Implementing Mental Health Screening for Adolescent Hematology and Oncology Patients: A Quality Improvement Initiative.

Purpose: Adolescents and young adults (AYA) with chronic illnesses experience an increase in mental health concerns. A mental health screening (MHS) process for hematology and oncology patients was implemented in a single institution. The quality improvement project was conducted to integrate a MHS process, educate providers about the importance of mental health in this patient population, and evaluate the process. Methods: The COM-B (capability, opportunity, motivation-behavior) model for behavior change was used to inform strategic planning and Plan-Do-Study-Act (PDSA) methodologies for process improvement. Retrospective chart reviews and surveys were conducted to determine missed screening rates and providers' perceptions, knowledge, attitudes, and skills of the MHS process. Results: Of 334 eligible patient encounters, the missed screening rate was 15.0%, the overall error rate of completing the screening was 3.8%, the error rate of completing the suicide or self-harm indicator was 2.6%, and the missed medical social worker touch point was 4.8%. Conclusion: The rising rates of mental health concerns in AYA hematology and oncology patients call for streamlined MHS processes to improve the identification of patients who may need intervention and services. Processes should be tailored to workflows and available resources. Future PDSA cycles will include providing dedicated nursing education and determining the cost needed to meet the rising mental health needs of the AYA hematology and oncology population.

Pituitary sellar spine in a pediatric patient with diabetes insipidus.

A sellar spine is a midline bony spur arising from the ventral aspect of the dorsum sellae. Representing a remnant of the anterior notochord, it is often an incidental finding and thought to be of no clinical significance. However, it has recently been suggested that a potential association may exist between sellar spine and pediatric pituitary endocrinopathies, possibly caused by deformation of the developing pituitary gland by the sellar spine. To our knowledge, this is the first case report demonstrating an association between sellar spine and clinical diabetes insipidus.

Tumefactive intracranial presentation of precursor B-cell acute lymphoblastic leukemia.

In children, leukemia is the most common malignancy, and approximately 75% of leukemias are acute lymphoblastic leukemia (ALL). Central nervous system leukemia is found at diagnosis in fewer than 5% of children with ALL. Leukemic intracranial masses have been described with acute myeloid leukemia, but ALL presenting as a mass lesion is rare. We describe a unique case of an intracranial confirmed precursor B cell (pre-B) ALL mass in a 13-year-old girl that was diagnosed by brain CT, MRI and cerebral angiography, and confirmed by biopsy. This report details pertinent history and distinguishing imaging features of an intracranial ALL tumefaction.

Expression of EWS-ETS fusions in NIH3T3 cells reveals significant differences to Ewing's sarcoma.

Ewing's sarcomas contain specific chromosomal translocations that fuse EWS to ETS family members, including FLI, ERG, FEV, ETV1 and ETV4. Prior work has suggested that functional differences exist between some of these EWS-ETS fusions. However, as the cell of origin of Ewing's sarcoma is unknown, this prior work was conducted in NIH3T3 cells, which have not been validated as an appropriate model for the study of EWS-ETS fusions. To determine if NIH3T3 cells are a good model for Ewing's sarcoma, we introduced all five EWS-ETS fusions into these cells, and analyzed their phenotypes and gene expression patterns. EWS-FLI, EWS-ERG, and EWS-FEV caused NIH3T3 cells to exhibit anchorage independent growth whereas EWS-ETV1 and EWS-ETV4 did not. In contrast, all the EWS-ETS fusions induced tumor formation in a xenograft model. We defined the core transcriptional profile of the EWS-ETS fusions using cDNA microarrays, and compared these to data derived from patient-derived Ewing's sarcoma cell lines. The NIH3T3 model did not recapitulate the gene expression pattern of bona fide Ewing's sarcoma. Based on these results, we conclude that while there may be functional differences between the various EWS-ETS fusions, the NIH3T3 cell model is inadequate to study the gene expression pattern induced by EWS-ETS proteins in Ewing's sarcoma. Thus, data derived from the NIH3T3 model system needs to be appropriately validated before they can be accepted as relevant to the human disease.