Social determinants of health contribute to inequalities in access to care and inferior outcomes in pediatric populations. Before the coronavirus disease 2019 (COVID-19) pandemic, telemedicine was shown to be an effective tool to bridge the gap between health care providers and rural or underserved populations. The pandemic has rapidly changed the current landscape of health care.
View Article and Find Full Text PDFDuodenal stenosis is one of the leading causes of duodenal obstruction in the pediatric population, usually diagnosed in newborns and in Down syndrome patients. It has historically been treated with duodeno-duodenostomy, an operation that is now commonly performed laparoscopically. We present a case of a 10-year-old child with a rare chromosomal abnormality who was diagnosed with a duodenal stricture after presenting with failure to thrive and inability to tolerate tube feeds.
View Article and Find Full Text PDFApproximately two-thirds of patients with neuroblastoma are found to have metastatic disease at time of diagnosis with frequent skeletal, lymph node, central nervous system, and liver involvement. Using a serial splenic injection model, we have isolated an aggressive subclone (BE(2)-C/LM2) from -amplified neuroblastomas that demonstrate an enhanced propensity to develop metastatic liver lesions. BE(2)-C/LM2 subclone cells demonstrate increased adherent, soft agar colony and tumorsphere growth .
View Article and Find Full Text PDFBackground: MYCN amplification is a key molecular hallmark of high-risk neuroblastoma. Previously considered an "undruggable" target, MYCN transcription can be disrupted by inhibiting the bromodomain and the extraterminal (BET) domain family of proteins that regulates MYCN transcription epigenetically. JQ1 is a potent, small-molecule BET inhibitor that induces cell-cycle arrest and initiates apoptosis in neuroblastoma.
View Article and Find Full Text PDFCell division cycle 42 (CDC42), a small GTPase of the Rho-subfamily, regulates diverse cellular functions including proliferation, cytoskeletal rearrangement and even promotes malignant transformation. Here, we found that increased expression of CDC42 correlated with undifferentiated neuroblastoma as compared to a more benign phenotype. CDC42 inhibition decreased cell growth and soft agar colony formation, and increased cell death in BE(2)-C and BE(2)-M17 cell lines, but not in SK-N-AS.
View Article and Find Full Text PDFBackground/aim: It is unknown whether hypoxia regulates aurora kinase A (AURKA), a serine/threonine kinase, in neuroblastoma to stimulate cell growth or migration. We sought to determine whether AURKA mediates hypoxia-induced regulation of neuroblastoma tumorigenicity.
Materials And Methods: Human neuroblastoma BE(2)-C cells were treated with CoCl2, a chemical hypoxia mimetic, and MLN8237, a pharmalogical inhibitor of AURKA, to assess cell viability, colony formation and transwell migration.