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Somatic mutations in arachidonic acid metabolism pathway genes enhance oral cancer post-treatment disease-free survival

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Listed:
  • Nidhan K. Biswas

    (National Institute of Biomedical Genomics, Netaji Subhas Sanatorium (2nd Floor))

  • Subrata Das

    (National Institute of Biomedical Genomics, Netaji Subhas Sanatorium (2nd Floor))

  • Arindam Maitra

    (National Institute of Biomedical Genomics, Netaji Subhas Sanatorium (2nd Floor))

  • Rajiv Sarin

    (Tata Memorial Centre, Advanced Centre for Treatment, Research and Education in Cancer)

  • Partha P. Majumder

    (National Institute of Biomedical Genomics, Netaji Subhas Sanatorium (2nd Floor))

Abstract

The arachidonic acid metabolism (AAM) pathway promotes tumour progression. Chemical inhibitors of AAM pathway prolong post-treatment survival of cancer patients. Here we test whether non-synonymous somatic mutations in genes of this pathway, acting as natural inhibitors, increase post-treatment survival. We identify loss-of-function somatic mutations in 15 (18%) of 84 treatment-naïve oral cancer patients by whole-exome sequencing, which we map to genes of AAM pathway. Patients (n=53) who survived ≥12 months after surgery without recurrence have significantly (P=0.007) higher proportion (26% versus 3%) of mutations than those who did not (n=31). Patients with mutations have a significantly (P=0.003) longer median disease-free survival (24 months) than those without (13 months). Compared with the presence of a mutation, absence of any mutation increases the hazard ratio for death (11.3) significantly (P=0.018). The inferences are strengthened when we pool our data with The Cancer Genome Atlas (TCGA) data. In patients with AAM pathway mutations, some downstream pathways, such as the PI3K–Akt pathway, are downregulated.

Suggested Citation

  • Nidhan K. Biswas & Subrata Das & Arindam Maitra & Rajiv Sarin & Partha P. Majumder, 2014. "Somatic mutations in arachidonic acid metabolism pathway genes enhance oral cancer post-treatment disease-free survival," Nature Communications, Nature, vol. 5(1), pages 1-9, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6835
    DOI: 10.1038/ncomms6835
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