59PD - Association of EGFR mutation subtypes with clinical and demographic characteristics of patients (pts) with aNSCLC: IGNITE and ASSESS pooled analysis

Date 14 April 2016
Event European Lung Cancer Conference 2016 (ELCC) 2016
Session Targeting EGFR and ALK driven tumours
Topics Aetiology, Epidemiology, Screening and Prevention
Pathology/Molecular Biology
Non-Small Cell Lung Cancer
Basic Scientific Principles
Presenter Baohui Han
Citation Journal of Thoracic Oncology (2016) 11 (supplement 4): S57-S166. S1556-0864(16)X0004-4
Authors B. Han1, M. Ratcliffe2, V. Haddad3, H. Brown2, S. Tjulandin4, K. Hagiwara5, M. Reck6, N. Normanno7
  • 1Department Of Respiratory Medicine, Shanghai Chest Hospital, Jiao Tong University, 200030 - Shanghai/CN
  • 2Personalised Healthcare And Biomarkers, AstraZeneca, Macclesfield/GB
  • 3Biostatistics & Information Sciences, AstraZeneca, Royston/GB
  • 4Department Of Clinical Pharmacology And Chemotherapy, Russian Cancer Research Centre, Moscow/RU
  • 5Comprehensive Medicine 1, Jichi Medical University Saitama Medical Center, Saitama/JP
  • 6Department Of Thoracic Oncology, LungenClinic Grosshansdorf GmbH, Airway Research Center North (ARCN), Grosshansdorf/DE
  • 7Cell Biology And Biotherapy Unit, Istituto Nazionale Tumori “Fondazione Pascale”, IRCCS, Naples/IT



Increased presence of EGFR mutations (EGFRm) in aNSCLC is associated with clinical/demographic characteristics (Asian ethnicity, female gender, never-smokers, adenocarcinoma [ADC] histology). However, it is less clear whether m subtypes are distributed differently across clinical/demographic groups.


Using pooled data from IGNITE (NCT01788163) and ASSESS (NCT01785888), association between tumour m (present vs absent or common vs rare) or different subtypes vs Exon 19 deletions as reference and clinical characteristics (ethnicity [Caucasian vs Asian], age [≤65 vs 65+], smoking status [never- vs ever-smoker], gender [male vs female], histology [non-ADC vs ADC], current disease status [IV vs IIIA, IIIB], WHO performance score and number of organs with metastases) was analysed (multinomial logistic regression model using stepwise forward selection).


Combining pts from IGNITE and ASSESS diagnostic studies gave a dataset of 4399 aNSCLC pts successfully tested for EGFR, 1242 with EGFRm. In addition to previously identified associations, an association was seen between disease stage IV and presence of an EGFRm (odds ratio [OR; 95% CI]) stage IIIA vs IV = 0.56 [0.40–0.81], stage IIIB vs IV = 0.62 [0.47–0.81] (table). Rare m subtypes were relatively more common in smokers than never-smokers compared with L858R/Exon 19 deletions (OR = 2.6 [1.5–4.5], p = 0.0005). EGFRm subtype heterogeneity was observed for smoking status, age, ethnicity and histology (p 


The finding that pts with later stage disease are more likely to have EGFRm suggests selection of EGFRm-positive cells as disease progresses. 59PDT1 Table: IGNITE and ASSESS pooled data (N = 1242)

 Exon 19 del, n (%)L858R, n (%)G719X, n (%)Exon 20 ins, n (%)L861Q/P, n (%)
 N = 609N = 506N = 17N = 25N = 17
ADC/non ADC/othera565/38/4 [93/6/1]452/50/4 [89/10/1]13/4/0 [76/24/0]24/0/0 [100/0/0]14/3/0 [82/18/0]
Male/Female259/350 [43/57]225/281 [44/56]9/8 [53/47]14/11 [56/44]12/5 [71/29]
Caucasian/Asian/Other121/482/6 [20/79/1]55/449/2 [11/89/0]2/15/0 [12/88/0]4/21/0 [16/84/0]5/12/0 [29/71/0]
WHO PS 0/1/2/3/4b199/315/68/17/9 [33/52/11/3/1]146/264/66/23/7 [29/52/13/5/1]5/6/5/0/1 [29/35/29/0/6]6/16/2/1/0 [24/64/8/4/0]4/12/1/0/0 [24/71/6/0/0]
Never/ever smoker408/201 [67/33]346/160 [68/32]9/8 [53/47]12/13 [48/52]6/11 [35/65]
Disease stage IIIA–B/IV59/550 [10/90]59/447 [12/88]2/15 [12/88]1/24 [4/96]4/13 [24/76]
Number of organs with metastases 0/1/2/3/>456/273/164/72/44 [9/45/27/12/7]60/232/119/62/33 [12/46/24/12/7]2/8/0/5/2 [12/47/0/29/12]1/9/10/2/3 [4/36/40/8/12]4/6/2/4/1 [24/35/12/24/6]
a Histological subtype data missing for three IGNITE pts (two with Exon 19 del and one with Exon 20 ins).b WHO PS data missing for one IGNITE pt (Exon 19 del).

Clinical trial identification


Legal entity responsible for the study





B. Han: Member of the speakers' bureau for AstraZeneca and Roche and a Consultant for AstraZeneca and Pfizer. M. Ratcliffe, V. Haddad, H. Brown: Employee of AstraZeneca and holds shares in AstraZeneca. S. Tjulandin: Member of the speakers' bureau for AstraZeneca, Pfizer and Sanofi-Aventis. K. Hagiwara: Member of the speakers' bureau for AstraZeneca, Chugai Pharmaceuticals and Pfizer and holds a patent with LSI Medience. M. Reck: Member of speakers' bureau for AstraZeneca, BMS, Boehringer Ingelheim, Daiichi-Sankyo, Hoffmann-La Roche, Lilly and Pfizer; Consultant for AstraZeneca, BMS, Boehringer Ingelheim, Daiichi-Sankyo, Hoffmann-La Roche, Lilly, MSD and Pfizer. N. Normanno: Has received grants/research support from, and been a Consultant for, AstraZeneca, Qiagen and Roche Diagnostics.