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Identification of the cell types from which relapse arises in acute myeloid leukaemia, by following leukaemia propagation from patient-derived leukaemia samples. AML relapse can develop from stem cells Relapse is frequently seen in patients with acute myeloid leukemia (AML). John Dick and colleagues now uncover the cell types from which relapse arises by following leukaemia propagation from patient-derived leukaemia samples. Surprisingly, they found that relapse can arise from two distinct leukaemia cell populations, both of which display stemness features. The first group consisted of rare leukaemia stem cells with a haematopoietic stem/progenitor cell phenotype, and the second were larger subclones of immunophenotypically committed leukaemia cells. These findings may help to better monitor and target relapse AML. In acute myeloid leukaemia, long-term survival is poor as most patients relapse despite achieving remission 1 . Historically, the failure of therapy has been thought to be due to mutations that produce drug resistance, possibly arising as a consequence of the mutagenic properties of chemotherapy drugs 2 . However, other lines of evidence have pointed to the pre-existence of drug-resistant cells 3 . For example, deep sequencing of paired diagnosis and relapse acute myeloid leukaemia samples has provided direct evidence that relapse in some cases is generated from minor genetic subclones present at diagnosis that survive chemotherapy 3 , 4 , 5 , suggesting that resistant cells are generated by evolutionary processes before treatment 3 and are selected by therapy 6 , 7 , 8 . Nevertheless, the mechanisms of therapy failure and capacity for leukaemic regeneration remain obscure, as sequence analysis alone does not provide insight into the cell types that are fated to drive relapse. Although leukaemia stem cells 9 , 10 have been linked to relapse owing to their dormancy and self-renewal properties 11 , 12 , 13 , and leukaemia stem cell gene expression signatures are highly predictive of therapy failure 14 , 15 , experimental studies have been primarily correlative 7 and a role for leukaemia stem cells in acute myeloid leukaemia relapse has not been directly proved. Here, through combined genetic and functional analysis of purified subpopulations and xenografts from paired diagnosis/relapse samples, we identify therapy-resistant cells already present at diagnosis and two major patterns of relapse. In some cases, relapse originated from rare leukaemia stem cells with a haematopoietic stem/progenitor cell phenotype, while in other instances relapse developed from larger subclones of immunophenotypically committed leukaemia cells that retained strong stemness transcriptional signatures. The identification of distinct patterns of relapse should lead to improved methods for disease management and monitoring in acute myeloid leukaemia. Moreover, the shared functional and transcriptional stemness properties that underlie both cellular origins of relapse emphasize the importance of developing new therapeutic approaches that target stemness to prevent relapse.

Toxic microcystins (MCs) produced by freshwater cyanobacteria such as Microcystis aeruginosa are of concern because of their negative health and economic impacts globally. An advanced oxidation process using UV/TiO2 offers a promising treatment option for hazardous organic pollutants such as microcystins. The following work details the successful degradation of MC-LA, MC-LR, and MC-RR using a porous titanium–titanium dioxide (PTT) membrane under UV-LED light. Microcystin quantitation was achieved by sample concentration and subsequent LC–MS/MS analysis. The PTT membrane offers a treatment option that eliminates the need for the additional filtration or separation steps required for traditional catalysts. Controlled periodic illumination was successfully used to decrease the total light exposure time and improve the photonic efficiency for a more cost-effective treatment system. Individual degradation rates were influenced by electrostatic forces between the catalyst and differently charged microcystins, which can potentially be adjusted by modifying the solution pH and the catalyst’s isoelectric point.

In this study, we evaluated the effectiveness of UV-LED-irradiated TiO2 in removing 24 commonly detected PPCPs in two water matrices (municipal wastewater effluent and Suwannee River NOM–synthetic water) and compared their performance with that of ultrapure water. Relatively fast removal kinetics were observed for 29% and 12% of the PPCPs in ultrapure water and synthetic surface water, respectively (kapp of 1–2 min−1). However, they all remained recalcitrant to photocatalysis when using wastewater effluent as the background matrix (kapp < 0.1 min−1). We also observed that the pH-corrected octanol/water partition coefficient (log Dow) correlated well with PPCP degradation rate constants in ultrapure water, whereas molecular weight was strongly associated with the rate constants in both synthetic surface water and wastewater. The electrical energy per order (EEO) values calculated at the end of the experiments suggest that UV-LED/P25 can be an energy-efficient method for water treatment applications (2.96, 4.77, and 16.36 kW h m−3 in ultrapure water, synthetic surface water, and wastewater effluents, respectively). Although TiO2 photocatalysis is a promising approach in removing PPCPs, our results indicate that additional challenges need to be overcome for PPCPs in more complex water matrices, including an assessment of photocatalytic removal under different background water matrices.