toyoaki

doi:10.3892/ol.2018.9158

Serum ProGRP and NSE levels predicting small cell lung cancer transformation in a patient with ALK rearrangement‑positive non‑small cell lung cancer: A case report

Authors:
- Yuko Oya
- Tatsuya Yoshida
- Takehiro Uemura
- Yoshiko Murakami
- Yoshitaka Inaba
- Toyoaki Hida
View Affiliations

Affiliations: Department of Thoracic Oncology, Aichi Cancer Center Hospital, Nagoya, Aichi 464‑8681, Japan, Department of Pathology and Molecular Diagnostics, Aichi Cancer Center Hospital, Nagoya, Aichi 464‑8681, Japan, Department of Diagnostic and Interventional Radiology, Aichi Cancer Center Hospital, Nagoya, Aichi 464‑8681, Japan
Published online on: July 17, 2018 https://doi.org/10.3892/ol.2018.9158
Pages: 4219-4222
Copyright: © Oya et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

The resistance mechanisms to anaplastic lymphoma kinase (ALK) inhibitors comprise ALK gene variations, such as ALK point mutations and copy‑number gains, the activation of bypass signaling through the activation of other oncogenes and small cell lung cancer (SCLC) transformation. To date, few studies have investigated whether tumor markers for SCLC correlate with the SCLC transformation in EGFR‑mutant NSCLC and ALK‑positive non‑SCLC (NSCLC). The present case study reported a patient with SCLC transformation after alectinib treatment. The patient exhibited elevation of pro‑gastrin‑releasing peptide precursor and neuron‑specific enolase levels, which may be predictive of SCLC transformation during the resistance to ALK‑tyrosine kinase inhibitors.

View Figures

View References

1	Katayama R, Khan TM, Benes C, Lifshits E, Ebi H, Rivera VM, Shakespeare WC, Iafrate AJ, Engelman JA and Shaw AT: Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK. Proc Natl Acad Sci USA. 108:7535–7540. 2011. View Article : Google Scholar : PubMed/NCBI
2	Katayama R, Shaw AT, Khan TM, Mino-Kenudson M, Solomon BJ, Halmos B, Jessop NA, Wain JC, Yeo AT, Benes C, et al: Mechanisms of acquired crizotinib resistance in ALK-rearranged lung cancers. Sci Transl Med. 4:120ra172012. View Article : Google Scholar : PubMed/NCBI
3	Sasaki T, Koivunen J, Ogino A, Yanagita M, Nikiforow S, Zheng W, Lathan C, Marcoux JP, Du J, Okuda K, et al: A novel ALK secondary mutation and EGFR signaling cause resistance to ALK kinase inhibitors. Cancer Res. 71:6051–6060. 2011. View Article : Google Scholar : PubMed/NCBI
4	Lovly CM, McDonald NT, Chen H, Ortiz-Cuaran S, Heukamp LC, Yan Y, Florin A, Ozretić L, Lim D, Wang L, et al: Rationale for co-targeting IGF-1R and ALK in ALK fusion-positive lung cancer. Nat Med. 20:1027–1034. 2014. View Article : Google Scholar : PubMed/NCBI
5	Fujita S, Masago K, Katakami N and Yatabe Y: Transformation to SCLC after treatment with the ALK inhibitor alectinib. J Thorac Oncol. 11:e67–e72. 2016. View Article : Google Scholar : PubMed/NCBI
6	Ou SI, Lee TK, Young L, Fernandez-Rocha MY, Pavlick D, Schrock AB, Zhu VW, Milliken J, Ali SM and Gitlitz BJ: Dual occurrence of ALK G1202R solvent front mutation and small cell lung cancer transformation as resistance mechanisms to second generation ALK inhibitors without prior exposure to crizotinib. Pitfall of solely relying on liquid re-biopsy? Lung Cancer. 106:110–114. 2017.PubMed/NCBI
7	Stieber P, Dienemann H, Schalhorn A, Schmitt UM, Reinmiedl J, Hofmann K and Yamaguchi K: Pro-gastrin-releasing peptide (ProGRP)-a useful marker in small cell lung carcinomas. Anticancer Res. 19:2673–2678. 1999.PubMed/NCBI
8	Gainor JF, Dardaei L, Yoda S, Friboulet L, Leshchiner I, Katayama R, Dagogo-Jack I, Gadgeel S, Schultz K, Singh M, et al: Molecular mechanisms of resistance to first- and second-generation ALK inhibitors in ALK-rearranged lung cancer. Cancer Discov. 6:1118–1133. 2016. View Article : Google Scholar : PubMed/NCBI
9	Paweletz CP, Sacher AG, Raymond CK, Alden RS, O'Connell A, Mach SL, Kuang Y, Gandhi L, Kirschmeier P, English JM, et al: Bias-corrected targeted next-generation sequencing for rapid, multiplexed detection of actionable alterations in cell-free DNA from advanced lung cancer patients. Clin Cancer Res. 22:915–922. 2016. View Article : Google Scholar : PubMed/NCBI
10	Lodrini M, Sprüssel A, Astrahantseff K, Tiburtius D, Konschak R, Lode HN, Fischer M, Keilholz U, Eggert A and Deubzer HE: Using droplet digital PCR to analyze MYCN and ALK copy number in plasma from patients with neuroblastoma. Oncotarget. 8:85234–85251. 2017. View Article : Google Scholar : PubMed/NCBI
11	Johnson AC, Dô P, Richard N, Dubos C, Michels JJ, Bonneau J and Gervais R: Identification of I1171N resistance mutation in ALK-positive non-small-cell lung cancer tumor sample and circulating tumor DNA. Lung Cancer. 99:38–40. 2016. View Article : Google Scholar : PubMed/NCBI
12	Bordi P, Tiseo M, Rofi E, Petrini I, Restante G, Danesi R and Del Re M: Detection of ALK and KRAS mutations in circulating tumor DNA of patients with advanced ALK-positive NSCLC with disease progression during crizotinib treatment. Clin Lung Cancer. 18:692–697. 2017. View Article : Google Scholar : PubMed/NCBI