Search
It is now known that the HOX11 gene is permanently activated in the leukaemia cells and it drives the disease.
A cutting edge cancer imaging facility will help specialist children's cancer researchers at Perth's Telethon Institute for Child Health Research.
Avantogen Limited (ACU:ASX) today announced that cancer researchers at Perth's The Kids for Child Health Research (TICHR) and Avantogen Limited
A national study is investigating diet, chemical exposure and genetic factors in a new bid to unravel the causes of childhood leukaemia.
West Australian families are being asked to play a vital role in a major new national study to unravel the causes of childhood leukaemia.
The WA Kids Cancer Centre has a suite of world-leading research projects to unlock new treatments for childhood cancers.
Leukaemia, also spelled leukemia, is a cancer that develops in the bone marrow and results in abnormal white blood cells. It is the most common cancer in children, accounting for almost a third of all childhood & teen cancers.
CD8+ T cells are an important weapon in the therapeutic armamentarium against cancer. While CD8+CD103+ T cells with a tissue-resident memory T (TRM) cell phenotype are associated with favorable prognoses, the tumor microenvironment also contains dysfunctional exhausted T (TEX) cells that exhibit a variety of TRM-like features.
Acute lymphoblastic leukaemia (ALL) is the most common paediatric malignancy and remains one of the most common causes of cancer-related death in children and adolescents. It is characterised by the proliferation of immature lymphoid cells capable of infiltrating bone marrow, blood and extramedullary sites. Five-year overall survival rates exceed 90% with current multidrug chemotherapeutic regimens. This manuscript reviews the abdominal imaging features of leukaemic infiltration in children with ALL at the time of initial diagnosis and following relapse.
Chemotherapy often kills a large fraction of cancer cells but leaves behind a small population of drug-tolerant persister cells. These persister cells survive drug treatments through reversible, non-genetic mechanisms and cause tumour recurrence upon cessation of therapy. Here, we report a drug tolerance mechanism regulated by the germ-cell-specific H3K4 methyltransferase PRDM9.