Showing posts with label Jody Haigh. Show all posts
Showing posts with label Jody Haigh. Show all posts

2 Mar 2017

Finding boosts target hopes for aggressive blood cancers

2016 Mammalian Functional Genetics Laboratory group
L- R: Dr Katharina Haigh, Mr John Drummond, Mr Mina Takawy,

Dr Catherine Carmichael, Assoc Prof Jody Haigh, Dr Maggie Costa,
Absent: Dr Thao Nguyen
by Anne Crawford 

In September last year this blog reported on some promising findings into ZEB2, a protein implicated in certain aggressive leukaemias, made by Australian Centre for Blood Diseases (ACBD) researcher, Associate Professor Jody Haigh as part of an international collaboration.

Associate Professor Haigh’s work has since been bolstered by the revelation of a novel partner of ZEB2. Combined, they may form a possible therapeutic target that could potentially have greater efficacy than targeting ZEB2 alone.

9 Sept 2016

Suspect exposed in aggressive blood cancers

Jody Haigh's group. L-R: Dr Katharina Haigh, Mr John Drummond,
Mr Mina Takawy, Dr Catherine Carmichael, A/Prof Jody Haigh,
Dr Maggie Costa. See more about the lab & its research.
by Anne Crawford

Monash researchers are progressing work into genes which they have revealed initiate aggressive forms of leukaemia. They hope that the genetic tools they have developed for their investigations will be used to identify novel compounds for the treatment of cancers including Early T-cell precursor leukaemia (ETP-ALL) and other related blood diseases.

19 Nov 2015

CCS successes in 2015 NHMRC funding

4 Sept 2015

Publication: Novel biological insights in T-cell acute lymphoblastic leukemia


Figure 2. Molecular mechanisms for IL7R/JAK/STAT
activation in T-cell acute lymphoblastic leukemia (T-ALL).
Review article on T-cell acute lymphoblastic leukemia (T-ALL), an aggressive type of blood cancer that accounts for about 15% of pediatric and 25% of adult acute lymphoblastic leukemia (ALL) cases. It is considered as a paradigm for the multistep nature of cancer initiation and progression. T-ALL originates from T-cell precursors at different stages of their development and is characterized by distinct and well characterized molecular genetic subtypes. Children affected by this disease respond fairly well to high-dose chemotherapy regimens. Unfortunately, the clinical response in adults remains problematic, and therapeutic options for relapsed T-ALL patients remain scarce.

13 Feb 2015

Driver discovered in aggressive form of T-cell acute lymphoblastic leukaemia

Zinc finger E-box binding homeobox 2 protein
Source: Wikipedia ZEB2
The disease Early Thymic Progenitor-cell acute lymphoblastic leukaemia (ETP-ALL) is aggressive, has poor survival rates and doesn't respond well to therapies currently available. Its exact causes have to date not been well understood.

A research group at Monash's Australian Centre for Blood Diseases (ACBD) has identified that increased expression in one transcription factor acts as a driver in the development of ETP-ALL. Dr. Steven Goossens and Associate Professor Jody J. Haigh, who is the leader of the Mammalian Functional Genetics group in the ACBD, have been working on the Zinc finger E-box-binding homeobox 2 (ZEB2) protein.

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