Correction: Guarnera et al. KMT2A Rearrangements in Leukemias: Molecular Aspects and Therapeutic Perspectives. Int. J. Mol. Sci. 2024, 25, 9023

There was an error in the original publication [1]. The oncogenic rearrangements in infant ALL are always somatic, not constitutive or inherited. As correctly indicated in the publication, there is a dramatic incidence of KMT2A rearrangements during infanthood, constituting the driver genetic alteration in 80% of acute leukemias during this period. KMT2A-rearranged ALL normally has a poor prognosis. In this manuscript, the term “germline KMT2A rearrangement” is incorrect and needs clarification. Instead, it was intended to specify that 20% of the infants with ALL which were not KMT2A-rearranged, also known as KMT2A-germline since the gene remained in its unaltered (germline) configuration, were found to carry rearrangements in other oncogenes. Similarly, the term “germline KMT2A::NUTM1” is not correct. Instead, in the KMT2A-germline cases, genetic analysis showed an enrichment in the NUTM1 and PAX5 rearrangements, which were fused to partners not including KMT2A. Genetic correlation studies revealed that NUTM1 rearrangements have a favorable prognosis (PFS of 75–95%), while PAX5 and other gene rearrangements have a high risk of relapse.

A correction has been made to “Chapter 3.1. Incidence, Clinical Features, and Prognosis in Infancy and Childhood”, first paragraph, as follows:

There is a dramatic incidence of KMT2A rearrangements in infants, constituting the driver genetic alteration in 80% of the acute leukemias during this period. Most of them are B-ALL (80–90%), followed by T-ALL, AML (up to 5–10% each), and other disease subtypes (<5%) [21]. Molecularly, the most frequent fusion partners of KMT2A are AFF1, MLLT1, and MLLT3 [1]. Infant-onset B-ALL with KMT2A rearrangement normally exerts a very immature phenotype (pro-B), with the frequent aberrant co-expression of myeloid markers. Patients normally present with hyperleukocytosis and extramedullary disease with central nervous system involvement and have a poor prognosis [22]. The other 20% of infant ALL cases that were not KMT2A-rearranged, also known as KMT2A-germline since the gene remained in its unaltered (germline) configuration, were found to carry somatic rearrangements in other oncogenes. Genetic analysis showed an enrichment in the NUTM1 and PAX5 rearrangements. Clinically, KMT2A-germline cases are normally B-ALLs with a more mature immunophenotype. Genetic correlation studies have revealed that NUTM1 rearrangements have an unusual favorable prognosis as compared to the rest of the infant ALL (PFS of 75–95%), while PAX5 and other gene rearrangements have a high risk of relapse [23–26].

The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.