Transformation Into Small Cell Lung Cancer : a Mode of Resistance to Treatment

The discovery of oncogenic mutations and the use of targeted therapies have transformed the management of certain tumors. Thus 12 to 15% of bronchial adenocarcinomas (AD) carry mutations of EGFR and receive from the first line inhibitors of this kinase (ITK). Despite spectacular results, relapse and resistance are quasi-general phenomena. In most known cases, EGFR-TKI resistance mechanisms involve secondary mutations of EGFR or the activation of alternative oncogenic pathways. However, in 5 to 15% of patients, resistance is manifested by the emergence of a small cell carcinoma (CPC), a cancer of neuroendocrine origin very different from AD by its cellular, molecular and epidemiological characteristics. This phenotypic transformation is an almost unique phenomenon in oncology and its molecular bases are not understood. To study this phenomenon, a Franco-Italian network was established that documented and collected cases of this rare tumor. This series is the subject of detailed anatomopathological, clinical and therapeutic documentation. This project aims to investigate the exome of one or more matched lesion regions to evaluate the evolutionary processes leading from the initial AD to the relapsing CPC. These results will guide future research on predictive markers of relapse and their targeted treatment.

Sex

All

Inclusion Criteria:

* Patient with no history of small cell cancer or Neuroendocrine cancer
* Patients with non-small cell lung cancer at baseline, stage IIIB or IV
* Transformation during treatment of non small cell lung cancer, in small cell cancer proven by biopsy

Exclusion Criteria:

* History of small cell cancer or Neuroendocrine cancer
* Absence of histological evidence of the transformation into small cell lung cancer after treatment of non small cell lung cancer
* Patients with non-small cell lung cancer at initial biopsy, stage I, II, IIIA

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