Indirect Co-Culture with Schwann Cells as a New Approach for Human Endometrial Stem Cells Neural Transdifferentiation Research Article 1 , 2*, 3 ,

Neurodegenerative diseases such as Spinal Cord Injury (SCI) refer to the loss of neuronal cells in the central nervous system. Cell replacement therapy is currently the most propitious approach for the treatment of such diseases. Endometrial Stem Cells (EnSC) due to their unique characteristics have recently gained extensive attention as a new source of mesenchymal-like stem cells for tissue engineering purposes. Research has shown the potency of these cells to differentiate into several cell lineages including osteocytes, adipocytes and neural cells using chemical induction. In this present study we describe how human EnSCs can be induced to differentiate into neuron-like cells when co-cultured with human Schwann cells via insert wells which inhibit intercellular contact of the two cell types. Quantitative gene expression analysis and immunocytochemistry was performed after one week of co-culture. The results confirmed neuronal differentiation of EnSCs which support the notion that Schwann cells produce and secrete neurotrophic factors that can act upon cells without physical contact. Our present findings support the differentiation of EnSCs and the potency of these cells for the treatment of degenerative and acquired disorders of the nervous system

Twists and Turns from 'Tumor in Tumor' Profiling: Surveillance of CLL leads to detection of a lung adenocarcinoma, whose genomic characterization alters the original hematologic diagnosis

Comprehensive characterization of somatic genomic alterations has led to fundamental shifts in our understanding of tumor biology. In clinical practice, these studies can lead to modifications of diagnosis and/or specific treatment implications, fulfilling the promise of personalized medicine. Herein, we describe a 78-yr-old woman under surveillance for long-standing untreated chronic lymphocytic leukemia (CLL). Molecular studies from a peripheral blood specimen revealed a TP53 p.V157F mutation, whereas karyotype and fluorescence in situ hybridization (FISH) identified a 17p deletion, trisomy 12, and no evidence of IGH-CCND1 rearrangement. Positron emission tomography-computed tomography scan identified multistation intra-abdominal lymphadenopathy and a pulmonary nodule, and subsequent pulmonary wedge resection confirmed the presence of a concurrent lung adenocarcinoma. Targeted next-generation sequencing of the lung tumor identified an EGFR in-frame exon 19 deletion, two TP53 mutations (p.P152Q, p.V157F), and, unexpectedly, a IGH-CCND1 rearrangement. Follow-up immunohistochemistry (IHC) studies demonstrated a cyclin D1-positive lymphoid aggregate within the lung adenocarcinoma. The presence of the TP53 p.V157F mutation in the lung resection, detection of an IGH-CCND1 rearrangement, and cyclin D1 positivity by IHC led to revision of the patient's hematologic diagnosis and confirmed the extranodal presence of mantle cell lymphoma within the lung mass, thus representing a "tumor in tumor." Manual review of the sequencing data suggested the IGH-CCND1 rearrangement occurred via an insertional event, whose size precluded detection by original FISH studies. Thus, routine imaging for this patient's known hematologic malignancy led to detection of an unexpected solid tumor, whose subsequent precision medicine studies in the solid tumor redefined the original hematological diagnosis