Annual Meeting Proceedings Part 1 - American Society of Clinical ...

7545 General Poster Session (Board #45C), Sat, 1:15 PM-5:15 PM
FGFR1 amplification and EGFR mutation in Chinese squamous cell lung
cancer. Presenting Author: Zhigang Wei, Department of Thoracic Medical
Oncology, Department of Thoracic Surgery, Peking University School of
Oncology, Beijing Cancer Hospital and Institute, Beijing, China
Background: Squamous cell lung cancer (SCC) lacks for effective targeted
therapies. FGFR1 amplification has emerged as a potential biomarker. This
study aimed to explore clinicopathologic characteristics of FGFR1 amplification
in Chinese SCC patients and further explore the correlation between
FGFR1 amplification and EGFR mutations. Methods: One hundred seventyseven
SCC patients were included in this retrospective study. Gene copy
number of FGFR1 and EGFR mutations were detected by fluorescence in
situ hybridization (FISH) and denaturing high-performance liquid chromatography
(DHPLC), respectively. Results: FGFR1 amplifications were detected
in 24.9% (44/177) Chinese SCC patients. FGFR1 amplification in
SCC was more common in male (28.0%, 40/143) and smokers (28.7%,
39/136) than female (11.8%, 4/34, p�0.049) and nonsmokers (12.2%,
5/41, p�0.032). FGFR1 amplification and EGFR mutations were mutually
exclusive (p�0.006), fourty-one of 139(29.4%) patients with wild-type
EGFR had FGFR1 amplification, while 3 of 38 (7.9%) patients with EGFR
mutation had FGFR1 amplification. Conclusions: FGFR1 amplification was
common in Chinese squamous cell lung cancer, and mutually exclusive
with EGFR mutations.
7547 General Poster Session (Board #45E), Sat, 1:15 PM-5:15 PM
Delay of chemotherapy through use of post-progression erlotinib in patients
with EGFR-mutant lung cancer. Presenting Author: Geoffrey R. Oxnard,
Dana-Farber Cancer Institute, Boston, MA
Background: 1st-line tyrosine kinase inhibitor (TKI) therapy for patients
(pts) with EGFR-mutant lung cancer prolongs progression free survival
(PFS) and improves quality of life. When pts develop acquired resistance to
TKI, chemotherapy is the only approved systemic treatment. Anecdotal
evidence suggests that change of therapy can be delayed in some pts
through continued TKI beyond progression (PD), but the effectiveness of
this approach has not been quantified. Methods: Through an IRB-approved
mechanism, pts with advanced lung cancer and EGFR sensitizing mutations
treated on 3 prospective trials of 1st-line erlotinib were identified.
Only pts with RECIST PD while on erlotinib were studied. Time from PD
until use of an alternate systemic therapy (or death) and characteristics at
PD (development of new extra-thoracic metastases or cancer-related
symptoms) were assessed. Results: 42 eligible pts were identified with the
following characteristics: median age 70, 86% female, 93% non-Asian,
50% never-smokers, 83% adenocarcinoma, 100% EGFR-mutant (55%
exon 19, 36% exon 21, 9% exon 18). Median PFS on erlotinib was 13
months. After PD, alternate systemic therapy was delayed �3 months in 19
pts (45%; 95%CI: 31%-60%), through a combination of post-PD erlotinib
(16 pts), radiation (6 pts), and/or surgery (3 pts), or on observation alone (2
pts). These 19 pts commonly had exon 19 deletions and were more likely to
have no cancer-related symptoms at PD (Table), and had a median post-PD
survival of 29 months. Alternate systemic therapy was delayed �12
months in 8 pts (19%). Conclusions: In a subset of pts with EGFR-mutant
lung cancer and acquired resistance to TKI, chemotherapy can be delayed
with the aid of post-PD TKI and local treatment modalities. This indolent
PD is likely due to ongoing tumor EGFR dependence. In pts who are
tolerating TKI and have asymptomatic progression, we recommend this
palliative treatment strategy as an option for delaying chemotherapy and
maximizing quality of life.
Delay of alternate systemic therapy
>3m
(n�19)