Wei-Ting Lu

Originally from Taiwan, Wei-Ting spent most of his childhood in the Malaysian island of Borneo. He did his undergraduate and PhD studies at the University of Sheffield, focusing on genome instability. Wei-Ting then joined the group of Prof. Martin Bushell where he investigated how non-coding RNAs and DNA-RNA hybrids are regulated to maintain genome stability. In 2018, Wei-Ting joined the group of Prof. Charles Swanton at the Crick Institute, where he led the functional characterisation of cancer drivers identified in the TRACERx lung cancer cohort. In September 2025, he joined the Department of Oncology as a Group Leader, studying the molecular processes contributing to whole genome doubling and chromosomal instability.

Normally, we store our genetic information in 23 pairs of chromosomes. However, cancer cells seldom conform to this number. Rather, cancer cells undergo whole genome doubling to duplicate all their 23 pairs of chromosomes to 46 pairs in one fell swoop. Following this, mutations and chromosomal rearrangements occur repeatedly in cancer cells, resulting in a population of highly variable chromosomal numbers. These events correlate with worse clinical outcomes, drug resistance and cancer metastasis.

Using existing population genomic and clinical data, our lab aims to functionally characterise the events that contribute to whole genome doubling and chromosomal instability. We are interested in FAT protocadherins,  a class of proteins which are often mutated in lung, breast, skin and oesophageal cancers. By understanding the role played by the FAT proteins, we aim to find novel treatment strategies.