Time filter

Source Type

Tiseo M.,University of Parma | Bersanelli M.,University of Parma | Rossi G.,University Hospital Policlinico | Ardizzoni A.,University of Bologna | Pelosi G.,University of Milan
Lung Cancer | Year: 2015

We present a very interesting case of lung adenocarcinoma carrying an uncommon EGFR exon 19 insertion with concomitant PIK3CA mutation showing dramatic and persisting improvement upon erlotinib therapy, after progression during PI3K inhibitor. © 2014 Elsevier Ireland Ltd.

Mengoli M.C.,University Hospital Policlinico | Barbieri F.,University Hospital Policlinico | Bertolini F.,University Hospital Policlinico | Tiseo M.,University of Parma | Rossi G.,University Hospital Policlinico
Lung Cancer | Year: 2016

The paradigm of mutually exclusive alterations among oncogenic drivers in non-small-cell lung cancer (NSCLC) is challenged by the increasing evidence of detection of two or more driver alterations in the same tumor using highly-sensitive molecular assays. We report here two cases of ALK-rearranged adenocarcinomas harboring concomitant exon 2 K-RAS mutations (G13D and Q61H). The patients, a 49-year-old smoker man and a 59-year-old non-smoking woman, experienced a rapid disease progression and primary resistance to crizotinib. Search for similar cases in the literature reveals that concomitant K-RAS mutations and ALK rearrangement occur in a subset of NSCLC and seems to lead to resistance to crizotinib. Among 8 similar cases receiving crizotinib previously reported (4 in first line and 4 in second line), 1 had a partial response, 1 stable disease and 6 disease progression. One patient still had progression disease when switching to ceritinib. At the end, K-RAS mutations seem to represent a negative predictive marker in ALK-rearranged adenocarcinomas treated with ALK inhibitor. © 2016 Elsevier Ireland Ltd.

Discover hidden collaborations