Transformation from non-small-cell lung cancer to small-cell lung cancer: molecular drivers and cells of origin

Summary Lung cancer is the most common cause of cancer deaths worldwide. The two broad histological subtypes of lung cancer are small-cell lung cancer (SCLC), which is the cause of 15% of cases, and non-small-cell lung cancer (NSCLC), which accounts for 85% of cases and includes adenocarcinoma, squa...

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Bibliographic Details
Published in:The lancet oncology 2015-04, Vol.16 (4), p.e165-e172
Main Authors: Oser, Matthew G, MD, Niederst, Matthew J, PhD, Sequist, Lecia V, MD, Engelman, Jeffrey A, Dr
Format: Article
Language:English
Subjects:
Adenocarcinoma - genetics
Adenocarcinoma - pathology
Biopsy
Carcinoma, Non-Small-Cell Lung - genetics
Carcinoma, Non-Small-Cell Lung - pathology
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - pathology
Clinical medicine
Drug Resistance, Neoplasm - genetics
Hematology, Oncology and Palliative Medicine
Histology
Humans
Lung cancer
Metastasis
Mutation
Patients
Protein expression
Protein Kinase Inhibitors - therapeutic use
Radiation therapy
Receptor, Epidermal Growth Factor - genetics
Small Cell Lung Carcinoma - genetics
Small Cell Lung Carcinoma - pathology
Surgery
Tumors
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Summary:Summary Lung cancer is the most common cause of cancer deaths worldwide. The two broad histological subtypes of lung cancer are small-cell lung cancer (SCLC), which is the cause of 15% of cases, and non-small-cell lung cancer (NSCLC), which accounts for 85% of cases and includes adenocarcinoma, squamous-cell carcinoma, and large-cell carcinoma. Although NSCLC and SCLC are commonly thought to be different diseases owing to their distinct biology and genomic abnormalities, the idea that these malignant disorders might share common cells of origin has been gaining support. This idea has been supported by the unexpected findings that a subset of NSCLCs with mutated EGFR return as SCLC when resistance to EGFR tyrosine kinase inhibitors develops. Additionally, other case reports have described the coexistence of NSCLC and SCLC, further challenging the commonly accepted view of their distinct lineages. Here, we summarise the published clinical observations and biology underlying tumours with combined SCLC and NSCLC histology and cancers that transform from adenocarcinoma to SCLC. We also discuss pre-clinical studies pointing to common potential cells of origin, and speculate how the distinct paths of differentiation are determined by the genomics of each disease.
ISSN:1470-2045
1474-5488
DOI:10.1016/S1470-2045(14)71180-5