Chromosomal microarray analysis (CMA) detects copy-number alterations and copy-neutral loss of heterozygosity (cnLOH), but the CMA landscape of adult T-ALL has been described in few cohorts. Day +70 measurable residual disease (MRD) is a surrogate marker of early treatment response, available only after induction. Thirty-nine adults with Ph-negative T-ALL on a single protocol underwent diagnostic CMA. Mosaic events were catalogued per chromosome and against a 57-gene panel and described in relation to day +70 MRD status (13 MRD-positive, 25 MRD-negative). The analysis is presented as descriptive without formal inference. Mosaic alterations were present in almost all patients, so groups differed in the amount rather than the presence of genomic change. Complex profiles (≥3 affected chromosomes) were seen in 46.2% of MRD-positive and 20.0% of MRD-negative patients. Biallelic 9p21.3 deletion occurred in both groups, whereas 9p cnLOH without deletion occurred predominantly in MRD-negative patients. Total cnLOH burden did not track with copy-number burden. Copy-number and copy-neutral events are mechanistically distinct and were not interchangeable here: 9p deletion and 9p cnLOH are separable by SNP array and should be reported separately rather than pooled. No association reached significance, although the cohort was too small to detect all but very large effects.

Background/Objectives: Acute leukemia (AL) alters both hematopoiesis and the bone marrow stromal microenvironment. Attempts to develop a culture of multipotent mesenchymal stromal cells (MSCs) from AL patients’ bone marrow are not always successful, as opposed to healthy donors’ bone marrow. Methods: To unveil the reason, healthy donors’ MSCs were cultured in the presence of sera from healthy donors (control group) or AL patients at the onset of the disease, in short- and long-term remission, and before and after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Results: The cell yield in the presence of patient sera was lower than in the control, regardless of the AL stage. It was assumed that the patients either lacked growth factors to sustain MSCs, or there were inhibitors of MSC growth present. The serum’s ability to support MSC growth correlated with platelet count and albumin and calcium concentrations in patients’ blood. Platelet-derived growth factors—PDGFA and PDGFB—are known to induce MSC growth. Their concentration in the serum of AL patients and healthy donors was analyzed. A decrease in PDGFA concentration was found in the sera of patients compared to healthy donors. PDGFB concentration was lower at disease onset, increased during remission and decreased again during relapse. PDGFB concentration correlated with platelet count, while PDGFA concentration did not. AL patients’ sera reflected systemic disturbances affecting MSC growth. So far, decreases in PDGFs, albumin and calcium concentration, as well as platelet count, are the parameters that might be among the causes of this observation.