Acute leukemia is the most common cancer in children, although it can occur at any age. Outcomes are generally more favorable in children than in adolescents or adults.
​
Acute leukemias progress rapidly and therefore require prompt treatment upon diagnosis. These aggressive blood cancers may present with symptoms such as fatigue, weakness, pale skin, easy bruising or bleeding, fever, weight loss, and bone or joint pain.
​
Although treatments have improved greatly, we still do not fully understand how acute leukemia develops, especially across different types of the disease. These gaps in knowledge make it harder to develop new and more targeted treatments.
Types of acute leukemia
ACUTE LYMPHOBLASTIC LEUKEMIA (ALL)
Most common in children, characterized by overproduction of dysfunctional lymphocytes (lymphoblasts or leukemic blasts). Different types, with the most common:​
-
B-cell ALL (B-ALL) – blasts displaying surface markers associated with B lineage;
-
T-cell ALL (T-ALL) – blasts characterized by T-cell development markers.
ACUTE
MYELOID LEUKEMIA (AML)
Mostly associated with old age, characterized by an overproduction of immature and dysfunctional myeloid cells (myeloblasts or leukemic blasts).
Name given to a group of acute leukemias associated with different types of myeloid cells (red blood cells, platelets, white blood cells excluding lymphocytes).
ACUTE LEUKEMIA OF AMBIGUOUS LINEAGE (ALAL)
Rare subset (<5%) associated with a markedly adverse clinical outcome.
Encompasses leukemias which fail to show commitment to myeloid, B-, or T-lymphoid lineages (ie, acute undifferentiated leukemia - AUL), or display surface markers from more than one lineage (ie, mixed-phenotype acute leukemias - MPAL).
Origin of relapse in acute leukemia
In acute leukemia, we refer to cell populations capable of propagating the disease and giving rise to relapse as leukemia stem cells (LSCs). Given their inherent capacity of tumor regeneration, LSCs are responsible for driving disease progression and relapse.
​
​
Furthermore, we have experimentally demonstrated that numerous signals from the microenvironment support LSCs, thereby actively promoting leukemia progression and relapse.
​
Despite these recent discoveries, the mechanisms of therapy-resistance in acute leukemia remain poorly defined, particularly in T-ALL.
OUR RESEARCH PROGRAM
Using bulk and single cell multi-omic (e.g., transcriptomic, genomic, proteomic) approaches, whilst taking advantage of in vivo tools that enable to study LSCs at any stage during leukemia development, our research team aims to understand how LSCs escape immune surveillance and current therapies, and how tumor cells interact with their microenvironment to drive relapse in acute leukemia.
​
We have successfully established a translational pipeline that incorporates cell-marking strategies and patient-derived xenograft (PDX) models of acute leukemia for pre-clinical testing of novel antileukemic therapies.
Using this translational pipeline, our ultimate goal is to develop new therapeutic strategies to eradicate relapse-inducing cells, and identify biomarkers for predicting therapy response or relapse in T-ALL and other subtypes of acute leukemia.
Support & funding
