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Medical Science Monitor Basic Research


Evident clinical response to erlotinib as third-line treatment in EGFR FISH (+) male smoker patient with adenocarcinoma of lung

Pawel Krawczyk, Wojciech Remiszewski, Elżbieta Czekajska-Chehab, Beata Gryglicka, Edward Warda, Maciej Pelak, Kamila Wojas-Krawczyk, Olga Jankowska, Tomasz Mazurkiewicz, Janusz Milanowski

Am J Case Rep 2009; 10:166-171

ID: 878220

Available online:

Published: 2009-10-14


Background: Bronchoalveolar carcinoma (BAC) is a “minimally invasive” form of adenocarcinoma, which spreads along the intraalveolar septum and is poorly associated with cigarette smoking. The EGFR tyrosine kinase inhibitors (TKIs), e.g. erlotinib or gefi tinib, have proven effective in some patients with advanced non-small cell lung cancer previously treated and progressive on chemotherapy. Female, never-smokers or histology of adenocarcinoma or BAC are uncertain favourable factors for positive clinical outcome in EGFR TKIs therapy. However, increased EGFR gene copy number without EGFR protein expression has been shown in several studies to be a good predictive marker for this treatment.
Case Report: In the present paper, we reported a rare case of adenocarcinoma with BAC pattern evidently responding to erlotinib in the absence of EGFR protein expression on cancer cells. However, increased EGFR gene copy number in cancer cells was detected by fl uorescent in situ hybridisation (FISH). Unusually, for 8 months we have observed partial remission in smoking male patient with multiple distant metastases after the failure of fi rst- and second-line chemotherapy. The complete regression of multiple cancer micronodules in the lung and brain metastases, partial reduction of metastases in mediastinal lymph nodes and liver as well as stabilisation of bone metastases were noted.
Conclusions: Tyrosine kinase inhibitors may play an important role in BAC treatment especially with increased EGFR gene copy number in tumour cells, even in smokers and in the absence of EGFR protein expression.

Keywords: lung adenocarcinoma , erlotinib, clinical response