<b>Conclusion:</b> Occurrence of muscle function deficit in childhood ALL is thus strongly modulated by variations in the <i>DUOX2, ADAMTS4</i> and <i>ALOX15</i> genes, which could lead to personalized prevention strategies in childhood ALL survivors.
<b>Results:</b> From a revision of 45 manuscripts, we found that miR-128 and miR-181 overexpression could represent markers for ALL diagnosis and underexpression of miR-708 and miR-99a could be markers for bad prognosis.
<i>ETV6/RUNX1</i> (+) ALL may be heterogeneous in terms of prognosis, and variables such as MRD at end ofremission induction or additional structural abnormalities of 12p could define a subset of patients who are likely to have poor outcome.
<i>CDKN2A/2B</i> deletions were associated with poor 2-year OS (P=0.045) and RFS (P=0.071) rates in Philadelphia chromosome positive (Ph<sup>+</sup>) B-ALL patients, as well as in the high risk (HR) B-ALL group (P=0.037 and P=0.047, respectively).
<i>In vivo</i>, KPT-8602 showed potent anti-leukemia activity in a mouse ALL model as well as in patient-derived T- and B-ALL xenograft models without affecting normal hematopoiesis.<b>Conclusions:</b> KPT-8602 is highly specific for XPO1 inhibition and demonstrates potent anti-leukemic activity supporting clinical application of the second-generation SINE compound for the treatment of ALL.<i></i>.
<i>Materials and methods</i> We compared DNA methylation of 1,505 selected promoter CpGs in chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL) with and without the Philadelphia chromosome t(9:22), CD34+ hematopoietic stem cells transfected with <i>BCR-ABL</i>, and other tumors without <i>BCR-ABL</i> (acute promyelocytic leukemia (APL) and gastrointestinal stromal tumors (GIST).
<i>TP53</i> alterations are present in almost all cases of ALL with low hypodiploidy and are associated with alterations of the lymphoid transcription factor <i>IKZF2</i> and the tumor-suppressor gene loci <i>CDKN2A</i> and <i>CDKN2B.</i> Remarkably, more than half of <i>TP53</i> mutations in low-hypodiploid ALL in children are present in nontumor cells, indicating that low-hypodiploid ALL is a manifestation of Li-Fraumeni syndrome.
11 out of 18 T-ALLs were T3 positive; alpha-chain gene rearrangements were demonstrated in only two of 18, indicating that the majority of T-ALLs would have rearrangements involving J alpha segments located upstream of these probes.
95% of Chronic Myelocytic (CML) and 15-25% of Acute Lymphoblastic Leukemia (ALL) patients are Ph1 producing a fusion transcript between the abl proto-oncogene and the bcr gene.
Acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) in infants have in common a high incidence of translocations of the MLL gene at chromosome band 11q23.
Acute lymphoblastic leukemia (ALL) in infants under 1 year is strongly associated with translocations involving 11q23 (MLL gene), CD10-negative B-lineage (proB) immunophenotype, and poor outcome.