Our results indicate that assistance with setting achievable goals, including individualised strategies and support from health care professionals to realise the goals, may assist in the rehabilitation to restore health and function after allo-SCT.

Purpose The purpose of this paper is to develop a deeper understanding of the organization-trainee relationship through a psychological contract lens, by exploring the psychological contract between the trainee and organization during and after the program and what factors may account for contract reciprocity. Design/methodology/approach Inductive qualitative study design. Findings Data suggested that factors accounting for contract reciprocity during the program included: trainees’ responsibilities, trainees’ personal and professional development, trainees’ commitment, trainees’ delivery, and managerial and supervisory support. Factors identified accounting for contract reciprocity after individuals completed the program were: career opportunities, future-oriented dialogue between former trainees and managers, wage-setting, job tasks, and working conditions. Originality/value This exploratory research is original in that it identifies different factors accounting for the reciprocity during and after the program, and how this may be particularly relevant when talents are recruited externally to specifically participate in the program.

Most chemotherapeutics target DNA integrity and thereby trigger tumour cell death through activation of DNA damage responses that are tightly coupled to the cell cycle. Disturbances in cell cycle regulation can therefore lead to treatment resistance. Here, a comprehensive analysis of cell cycle checkpoint activation following doxorubicin (doxo) treatment was performed using flow cytometry, immunofluorescence and live-cell imaging in a panel of TP53 mutated ultra high-risk neuroblastoma (NB) cell lines, SK-N-DZ, Kelly, SK-N-AS, SK-N-FI, and BE(2)-C. Following treatment, a dose-dependent accumulation in either S- and/or G2/M-phase was observed. This coincided with a heterogeneous increase of cell cycle checkpoint proteins, i.e., phos-ATM, phos-CHK1, phos-CHK2, Wee1, p21Cip1/Waf1, and p27Kip among the cell lines. Combination treatment with doxo and a small-molecule inhibitor of ATM showed a delay in regrowth in SK-N-DZ, of CHK1 in BE(2)-C, of Wee1 in SK-N-FI and BE(2)-C, and of p21 in Kelly and BE(2)-C. Further investigation revealed, in all tested cell lines, a subset of cells arrested in mitosis, indicating independence on the intra-S- and/or G2/M-checkpoints. Taken together, we mapped distinct cell cycle checkpoints in ultra high-risk NB cell lines and identified checkpoint dependent and independent druggable targets.