Research in the Cancer Bioinformatics group centres around the application of computational methods to two areas: alterations in the cancer genome and the tumour immune environment. By integrating different modalities of next generation sequencing, microarray and nanoString data, we aim to expand our knowledge of cancer biology and identify potential therapeutic targets and biomarkers for patient stratification.

In 2015, we have identified the meiotically expressed cancer/testis antigen (CT antigen) HORMAD1 as a driver of certain copy number aberrations in Triple Negative Breast Cancers. Our close link with the target & biomarker validation laboratory of Professor Andrew Tutt, a molecular oncologist and Director of Breast Cancer Now Centre and Research Unit, gives us the opportunity to study human primary tumour specimens, metastatic lesions and clinical trial data, as well as mouse and isogenic in vitro models. Our research provided insight into potential therapeutic avenues of patients with TNBC, of which nearly 60% are considered HORMAD1 positive.

In collaboration with Professors Tony Ng, Professor Sarah Pinder and Professor Ton Coolen, we found molecular signals in the pre-metastatic and metastatic lymph nodes of breast cancers that might facilitate tumour metastasis, and thereby inform novel therapeutic targets to control disease progression. We recently identified robust mechanism-based biomarkers of immunohistochemically assessed immune and stroma patterns, which dichotomise lymph node-positive breast cancers with short or long-term metastatic free survival. In parallel, we determined somatic mutations in DNA damage repair and immune-related genes in metastatic lymph nodes of breast cancers.

Together with Professor Arnie Purushotham, we are working on a sizable primary breast cancers cohort (n:1300) with extensive long-term clinico-pathological annotation to decipher risk factors of organotropic metastatic spread.

By collaborating with Dr Mieke van Hemelrijck, we have extracted genomic features indicative of upgrading in low Gleason-grade prostate cancers genomes on active surveillance.