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Poster display session

88P - The Sidra LUMC advanced colon cancer NGS cohort


23 Nov 2019


Poster display session


Tumour Site

Colon and Rectal Cancer


Wouter Hendrickx


Annals of Oncology (2019) 30 (suppl_9): ix30-ix41. 10.1093/annonc/mdz421


W.R.L. Hendrickx1, J. Roelands2, P. Kuppen3, F. Marincola4, D. Bedognetti5

Author affiliations

  • 1 Immunology Inflammation And Metabolism, Sidra Medicine, 26999 - Al-Rayyan/QA
  • 2 Immunology Inflammation And Metabolism, Sidra Medicine, 26999 - Doha/QA
  • 3 Department Of Surgery, Leiden University Medical Center, 2300RC - Leiden/NL
  • 4 Rnd, Refuge Biotechnologies, 94059 - Redwood City/US
  • 5 Immunology Inflammation And Metabolism, Sidra Medicine, 26999 - Doah/QA


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Abstract 88P


It is now clear that the immune system has a substantial effect on the progression of colon cancer. Typically, an immune response defined by a polarized Th1 phenotype, characterized by expression of CXCR3/CCR5 chemokine-receptor ligands, activation of interferon stimulated genes and production of cytotoxic molecules by effector immune cells, has been associated with immune-mediated tumor rejection. We have previously introduced a gene signature, called Immunology Constant of Rejection (ICR), that reflects these immune components. This signature was able to differentiate quite well the patients with an active immune environment and improved survival vs those who did not display this phenotype. This phenomenon although expected based on other immune infiltration studies could not be observed in the TCGA colon cancer cohort, likely due to the per protocol exclusion of samples with low purity. To gain more insight in the underlying mechanism of cancer tissue rejection by the immune system, we build an extensive data repository from high quality colon cancer samples unbiased for tumor purity.


RNA and DNA were isolated from fresh frozen tissue samples of a cohort of 366 colon cancer patients collected over the last decade at the University of Leiden, Netherlands. Tissue sections flanking the corresponding samples were hematoxylin and eosin stained. RNA-seq (HiSeq4000) data was obtained using HISAT2 alignment and quantile normalization of the GC corrected raw counts. Whole Exome Sequencing (>100X) for our cohort for normal and cancer tissue respectively. T-cell repertoire profiling of 150 tumors was achieved using Adaptive immunoSEQ. Tumor immune phenotype classification was done using unsupervised consensus clustering based on the expression of ICR genes.


Our preliminary data supports a positive impact of ICR gene expression in our colon cancer cohort: patients in ICR High cluster had a significantly improved survival compared to other clusters.


This newly generated immune centric NGS dataset, generated in Qatar, will is used to elucidate the genetic determinants of immune phenotype in colon cancer and the relationship of the immune phenotype, the tumors genetics the TCR diversity.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

Sidra Medicine.


Qatar National Research Fund.


All authors have declared no conflicts of interest.

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