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D. Jain
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Poster Display session (Friday) (ID 65)
- Event: ELCC 2018
- Type: Poster Display session
- Track:
- Presentations: 2
- Now Available
- Moderators:
- Coordinates: 4/13/2018, 12:30 - 13:00, Hall 1
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54P - Epidermal growth factor receptor expression (EGFR) in serum as a marker of treatment response and survival in advanced squamous cell lung cancer (Now Available) (ID 353)
12:30 - 12:30 | Author(s): D. Jain
- Abstract
Background:
Reliable biomarkers are needed to prognostigate patients with advanced lung cancer following chemotherapy. This study evaluated the association of serum EGFR expression with disease severity and treatment response in advanced Squamous cell lung cancer.
Methods:
Newly diagnosed subjects with advanced Squamous cell lung cancer (stage IIIB and IV) were enrolled. Relevant demographic data were recorded, including performance status (assessed by Karnofsky performance status [KPS] and European Co-operative Oncology Group [ECOG] scoring system). Epidermal growth growth factor receptor (EGFR) expression was estimated in serum using reverse transcriptase polymerase chain reaction (RT-PCR) at baseline and following four cycles of Carboplatin – Paclitaxel chemotherapy. Response was assessed using the RECIST 1.1 criteria. Objective response rate (ORR) was defined as Complete remission (CR) or partial response (PR) and Disease control rate (DCR) was defined as CR/PR/Stable disease (SD). Kaplan meier curve was used to compare the overall survival (OS) between subjects based on median EGFR expression level as the cut-off.
Results:
A total of 82 subjects were enrolled. These included 79 (96.3%) males with mean (SD) age of 61.9 (9.8) years and 48.8% having metastatic disease. Majority were current / former smokers (97.6%); 59.7% had KPS ranging between 40 -70 and 48.1% had ECOG of 0/II. The baseline mean (± SD) serum EGFR expression was 17.8 ± 9.3 fold increase over control values, with median (min., max.) of 18.2 (4.4, 42.8). Following chemotherapy, ORR and DCR were 59.7% and 77.3% respectively. Significant reduction in EGFR expression was observed with median (min, max.) absolute and percentage reduction of 6.2 fold (−3.1, 33.6), and 54.2 % (−55.6, 78.4) respectively; p < 0.001. No significant association was observed between change in EGFR expression and age, gender, disease stage, performance status, ORR or DCR. Subjects with baseline EGFR expression of greater than 16.0 fold had significantly worse OS than those with <16.0 fold increase.
Conclusions:
EGFR is over-expressed in advanced squamous cell lung cancer and is significantly down-regulated following chemotherapy; additionally, baseline expression is a useful marker of overall survival following chemotherapy.
Clinical trial identification:
Legal entity responsible for the study:
N/A
Funding:
Department of Biotechnology, India
Disclosure:
All authors have declared no conflicts of interest.
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62P - MAP kinase signaling pathway in pulmonary adenocarcinomas: A study from India (ID 553)
12:30 - 12:30 | Author(s): D. Jain
- Abstract
Background:
Tyrosine kinase inhibitors (TKIs) are effective in EGFR and ALK driven non-small cell lung cancer (NSCLC). However, drug insensitivity, tumor recurrence, and resistance caused by second mutations in the EGFR or aberrant bypass signaling are key challenges. To overcome this, the focus has been shifted to genomic analysis of various EGFRdownstream signaling pathways. One of the vital EGFR downstream signaling pathways that perhaps provide roadmaps for targeted therapy is MAP kinase pathway. We aim to study key genes of MAP kinase pathway in patients with pulmonary adenocarcinomas (PADC).
Methods:
All PADC patients since 2015 were included after obtaining clinical details. Histomorphology was ascertained prior to mutational analysis. Real-Time PCR (EGFRexon 18–21 and KRASexon 2) and Sanger Sequencing (BRAFexon 11 and 15 and MEK1exon 2) technologies were used. The clinical and pathologic correlation was done.
Results:
Of 118 PADC patients (M: F-2.3:1), 26.2% (31/118) patients harboured EGFR mutations and were predominantly females. The most common EGFR mutation was exon 19 deletion. EGFR mutation positive cases showed mostly acinar histology. KRAS mutations (G12A) were observed in 21.1% (25/118) patients and were predominantly older males with mucinous histology. Four (3.3%) patients harboured coexisting EGFR and KRAS mutations. BRAF mutations (L597V, I953V) were seen in 2.5% (3/118) patients, however, there was no coexistence of BRAF mutations with other oncogenic drivers such as KRAS, EGFR mutations or ALK fusion. Additionally, BRAFpolymorphism was seen in 15.0% cases. None of the cases showed MEK1 mutation.
Conclusions:
This study examined the genetic alterations of genes involved in MAP kinase pathway in PADC of Indian patients. The frequency of KRAS mutation is higher than reported previously in the literature. Secondly, mutations in EGFR and KRAS showed coexistence. The high rate of KRAS mutations and coexistence of genomic alterations in Indian patients should be validated in a large number of cases for better patient management.
Clinical trial identification:
Legal entity responsible for the study:
AIIMS, New Delhi, India
Funding:
ICMR, Lady Tata Trust, and AIIMS
Disclosure:
All authors have declared no conflicts of interest.
