The Effect of Social Determinants of Health on Telemedicine Access During the COVID-19 Pandemic.

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.

Robotic duodeno-duodenostomy creation in a pediatric patient with idiopathic duodenal stricture.

Duodenal 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.

Elevated TIMP-1 expression is associated with a prometastatic phenotype, disease relapse, and poor survival in neuroblastoma.

Approximately 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 .

Bromodomain and extraterminal inhibition blocks tumor progression and promotes differentiation in neuroblastoma.

Background: 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.

Silencing gastrin-releasing peptide receptor suppresses key regulators of aerobic glycolysis in neuroblastoma cells.

Background: Under normoxic conditions, cancer cells use aerobic glycolysis as opposed to glucose oxidation for energy production; this altered metabolism correlates with poor outcomes in neuroblastoma. Hypoxia-inducible factor-1 alpha (HIF-1α) and pyruvate dehydrogenase kinase 4 (PDK4) regulate aerobic glycolysis, while pyruvate dehydrogenase phosphatase 2 (PDP2) promotes glucose oxidation. Here, we sought to determine whether gastrin-releasing peptide receptor (GRP-R) signaling regulates glucose metabolism.

Silencing of CDC42 inhibits neuroblastoma cell proliferation and transformation.

Cell 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.

Targeting aurora kinase A inhibits hypoxia-mediated neuroblastoma cell tumorigenesis.

Background/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.

Targeting Aurora kinase-A downregulates cell proliferation and angiogenesis in neuroblastoma.

Purpose: Aurora kinase A (AURKA) overexpression is associated with poor prognosis in neuroblastoma and has been described to upregulate VEGF in gastric cancer cells. However, the exact role of AURKA in the regulation of neuroblastoma tumorigenesis remains unknown. We hypothesize that AURKA-mediated stabilization of N-Myc may affect VEGF expression and angiogenesis in neuroblastoma.

Targeting gastrin-releasing peptide suppresses neuroblastoma progression via upregulation of PTEN signaling.

We have previously demonstrated the role of gastrin-releasing peptide (GRP) as an autocrine growth factor for neuroblastoma. Here, we report that GRP silencing regulates cell signaling involved in the invasion-metastasis cascade. Using a doxycycline inducible system, we demonstrate that GRP silencing decreased anchorage-independent growth, inhibited migration and neuroblastoma cell-mediated angiogenesis in vitro, and suppressed metastasis in vivo.