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Dr Seong Lin Khaw
Dr Seong Lin Khaw is a clinician-scientist, with current appointments as Children's Cancer Foundation Clinical Research Fellow at the MCRI and Consultant Paediatric Oncologist at the Children's Cancer Centre, Royal Children's Hospital (RCH).
Dr Khaw undertook basic paediatric training at the RCH and Sydney Children's Hospital, before completing fellowship training in paediatric haematology/oncology at the RCH and Monash Medical Centre (MMC) in 2006. He has been a consultant paediatric oncologist since 2010, first at MMC (2010- 2012) and then RCH (2012-present). His clinical focus is on haematological malignancies and haematopoietic stem cell transplantation, as well as early phase clinical trials.
Dr Khaw has been an active translational researcher since 2007, first completing a PhD and then working as a postdoctoral researcher with Prof Andrew Roberts and Prof David Huang at the Walter and Eliza Hall Institute of Medical Research in the field of apoptosis, particularly the clinical translation of BH3-mimetic therapy in haematological malignancies. In 2017, he joined A/Prof Paul Ekert in the Cancer Research Group at MCRI to focus on developing platforms to improve therapy of childhood acute lymphoblastic leukaemia.
2015 Thomson Reuters Citation Award in Molecular Biology and Genetics
· One of 11 WEHI researchers whose research papers on cell death published in the past seven years have been the most frequently cited of any Australian researchers in molecular biology and genetics
2017 Kellaway Translation Award (WEHI)
· With Dr Mary Ann Anderson and Dr Kylie Mason
· For translational research undertaken at WEHI in the clinical development of BH3-mimetics in CLL and other blood cancers
Dr Khaw's research centres on improving the treatment of childhood acute lymphoblastic leukaemia (ALL). ALL is the most common childhood malignancy, and leading cause of cancer-related death in young people. Contemporary chemotherapeutic regimens confer an overall probability of cure approaching 90%. However, patients in the very-high-risk (VHR-ALL) subgroup, defined on the basis of clinical features, adverse molecular aberrations and/or poor treatment response, continue to have a markedly inferior outcome even with the most intensive current therapy, including hematopoietic stem cell transplantation.
In the last decade, significant advances in characterizing individual leukaemias, particularly with the increasing integration of genomic technologies into clinical care, have made possible in some patients a shift to more rational, biology-directed therapy. This is especially where there has been a clear understanding of the consequences of, and capacity to target the molecular aberrations identified. For example, some patients with Ph-like ALL, a recently identified disease subgroup characterized by clinical and biological features which overlap with Philadelphia-positive (Ph+) ALL, but who lack the signature t(9;22) or BCR-ABL1 fusion, have been found to have other chromosomal translocations which result in similarly aberrant activation of tyrosine kinases, which in some cases is amenable to treatment with specific small molecule inhibitors.
Conversely, in many patients with VHR-ALL where no actionable mutations are identified, there is a need for other approaches to improve treatment efficacy. For example, there is an increasing understanding of the mechanisms by which cancer cells can escape killing by standard chemotherapeutic drugs. These include perturbations in cell death pathways involving members of the BCL-2 protein family. These insights have led to the design of a new class of medications called BH3-mimetics, which can bypass many of these mechanisms of chemoresistance. Venetoclax, a BH3-mimetic which selectively blocks the BCL-2 protein, is now an established treatment for patients with an aggressive form of chronic lymphocytic leukaemia (CLL) including those where all standard therapies have failed. An ongoing focus of Dr Khaw's research is the clinical translation of BH3-mimetic drugs such as venetoclax in childhood ALL.
· Developing laboratory models to identify therapeutic vulnerabilities in very high risk ALL
· In collaboration with A/Prof Ekert, characterising the biology of novel leukaemic fusion genes
· Translational and clinical studies with BH3-mimetics in childhood leukaemias
· Children's Cancer Foundation Research Support Package 2017-2021
· Cancer Council of Victoria Postdoctoral Cancer Research Fellowship
· Leukaemia Foundation Clinical Fellowship
· Royal Melbourne Hospital Haematology and Bone Marrow Transplant Scholarship
· Cancer Trials Australia Specialist Certificate in Clinical Research (Oncology) Funded Place
· HOTT Fellowship Award (Roche, COSA, HSANZ)
· ANZCHOG-Amgen Australia Travel Grant for ANZCHOG Annual Scientific Meeting