Our people

Steve Stick

Graham Hall

Sarath Ranganathan

Anthony Kicic

 Helen Lester

(Consumer Representative)

Kate McDonald

(Consumer Representative)

 Mitch Messer

(Consumer Representative)

 Erika Sutanto

 Ingrid Laing

 Craig Schofield 

Samantha McLean 

Liz Starcevich

Kevin Looi

Jessica Hillas 

Luke Berry

Emma de Jong

Patricia Agudelo Romero

Alana Harper

Renée La Grange

Samantha Grogan

Sally McCappin

 
Nat Eiffler

 
Joseph Bartlett

 
Alexia Foti

Georgia Banton

Oded Breuer

 

Connor Murray

Rachel Foong

Steven Oo

Alya Ishak 

Barry Clements

Thomas Iosifidis

Nick de Klerk

Nicole Shaw 

Louise King

Suzanna Vidmar

Rosemary Carzino

Nadeene Clarke

Phil Robinson

Rebecca McElroy

Natalie Zajakovski

Katherine Frayman

Jo Harrison

John Massie

Julie Smith

Colin Robertson 

Peter Sly

Linda Shields 

Clara Mok (PhD)

Characterising low attenuation regions (LAR) on CT scans in children with cystic fibrosis

Repurpose and validate the use of a novel quantitative CT scoring technique (PRAGMA-CF) in MRI images. Using a mathematical model of the lung, assess how the extent and geographic distribution of CT LARs change over time and correlate these findings with clinical markers of disease. Determine the cause of CT LARs (ventilation, perfusion or combined defect) using functional MRI.

Email: Clara.mok@telethonkids.org.au  

Shivanthan Shanthikumar (PhD)

The aim of my research is to identify epigenetic markers from early life which predict the severity of lung disease at 9 years of age.  I will do this by comparing two groups, one with mild lung disease and one with severe lung disease at 9 years of age (based on CT scan results), and I will perform whole genome methylation analysis on broncho-alveolar lavage from early life with the aim of identifying differential methylation patterns between the two groups.

The study involves patients with CF - so the 2 groups of kids will be kids with CF from the AREST CF cohort.

Contact: Shivanthan.shanthikumar@rch.org.au 

Kelly Martinovich (PhD)

Personalized antisense oligonucleotide therapy to correct CFTR function in Cystic Fibrosis (CF) patients

In 2016 I enrolled in a PhD to test whether Antisense Oligonucleotide therapy is capable of rescuing CFTR function in specific Cystic Fibrosis patients

I aim to develop a new treatment that targets specific CF gene types. The message that the CF gene holds makes the CF transmembrane regulator (CFTR) protein. A faulty gene message results in the CFTR protein not be produced or able to work properly. A non-functioning protein allows mucous build up and infections to establish that are hard to treat. Over time, these infections and the inflammation that follow leads to permeant lung damage.

The treatments we are developing are small molecules called antisense oligonucleotides (AOs). AOs can change the message that is sent from the gene to protein. AOs are made to target the specific site in the CFTR gene where the faulty message is. In selected CF cases, AOs could improve disease symptoms.

I am currently working with Telethon Kids Institute, the University of Western Australia and the Centre for Comparative Genomics to perform my research.

Kak-Ming Ling (PhD) 

Growing evidence has linked respiratory virus infection in Cystic Fibrosis (CF) with lung function decline and pulmonary exacerbation. Currently, rhinovirus is the most prevalent virus detected, predominantly in children with CF less than 5 years old who suffer an exacerbation. Although these children are prone to repeat and prolonged infection, there is no effective targeted treatment. My project will elucidate the mechanisms of viral infection at the primary site of infection, namely the airway epithelium. The first phase of my study will identify dysregulation in innate immune pathways in CF airway epithelium in response to rhinovirus infection utilising RNA-sequencing technology in conjunction with our collaborators (Hancock Laboratory; University of British Columbia). The second phase will validate the proposed candidate pathways and determine their role in regulating innate immune responses during viral infection. The last phase will focus on screening databases of known drugs for desirable interactions with these identified pathways. The anticipated translation of this research is a new area of anti-viral intervention in young children with CF, prior to severe lung disease and irreversible structural damage. By limiting the harmful consequences of viral infection at this early stage, we aim to ultimately reduce viral associated morbidity in CF. 

Samuel Montgomery (PhD)

"The Role of Hypoxia and Necrosis in Sterile Neutrophilic Inflammation in Children with Cystic Fibrosis"

Samuel is a fourth-year PhD student who focuses on an important but poorly researched area in CF; early life inflammation in the absence of infection. Specifically, his research aims to investigate the IL-1R inflammatory pathway in CF and the mechanisms surrounding inflammation arising from cell death following airway hypoxia and viral infections.

Daniel Laucirica (PhD)

"Early life airway infections in children with Cystic Fibrosis"

My research focuses on early life airway infections in children with Cystic Fibrosis (CF). The goal of my project is to assess innate immune responses of the CF airway epithelium to infection by a variety of CF associated pathogens, and connect these responses to functional changes in airway neutrophil activity observed in vivo. One of my key interests is modeling pathogenic interactions in CF airways that may enhance microbial dissemination, predisposition to further infection, and exacerbate epithelial immune responses. In addition to contributing new knowledge on early life airway infections in CF, results may also inform new strategies for the management or prevention of airway inflammation in CF lung disease.

Peter Van Mourik (PhD)

Generating 3D organoid as a cell model for drug discovery and therapy in cystic fibrosis

Intestinal organoids can be used to study the function of the CFTR-protein in patients with Cystic Fibrosis, and to predict whether someone will respond to CFTR-modulating drugs. We aim to study the effect of drugs in intestinal organoids of persons with rare CFTR-mutations to identify persons that might benefit from treatment.