All people manage their boundaries of privacy. Therapists should thoroughly consider circumstances, and personal or situational risk factors, which lead to crossing or violating these boundaries. They need to reflect upon the social and personal limitations associated with their occupation and the price they have to pay for the high status role.

T-cell acute lymphoblastic leukemia (T-ALL) is a highly heterogeneous disease, and numerous genetic aberrations in the leukemic genome are responsible for the biological and clinical differences among particular ALL subtypes. However, there is limited knowledge regarding the association of whole-genome copy number abnormalities (CNAs) in childhood TALL with the course of leukemia and its outcome. The aim of this study was to identify the pattern of whole-genome CNAs in 86 newly diagnosed childhood TALL cases using a high-density single-nucleotide polymorphism array. We analyzed the presence of whole-genome CNAs with respect to immunophenotype, clinical features, and treatment outcomes. A total of 769 CNAs, including trisomies, duplications, deletions, and segmental loss of heterozygosity, were detected in 86 analyzed samples. Gain or loss of chromosomal regions exceeding 10 Mb occurred in 46 cases (53%), including six cases (7%) with complex chromosomal alterations. We observed that microdeletions in selected genes (e.g., FIP1L1 and PDGFRB) were related to the clinical features. Interestingly, 13% of samples have a duplication of the two loci (MYB and AIH1-6q23.3), which never occurred alone. Single-nucleotide polymorphism array significantly improved the molecular characterization of pediatric TALL. Further studies with larger cohorts of patients may contribute to the selection of prognostic CNAs in this group of patients.

Background: The use of high-throughput analytical techniques has enabled the description of acute lymphoblastic leukaemia (ALL) subtypes. The TCF3-HLF translocation is a very rare rearrangement in ALL that is associated with an extremely poor prognosis. The TCF3-HLF fusion gene in the described case resulted in the fusion of the homeoboxrelated gene of TCF3 to the leucine zipper domain of HLF. The TCF3-HLF fusion gene product acts as a transcriptional factor leading to the dedifferentiation of mature B lymphocytes into an immature state (lymphoid stem cells). This process initiates the formation of pre-leukaemic cells. Due to the rarity of this chromosomal aberration, only a few cases have been described in the literature. The advantage of this work is the presentation of an interesting case of clonal evolution of cancer cells and the cumulative implications (diagnostic and prognostic) of the patient's genetic alterations. Case presentation: This work presents a patient with diagnosed with TCF3-HLF-positive ALL. Moreover, the additional genetic alterations, which play a key role in the pathogenesis of ALL, were detected in this patient: deletion of a fragment from the long arm of chromosome 13 (13q12.2-q21.1) containing the RB1 gene, intragenic deletions within the PAX5 gene and NOTCH1 intragenic duplication. Conclusions: A patient with coexistence of chromosomal alterations and the TCF3-HLF fusion has not yet been described. Identifying all these chromosomal aberrations at the time of diagnosis could be sufficient to determine the cumulative effects of the described deletions on the activity of other oncogenes or tumour suppressors, as well as on the clinical course of the disease. On the other hand, complex changes in the patient's karyotype and clonal evolution of cancer cells call into question the effectiveness of experimental therapy.

Background: Nijmegen breakage syndrome (NBS) is a rare genetic disorder inherited in an autosomal recessive pattern associated with an increased risk of developing lymphoproliferative disorders, mainly non-Hodgkin lymphoma (NHL) and acute lymphoblastic leukemia (ALL). NBS patients are 50 times more likely to develop malignancy than healthy controls. Moreover, in NBS, mortality rate from cancers, mainly lymphomas, is the highest among all diseases associated with excessive fragility of chromosomes. Case presentation: This work presents a patient previously diagnosed with Nijmegen breakage syndrome who rapidly developed T-NHL despite of constant medical supervision. Cytogenetic karyotype and microarray tests revealed complex aberrations, indicating enhanced chromosomal instability. Despite initial steroid therapy, the patient passed away due to multiorgan failure. Conclusions: The lack of well-established diagnostic procedures in NBS patients make it difficult to determine any therapeutic target or predictive marker. Moreover, anticancer treatment is the biggest challenge in NBS patients due to therapy-related toxicity and immunodeficiency. Our case indicates the importance of identifying parameters useful in prognosis of disease outcome, as main risk factor affecting overall survival in NBS patients is an extremely high incidence of malignancy development.

B-cell precursor acute lymphoblastic leukemia (BCP-ALL) is the most common childhood cancer. A special subtype of high risk BCP-ALL is Philadelphia-like ALL (Ph-like ALL), in which the gene expression profile is similar to BCR-ABL1-positive leukemia; however, fusion of the mentioned genes does not occur. The unfavourable clinical course and incidence of 15% of cases means that the diagnosis and therapeutic strategy of Ph-like ALL must be carefully developed and implemented into clinical practice. The study presents the case of a patient with diagnosed Ph-like ALL. The use of molecular analytical techniques has made it possible to identify a patient who is likely to relapse and who may benefit from personalized therapy This study shows the advantages of using genomic analyses to identify therapeutic targets, which is especially important for patients with high-risk disease. This model of management could be extended to other cancer subtypes, allowing for tailored diagnosis.