Han Leng Ng

Current research

Across each generation, an offspring acquires ~30-90 de novo mutations (DNMs) in their genome. These mutations are absent in the somatic cells of the parents, but are present in the parents germ cells. It is now understood that the male germ cells contribute to ~80% of DNMs found in his offspring. The number of inherited DNMs increases linearly with the age of the father. However, a class of DNMs exists that does not follow this linear correlation, which is termed as 'selfish' mutations.

'Selfish' mutations provide mutant spermatogonial stem cells with a selective advantage over neighbouring healthy cells. Over time, there is an accumulation of mutant sperm, with an increased risk of transmission to their offspring, known as 'paternal age effect' disorders.

I am interested in using next-generation sequencing technology to identify novel rare 'selfish' mutations.

Background

I graduated from the University of Western Australia with a Bachelor of Sciences in molecular biology. Following which, I obtained a Bachelor of Science with Honours in genetics, before pursuing a PhD. I completed my PhD in 2019 with Professor Daniela Ulgiati, at the University of Western Australia, where I investigated the role of Notch signalling in regulating the expression of Complement Receptor 2 (CR2/CD21) during B-cell development. In 2020, I joined the lab of Dr Niklas Feldhahn at Imperial College London as a postdoctoral researcher. During my time there (2020-2023), I investigated the transcriptional landscape changes of BCR::ABL1+ B-cell acute lymphoblastic leukaemia. My research involved using several high-throughput techniques, including promoter-capture Hi-C, ChIP-seq and RNA-seq,