In recent years numerous studies have been focused on the genomic analysis of acute leukemias with the purpose to improve the biology of these diseases and to identify key alterations relevant for diagnosis, risk stratification, prognosis and relapse.These studies revolutionized our understanding of leukemia, leading to the definition of novel leukemia subgroups harboring genomic aberrations with a peculiar age-related distribution and a prognostic significance.
Noteworthy, some of these researches revealed the sequential order the genetic mutations occur and the clonal contribution of these mutations to leukemia predisposition, onset and relapse. For both lymphoid and myeloid malignancies, there are key mutations that contribute to a pre-leukemic background, and further subclonal lesions and/or epigenetic events that lead to full leukemic transformation. Importantly, several mutations can occur before birth and increase the susceptibility to leukemias. In addition, inherited genetic variation affects both leukemia predisposition and drug responsiveness. Besides leukemia onset, the sequential acquisition of genetic and epigenetic alterations might affect leukemia prognosis. Indeed, multiple subclones exist in parallel, and the clonal expansion of those cells which survive during treatment contributes to leukemia transformation and relapse.
With this Research Topic, we aim to provide an extensive overview of the recently identified acute leukemia predisposing conditions along with the potential consequences for diagnosis and treatment of preleukemic clones.
We welcome Original Research, Review and Mini-review articles related to, but not limited to the following topics:
- the longitudinal genomic characterization of both myeloid and lymphoid neoplasms.
- the clonal genetic and epigenetic heterogeneity of acute leukemias including single-cell studies.
- the epistatic interactions between alterations promoting acute leukemia onset and those responsible for relapse.
- the role of inherited genetic variation in predisposition to acute leukemias.
In recent years numerous studies have been focused on the genomic analysis of acute leukemias with the purpose to improve the biology of these diseases and to identify key alterations relevant for diagnosis, risk stratification, prognosis and relapse.These studies revolutionized our understanding of leukemia, leading to the definition of novel leukemia subgroups harboring genomic aberrations with a peculiar age-related distribution and a prognostic significance.
Noteworthy, some of these researches revealed the sequential order the genetic mutations occur and the clonal contribution of these mutations to leukemia predisposition, onset and relapse. For both lymphoid and myeloid malignancies, there are key mutations that contribute to a pre-leukemic background, and further subclonal lesions and/or epigenetic events that lead to full leukemic transformation. Importantly, several mutations can occur before birth and increase the susceptibility to leukemias. In addition, inherited genetic variation affects both leukemia predisposition and drug responsiveness. Besides leukemia onset, the sequential acquisition of genetic and epigenetic alterations might affect leukemia prognosis. Indeed, multiple subclones exist in parallel, and the clonal expansion of those cells which survive during treatment contributes to leukemia transformation and relapse.
With this Research Topic, we aim to provide an extensive overview of the recently identified acute leukemia predisposing conditions along with the potential consequences for diagnosis and treatment of preleukemic clones.
We welcome Original Research, Review and Mini-review articles related to, but not limited to the following topics:
- the longitudinal genomic characterization of both myeloid and lymphoid neoplasms.
- the clonal genetic and epigenetic heterogeneity of acute leukemias including single-cell studies.
- the epistatic interactions between alterations promoting acute leukemia onset and those responsible for relapse.
- the role of inherited genetic variation in predisposition to acute leukemias.