Epidermal Growth Factor Receptor-Activating Mutation and Anaplastic lymphoma Kinase Gene Rearrangement as Oncogenic Co-Addiction: A Case Report of Adenocarcinoma Treated with Sequential Tyrosine Kinase- EGFR and ALK-Tyrosine Kinase Inhibitors

Benoit Roch, vanessa Szablewski, Isabelle Serre, Julie Vendrell, Jerome Solassol and Jean-louis Pujol

Department of Thoracic Oncology, Arnaud de Villeneuve Hospital, Montpellier, France
Department of Pathology, Arnaud de Villeneuve Hospital, Montpellier, France
Cancer Research Institute of Montpellier, Montpellier, France

^*Correspondance to: Jean-louis Pujol 

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Abstract:

Epidermal Growth Factor Receptor (EGFR)-activating mutation and Anaplastic Lymphoma Kinase (ALK) gene rearrangement are the two most frequently observed druggable oncogenic addictions in adenocarcinoma of the lung. Hitherto, they are considered as mutually exclusive and searching for ALK rearrangement when EGFR sensitizing mutation has been demonstrated is considered by many guidelines as not mandatory [1]. Recently coaltered EGFR and ALK genes in the same tumor have been described using micro-dissection techniques in two out of 629 adenocarcinomas [2]; this phenomenon is supposed to be linked with tumor heterogeneity. However, whether both altered genes behave as oncogenic drivers is not known. We report here a case of adenocarcinoma with concomitant EGFR/ALK gene alterations for which sequential therapy with EGFR-Tyrosine Kinase Inhibitors (TKI) and ALK-tyrosine kinase inhibitors demonstrated druggable status of both altered genes.

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Cite the Article:

Roch B, Szablewski V, Serre I, Vendrell J, Solassol J, Pujol J-l. Epidermal Growth Factor Receptor-Activating Mutation and Anaplastic lymphoma Kinase Gene Rearrangement as Oncogenic Co-Addiction: A Case Report of Adenocarcinoma Treated with Sequential Tyrosine Kinase-EGFR and ALK-Tyrosine Kinase Inhibitors. Clin Oncol. 2018; 3: 1482.