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Background  Lung cancer with EGFR mutation was shown to be a specific clinical entity. In order to better understand the biology behind this disease we used a genome wide characterization of loss of heterozygosity and amplification by Single Nucleotide Polymorphism (SNP) Array analysis to point out chromosome segments linked to  EGFR  mutations. To do so, we compared genetic profiles between  EGFR  mutated adenocarcinomas (ADC) and  KRAS  mutated ADC from 24 women with localized lung cancer.    Results  Patterns of alterations were different between  EGFR  and  KRAS  mutated tumors and specific chromosomes alterations were linked to the  EGFR  mutated group. Indeed chromosome regions 14q21.3 (p = 0.027), 7p21.3-p21.2 (p = 0.032), 7p21.3 (p = 0.042) and 7p21.2-7p15.3 (p = 0.043) were found significantly amplified in EGFR mutated tumors. Within those regions 3 genes are of special interest  ITGB8 ,  HDAC9  and  TWIST1 . Moreover, homozygous deletions at  CDKN2A  and LOH at  RB1  were identified in  EGFR  mutated tumors. We therefore tested the existence of a link between EGFR mutation, CDKN2A homozygous deletion and cyclin amplification in a larger series of tumors. Indeed, in a series of non-small-cell lung carcinoma (n = 98) we showed that homozygous deletions at  CDKN2A  were linked to  EGFR  mutations and absence of smoking whereas cyclin amplifications ( CCNE1  and  CCND1 ) were associated to  TP53  mutations and smoking habit.    Conclusion  All together, our results show that genome wide patterns of alteration differ between  EGFR  and  KRAS  mutated lung ADC, describe two models of oncogenic cooperation involving either  EGFR  mutation and  CDKN2A  deletion or cyclin amplification and  TP53  inactivating mutations and identified new chromosome regions at 7p and 14q associated to EGFR mutations in lung cancer.

bmc medical genomics

Genome wide SNP comparative analysis between EGFR and KRAS mutated NSCLC and characterization of two models of oncogenic cooperation in non-small cell lung carcinoma