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Poster display session

4139 - Mutational status and metastatic patteRn in a cohort Of ADvanced colorectal cancer (aCRC) patients (pts): the ROAD study.

Date

09 Sep 2017

Session

Poster display session

Topics

Colon and Rectal Cancer

Presenters

Elena Ongaro

Citation

Annals of Oncology (2017) 28 (suppl_5): v158-v208. 10.1093/annonc/mdx393

Authors

E. Ongaro1, G. De Maglio2, L. Gerratana1, M. Bonotto1, S.K. Garattini1, D. Basile1, M. Cattaneo1, V.J. Andreotti1, F. Cortiula1, A. Parnofiello1, V. Fanotto1, S. Pizzolitto2, G.G. Cardellino1, M. Casagrande1, F. Puglisi1, G. Aprile3, N. Pella1, G. Fasola1

Author affiliations

  • 1 Department Of Oncology, University and General Hospital of Udine, 33100 - Udine/IT
  • 2 Department Of Pathology, University and General Hospital of Udine, 33100 - Udine/IT
  • 3 Department Of Oncology, San Bortolo General Hospital, 36100 - Vicenza/IT
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Resources

Abstract 4139

Background

Somatic mutation status in aCRC is becoming increasingly relevant as it may predict efficacy of biological therapies but also site-specific patterns of metastatic spread and outcome.

Methods

We retrospectively analysed a cohort of 640 consecutive aCRC pts diagnosed at University Hospital of Udine, Italy, from 1st January 2000 to 15th March 2017. KRAS, NRAS, BRAF and PIK3CA status was all locally determined by pyrosequencing and/or mass-Spectrometry Assay, with commercially available kits (diatech pharmacogenetics). Pearson’s Χ2 test was performed with uni- and multivariate models to test association of mutational status and site-specific metastatic spread at the time of diagnosis, death or last follow-up.

Results

Overall, we detected 283 (47%) KRAS mutations, 21 (4%) NRAS mutations, 40 (7%) BRAF mutations, and 61 (14%) PIK3CA mutations. Most common mutations in KRAS gene were located in exon 2 (86%), while about 3% of mutations involved exon 3 and 5% exon 4. NRAS mutations involved equally exons 2 and 3. All BRAF mutated tumours except for one, exhibited exon 15 V600E mutations. Pts with KRAS mutations had an increased risk to develop lung metastases (odds ratio, OR 2.56, 95% CI 1.76-3.71; p 

Conclusions

Our findings suggest that molecular biology may help predicting the metastatic spread in aCRC pts. If confirmed by further studies, these observations could translate into tailored surveillance and follow-up protocols.

Clinical trial identification

Legal entity responsible for the study

University and General Hospital of Udine, Italy

Funding

None

Disclosure

All authors have declared no conflicts of interest.

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