Author of

• 25520

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  Poster Display session (Friday) (ID 65)

  • Event: ELCC 2018
  • Type: Poster Display session
  • Track:
  • Presentations: 1
  • Moderators:
  • Coordinates: 4/13/2018, 12:30 - 13:00, Hall 1

  • 25286

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    62P - MAP kinase signaling pathway in pulmonary adenocarcinomas: A study from India (ID 553)

    12:30 - 13:00  |  Presenting Author(s): V. Singh
    • 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.