Continuing education: The original scientific article

El artículo científico original proporciona un método para que los científicos puedan comunicarse con otros científicos sobre los resultados de sus investigaciones. El propósito de esta segunda parte de Educación Continua es dar una breve guía con consejos para ayudar al proceso de una mejor redacción científica y delinear los principios de la escritura y la edición. Escribir un artículo científico en una revista revisada por pares es un proceso exigente que requiere tiempo y habilidad. El artículo científico que informa sobre una investigación original incluye tres partes importantes: preliminares, cuerpo principal y parte final. El cuerpo principal debe seguir una estructura estándar resumido por el acrónimo IMRAD: Introducción, Métodos, Resultados y Discusión / conclusión. Cada sección tiene su propio estilo de la estructura y lenguaje de presentación. Se explica la importancia del empleo de tablas y figuras y se analizan otras secciones relevantes como la autoría, afiliación, conflicto de intereses y referencias.Scientific research articles provide a method for scientists to communicate with other scientists about the results of their research. The purpose of this second part of Continuing Education is to give a brief guide with tips to aid the process of better scientific writing and outline the principles of writing and publishing. Writing a scientific article in a peer-reviewed journal is a demanding process that requires time and skill. The paper reporting original research includes three important parts: preliminary, main body and final part. The main body should follow a standard structure summarized by the acronym IMRAD: Introduction, Methods, Results, and Discussion / Conclusion. Each section has its own style of structure and language of presentation. The significance of tables and figures is also explained and others relevant sections as authorship, affiliation, conflict of interest and references are also analyzed.Facultad de Ciencias Médica

Continuing education: The original scientific article

El artículo científico original proporciona un método para que los científicos puedan comunicarse con otros científicos sobre los resultados de sus investigaciones. El propósito de esta segunda parte de Educación Continua es dar una breve guía con consejos para ayudar al proceso de una mejor redacción científica y delinear los principios de la escritura y la edición. Escribir un artículo científico en una revista revisada por pares es un proceso exigente que requiere tiempo y habilidad. El artículo científico que informa sobre una investigación original incluye tres partes importantes: preliminares, cuerpo principal y parte final. El cuerpo principal debe seguir una estructura estándar resumido por el acrónimo IMRAD: Introducción, Métodos, Resultados y Discusión / conclusión. Cada sección tiene su propio estilo de la estructura y lenguaje de presentación. Se explica la importancia del empleo de tablas y figuras y se analizan otras secciones relevantes como la autoría, afiliación, conflicto de intereses y referencias.Scientific research articles provide a method for scientists to communicate with other scientists about the results of their research. The purpose of this second part of Continuing Education is to give a brief guide with tips to aid the process of better scientific writing and outline the principles of writing and publishing. Writing a scientific article in a peer-reviewed journal is a demanding process that requires time and skill. The paper reporting original research includes three important parts: preliminary, main body and final part. The main body should follow a standard structure summarized by the acronym IMRAD: Introduction, Methods, Results, and Discussion / Conclusion. Each section has its own style of structure and language of presentation. The significance of tables and figures is also explained and others relevant sections as authorship, affiliation, conflict of interest and references are also analyzed.Facultad de Ciencias Médica

Modulatory Role of microRNAs in Triple Negative Breast Cancer with Basal-Like Phenotype

Development of new research, classification, and therapeutic options are urgently required due to the fact that TNBC is a heterogeneous malignancy. The expression of high molecular weight cytokeratins identifies a biologically and clinically distinct subgroup of TNBCs with a basal-like phenotype, representing about 75% of TNBCs, while the remaining 25% includes all other intrinsic subtypes. The triple negative phenotype in basal-like breast cancer (BLBC) makes it unresponsive to endocrine therapy, i.e., tamoxifen, aromatase inhibitors, and/or anti-HER2-targeted therapies; for this reason, only chemotherapy can be considered an approach available for systemic treatment even if it shows poor prognosis. Therefore, treatment for these subgroups of patients is a strong challenge for oncologists due to disease heterogeneity and the absence of unambiguous molecular targets. Dysregulation of the cellular miRNAome has been related to huge cellular process deregulations underlying human malignancy. Consequently, epigenetics is a field of great promise in cancer research. Increasing evidence suggests that specific miRNA clusters/signatures might be of clinical utility in TNBCs with basal-like phenotype. The epigenetic mechanisms behind tumorigenesis enable progress in the treatment, diagnosis, and prevention of cancer. This review intends to summarize the epigenetic findings related to miRNAome in TNBCs with basal-like phenotype

T‐cell depleted HLA‐haploidentical HSCT in a child with neuromyelitis optica

Neuromyelitis optica is an immune-mediated disease characterized by a relapsing course, resulting in progressive disability. In children, given the long life expectancy, a disease-modifying treatment could be particularly desirable. Unfortunately, the currently available treatment strategies with this potential are scarce. Very limited data are available about the use of allogeneic hematopoietic stem cell transplantation (HSCT) for autoimmune neurological diseases. In this report, we present a pediatric case successfully treated with allogeneic HSCT from an HLA-haploidentical donor, after ex vivo TCR/CD19-depletion of the graft. To the best of our knowledge, this is the first case of a pediatric patient to benefit from such a treatment

Analysis of PIK3CA Mutations and Activation Pathways in Triple Negative Breast Cancer.

Triple Negative Breast Cancer (TNBC) accounts for 12-24% of all breast carcinomas, and shows worse prognosis compared to other breast cancer subtypes. Molecular studies demonstrated that TNBCs are a heterogeneous group of tumors with different clinical and pathologic features, prognosis, genetic-molecular alterations and treatment responsivity. The PI3K/AKT is a major pathway involved in the regulation of cell survival and proliferation, and is the most frequently altered pathway in breast cancer, apparently with different biologic impact on specific cancer subtypes. The most common genetic abnormality is represented by PIK3CA gene activating mutations, with an overall frequency of 20-40%. The aims of our study were to investigate PIK3CA gene mutations on a large series of TNBC, to perform a wider analysis on genetic alterations involving PI3K/AKT and BRAF/RAS/MAPK pathways and to correlate the results with clinical-pathologic data.PIK3CA mutation analysis was performed by using cobas® PIK3CA Mutation Test. EGFR, AKT1, BRAF, and KRAS genes were analyzed by sequencing. Immunohistochemistry was carried out to identify PTEN loss and to investigate for PI3K/AKT pathways components.PIK3CA mutations were detected in 23.7% of TNBC, whereas no mutations were identified in EGFR, AKT1, BRAF, and KRAS genes. Moreover, we observed PTEN loss in 11.3% of tumors. Deregulation of PI3K/AKT pathways was revealed by consistent activation of pAKT and p-p44/42 MAPK in all PIK3CA mutated TNBC.Our data shows that PIK3CA mutations and PI3K/AKT pathway activation are common events in TNBC. A deeper investigation on specific TNBC genomic abnormalities might be helpful in order to select patients who would benefit from current targeted therapy strategies

TCRαβ/CD19 depleted HSCT from an HLA-haploidentical relative to treat children with different nonmalignant disorders

Several nonmalignant disorders (NMDs), either inherited or acquired, can be cured by allogeneic hematopoietic stem cell transplantation (HSCT). Between January 2012 and April 2020, 70 consecutive children affected by primary immunodeficiencies, inherited/acquired bone marrow failure syndromes, red blood cell disorders, or metabolic diseases, lacking a fully matched donor or requiring urgent transplantation underwent TCRab/CD19-depleted haploidentical HSCT from an HLA-partially matched relative as part of a prospective study. The median age at transplant was 3.5 years (range 0.3-16.1); the median time from diagnosis to transplant was 10.5 months (2.7 for SCID patients). Primary engraftment was obtained in 51 patients, while 19 and 2 patients experienced either primary or secondary graft failure (GF), the overall incidence of this complication being 30.4%. Most GFs were observed in children with disease at risk for this complication (eg, aplastic anemia, thalassemia). All but 5 patients experiencing GF were successfully retransplanted. Six patients died of infectious complications (4 had active/ recent infections at the time of HSCT), the cumulative incidence of transplant-related mortality (TRM) being 8.5%. Cumulative incidence of grade 1-2 acute GVHD was 14.4% (no patient developed grade 3-4 acute GVHD). Only one patient at risk developed mild chronic GVHD. With a median follow-up of 3.5 years, the 5-year probability of overall and disease-free survival was 91.4% and 86.8%, respectively. In conclusion, TCRab/CD19-depleted haploidentical HSCT from an HLA-partially matched relative is confirmed to be an effective treatment of children with NMDs. Prompt donor availability, low incidence of GVHD, and TRM make this strategy an attractive option in NMDs patients. The study is registered at ClinicalTrial.gov as NCT01810120