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P1.01 - Poster Session 1 - Cancer Biology (ID 143)
- Event: WCLC 2013
- Type: Poster Session
- Track: Biology
- Presentations: 1
- Coordinates: 10/28/2013, 09:30 - 16:30, Exhibit Hall, Ground Level
P1.01-019 - Study of aberrant copy number of genes in adenocarcinoma of lung in never-smokers with respect to EGFR mutations by multiplex ligation-dependent probe amplification (MLPA®) (ID 2546)
09:30 - 16:30 | Author(s): P.P.F. So
MLPA® is a robust method that detects aberrant copy numbers in one simple PCR reaction by using one primer-pair. The SALSA® MLPA® kits P171, P172-B1 and P173 (MRC-Holland, Amsterdam, Netherlands) containing 42, 42 and 43 probes respectively for genes that often have an increased copy number in one or more types of tumours were used.
Tumor samples from 42 lung adenocarcinoma of never-smokers were studied (17 with EGFR L858R mutation, 9 with EGFR exon 19 deletions, and 16 with wild type EGFR). Normal lung parenchyma from the same individual was used as internal control. The normalization with reference controls and data analysis was done according to the MLPA® protocol and Coffalyser developed at MRC-Holland.
Significant copy number gains in > 15% cases (incidence rates indicated in brackets) were reported here. For tumours with EGFR L858R mutation, significant gains were detected in EGFR (60%), RNF139 (50%), TERT (28%), NFKBIE (22%), UCKL1 (23%), MYC (18%), NTRK1 (17%), RUNX1 (17%) and SERPINB9 (17%). For tumours with EGFR exon 19 mutations, significant gains were detected in PSMB4 (50%), EGFR (45%), UCKL1 (23%), MYC (23%), MET (23%), CENPF (23%), CYP27B1 (23%), CDK4 (23%) and ERBB4 (23%). For tumours with wild-type EGFR, significant gains were detected in STK6 (25%), IRS2 (20%) and MYC (20%). Therefore, gains in MYC copy numbers were common in all 3 groups. Gains in EGFR and UCKL1 were common in the 2 groups with EGFR mutations. Gains in STK6 were common to L858R mutation and wild-type EGFR groups.
The 3 groups of adenocarcinoma in never-smokers with respect to the absence, presence and types of EGFR mutation showed quite different patterns of aberrant copy numbers in other cancer-associated genes. This in turn reflected the distinctively different patterns of genetic instability.