Características clínicas, epidemiológicas y quirúrgicas de pacientes con afecciones nodulares tiroideas / Clinical, Epidemiological and Surgical Characteristics of Patients with Thyroid Nodular Conditions

Introducción: En las últimas décadas la incidencia del cáncer tiroideo en el curso de la enfermedad nodular se ha incrementado debido a las novedosas técnicas de diagnóstico; sin embargo, la tasa de mortalidad se ha mantenido muy baja. Objetivo: Evaluar las características clínicas, epidemiológicas y quirúrgicas de pacientes con afecciones nodulares tiroideas. Métodos: Se realizó un estudio descriptivo observacional de cohorte prospectivo, longitudinal con los pacientes operados de afecciones tiroideas durante el período comprendido entre enero del 2008 y diciembre del 2018. El universo y la muestra quedaron constituidos por 467 pacientes que cumplieron con los criterios de inclusión. Resultados: Predominaron el sexo femenino (89,5 por ciento) y el grupo etario de 45-60 años (29,5 por ciento). Asociaron comorbilidades 338 pacientes y algún factor de riesgo de malignidad (6,2 por ciento). Un total de 174 pacientes manifestaron síntomas y 264 mostraron algún signo. Predominaron los reportes ecográficos (TI-RADS) y citológicos (Bethesda) tipo II (54,3 por ciento) y (55,5 por ciento), respectivamente. La hemitiroidectomía fue el procedimiento más realizado (59,9 por ciento) y la disfonía la complicación más encontrada (1,9 por ciento). Conclusiones: El diagnóstico oportuno del cáncer tiroideo en el curso de una enfermedad nodular contribuye a individualizar todas las decisiones terapéuticas atendiendo a las características de cada paciente y sus circunstancias(AU)

Introduction: In recent decades, the incidence rates of thyroid cancer in the course of nodular disease has increased due to novel diagnostic techniques; however, the mortality rate has remained very low. Objective: To evaluate the clinical, epidemiological and surgical characteristics of patients with nodular thyroid disease. Methods: A descriptive, observational, of prospective cohort, longitudinal and observational study was conducted with patients operated on for thyroid disorders during the period from January 2008 to December 2018. The study universe and sample consisted of 467 patients who met the inclusion criteria. Results: The female sex (89.5 percent) and the age group 45-60 years (29.5 percent) predominated. Comorbidities were present in 338 patients, as well as some risk factor for malignancy in 6.2 percent. A total of 174 patients manifested symptoms and 264 showed some sign. There was a predominance of echography (TI-RADS) and cytology (Bethesda) type II reports, accounting for 54.3 percent and 55.5 percent, respectively. Hemithyroidectomy was the most performed procedure (59.9 percent), while dysphonia was the most encountered complication (1.9 percent). Conclusions: Timely diagnosis of thyroid cancer in the course of nodular disease contributes to individualizing all therapeutic decisions considering the characteristics of each patient and their circumstances(AU)

Progress of research on oncogene PTEN in thyroid malignant tumors / 中华内分泌外科杂志

The phosphatase and tensin homolog deleted on chromosome ten (PTEN) is a common oncogene located in the 10q23.3 region on the long arm of human chromosome l0, which regulates a variety of biological processes such as proliferation, survival, cell structure, motility, energy metabolism and genomic stability. Inactivation of PTEN is prevalent in almost all malignancies and correlates with tumor progression. Thyroid malignancies are among the most common endocrine malignancies, and PTEN has been shown to be critically associated with their development. The aim of this review is to describe the structural function of PTEN, as well as to summarize and discuss the recent findings of PTEN in thyroid malignancies.

Advancement on the pathogenesis of hereditary multiple exostoses / 中华骨科杂志

Hereditary multiple exostoses (HME) are benign bone tumors characterized by autosomal dominant inheritance, which can cause skeletal malformation in adolescents, seriously affecting the body's aesthetic and motor functions. Currently, there are no guidelines for diagnosing and treating HME, and the main treatment is surgical treatment to remove the tumor and correct the deformity. However, osteochondroma is multiple and difficult to be completely resected. Therefore, more and more scholars are exploring the method of conservative treatment. However, the current understanding of the pathogenesis of HME is limited, and there are no safe and effective drugs in the clinic. Most hypotheses regarding the pathogenesis of HME are based on genetic mutations. Patients with HME may have EXT tumor suppressor gene mutations and function loss caused by secondary mutations such as loss of gene heterozygosity, which ultimately induce abnormal proliferation and differentiation of cartilage in growth plates. Abnormal EXT gene expression causes a decrease in the level of heparan sulphate (HS), leading to abnormalities in multiple molecular pathways that regulate the development and differentiation of growth plate chondrocytes, which together participate in the entire process of HME development and progression. This paper reviews the relevant studies on the pathogenesis of HME in recent years, in order to better understand the pathological process of HME, provide a theoretical basis for the diagnosis and treatment of HME, and also provide ideas for the development of drugs targeting HME.

Consideraciones actuales sobre el diagnóstico y tratamiento del cáncer tiroideo

Introducción: Desde los inicios de este siglo se ha producido un notable incremento mundial de la tasa de incidencia del cáncer de tiroides, el cual generalmente tiene un curso larvado y asintomático. Objetivo: Profundizar en el conocimiento de los aspectos novedosos del diagnóstico oportuno y tratamiento personalizado del cáncer tiroideo. Desarrollo: El cáncer tiroideo es la enfermedad maligna más frecuente del sistema endocrino. En las últimas décadas, su incidencia se ha incrementado aceleradamente, aunque la mortalidad se ha mantenido baja. El descubrimiento y desarrollo de nuevas técnicas de imágenes, inmunológicas y moleculares, han permitido estudiar en profundidad la neoplasia de la tiroides. Esto ha favorecido avanzar en los aspectos que más han modificado la nueva actitud respecto al diagnóstico oportuno y su tratamiento. Conclusiones: En años recientes, los avances de las investigaciones básicas, clínicas y traslacionales (aplicación real de los conocimientos básicos en la práctica clínica), han transformado antiguos conceptos relacionados con el cáncer tiroideo y han dotado de nuevas herramientas para el diagnóstico oportuno y tratamiento personalizado.

Introduction: Since the beginning of this century there has been a notable increase worldwide in the incidence rate of thyroid cancer, which generally has a latent and asymptomatic course. Objectives: To deepen the knowledge of the novel aspects of timely diagnosis and treatment of thyroid cancer. Development: Thyroid cancer is the most frequent malignant disease of the endocrine system. In recent decades, its incidence has increased rapidly, although mortality has remained low. The discovery and development of new imaging, immunological and molecular techniques have made it possible to study thyroid neoplasm in depth. This has favored advancing in the aspects that have most modified the new attitude regarding timely diagnosis and its treatment. Conclusions: In recent years, advances in basic, clinical and translational research have transformed old concepts related to thyroid cancer and have equipped with new tools for timely diagnosis and personalized treatment.

Caracterización molecular de pacientes con cáncer colorrectal / Molecular characterization of colorectal cancer patients

Introducción. El cáncer colorrectal tiene una alta incidencia en la población mundial. Diversas vías moleculares están involucradas en su desarrollo, entre ellas, la inestabilidad cromosómica, la inestabilidad microsatelital y la epigenética. Objetivo. Hacer la caracterización molecular de 44 individuos con cáncer colorrectal esporádico. Materiales y métodos. El análisis de mutaciones en los genes APC, KRAS, TP53 y BRAF se hizo mediante secuenciación de Sanger; la inestabilidad microsatelital se determinó mediante electroforesis capilar utilizando cinco marcadores de repetición corta en tándem (Short Tandem Repeat) y el estado de metilación del promotor del gen MLH1 se hizo con la técnica MS-PCR (Methylation-Specific PCR). Resultados. La frecuencia de mutación de los genes APC, KRAS y TP53 fue del 18,1, 25 y 4,5 %, respectivamente; las mutaciones detectadas se localizaron con mayor frecuencia en el colon derecho. La frecuencia de inestabilidad microsatelital fue del 27,2 % y el 73,1 % en los tumores con metilación en el gen MHL1, y el 91,6 % de los tumores con inestabilidad microsatelital presentaba metilación en el gen MLH1. En el grupo de tumores con estabilidad microsatelital, las mutaciones en los genes APC, KRAS y TP53 fueron más frecuentes que en el grupo de tumores con inestabilidad microsatelital. La metilación del gen MLH1 fue la alteración más predominante. Conclusiones. En los pacientes con cáncer colorrectal evaluados se demostró la presencia de alteraciones moleculares en las diferentes vías genéticas, las cuales son comunes en su carcinogénesis. Los pacientes presentaron un perfil de mutaciones diferente al de otras poblaciones. Los hallazgos obtenidos en este estudio confirman la heterogeneidad molecular descrita en el desarrollo del cáncer colorrectal.

Introduction: Colorectal cancer has a high incidence in the world population. Different molecular pathways, such as chromosomal instability, microsatellite instability, and epigenetics are involved in its development. Objective: To perform molecular characterization in 44 individuals with sporadic colorectal cancer. Materials and methods: We conducted mutation analyses of the APC, KRAS, TP53 y BRAF genes using Sanger sequencing techniques; microsatellite instability was determined by capillary electrophoresis with five STR genetic markers while the methylation status of the MHL1 promotor gene was analyzed using methylation-specific PCR. Results: APC, KRAS, and TP53 genes mutation frequency was 18.1%, 25%, and 4.5%, respectively; the somatic mutations detected were located more frequently in the right colon. The frequency of microsatellite instability was 27.2% and 73.1% of the tumors had the MHL1 gene methylated while 91.6% of microsatellite instability-positive tumors had the methylated MLH1 gene. The mutation profile of microsatellite stability tumors APC, KRAS, and TP53 genes was more frequent than in the microsatellite instability-positive tumors. The methylation of the MLH1 gene was the most predominant molecular alteration. Conclusions: We identified molecular alterations in different genetic pathways of the colorectal cancer patients evaluated, which are common in the carcinogenesis of this cancer. These patients showed a different mutational profile compared to other populations. Our findings confirm the molecular heterogeneity described in the development of colorectal cancer.

Bases biológicas del cáncer: una propuesta de contenidos mínimos para las carreras de la salud / Biological bases of cancer: a proposal of minimum contents for health schools

El cáncer constituye la segunda de causa de muerte a nivel mundial y se estima será la primera, superando a las cardiovasculares. El estudio de sus bases moleculares ha permitido el desarrollo de la quimioterapia clásica, como de nuevas terapias biológicas. Si bien estos avances han redundado en un aumento en la sobrevida, no ha impactado en una menor incidencia de los casos. Esto último se debe, en parte, al desconocimiento de los múltiples factores carcinogénicos existentes y los efectos de sus interacciones para cada uno de los tumores. En este sentido, es interesante notar que, en los currículos de las escuelas de salud de las universidades chilenas, el cáncer u oncología como tal, no constituye una cátedra en sí misma, siendo sus contenidos tangencialmente abordados en distintos momentos de la formación; en biología celular, medicina interna y cirugía, entre otros. Con estos antecedentes, el propósito de este trabajo es ofrecer un propuesta sencilla y accesible para los estudiantes, respecto de los contenidos que, a nuestro juicio, son esenciales para comprender las bases biológicas de esta enfermedad y enfrentar con mejores conocimientos el ciclo clínico posterior. A continuación, el lector se encontrará con principios fundamentales de la biología humana normal (como el ciclo celular y el dogma central de la biología molecular), que permiten obtener una visión global de los mecanismos fisiológicos cuya desregulación conlleva a una neoplasia maligna. Luego se entregarán algunas definiciones amplias en relación con los conceptos de neoplasia, tumor benigno y maligno. Para, finalmente, abordar las principales etapas que permiten el desarrollo del cáncer; (i) iniciación, (ii) promoción y (iii) progresión. En esta última, se profundizará por separado, en angiogénesis, degradación de la matriz extracelular, migración y evasión de la respuesta inmune. Este trabajo no aborda materias relacionadas con la hipótesis metabólica del cáncer.

Cancer constitutes the second most common cause of death worldwide and is expected to become the leading one, even above cardiovascular diseases. The understanding of the cellular and molecular basis of cancer has led not only to the proper development of chemotherapy but also of target therapies. Although these advances are related with improved survival rates among cancer patients, it has poorly impacted its incidences. In this regard, the lack of knowledge regarding the impact that the several carcinogenic factors and their interactions have on different types of cancers may explain at least in part the difficulties to reduce incidence rates. However, is worth noticing that in several health schools of chilean universities, cancer does not constitute a formal course, being only partially approached during other courses, such as cell biology, internal medicine, and surgery. Thus, the aim of our work is to provide students a simple and resumed manuscript about essential topics necessary to understand the biological basis of cancer. First, the reader will find some fundamentals about human biology including the cell cycle and the central dogma of molecular biology, which offers an overview of the physiological mechanisms leading to malignant neoplasia. Then, we will provide current definitions of neoplasia, benign and malignant tumors are provided. Finally, the different stages of tumor progression will be approached to allow the understanding of cancer development. These stages include (i) initiation, (ii) promotion, and (iii) progression. For the last one, metastasis, angiogenesis, extracellular matrix degradation, migration, and immune evasion will also be addressed. This work will not consider the metabolic hypothesis of cancer.

Genes involucrados en el cáncer pulmonar / Genes involved in lung cancer

Introducción: El cáncer pulmonar constituye un serio problema de salud mundial por su elevada prevalencia y mortalidad. En la carcinogénesis pulmonar están implicados oncogenes y genes supresores tumorales, que en una compleja interacción con factores ambientales favorecen la transformación cancerosa. Objetivo: Describir los principales genes implicados en el cáncer pulmonar. Métodos: Se buscaron referencias en las bases de datos PubMed Central, Annual Reviews y SciELO. Se revisaron preferentemente los artículos originales, las revisiones bibliográficas, las revisiones sistemáticas y los metaanálisis de los últimos cinco años. Análisis e integración de la información: En la carcinogénesis pulmonar se involucran los oncogenes JUN, FOS, ABL1, BRAF, RAF1, GNAS, KRAS, NRAS, HRAS, CSF 1R, MYC, EGFR, MET, ALK, CCNE1, DDR2, ERBB3, FGFR1, MDM2, ROS1, SOX2 y TP63 y los genes supresores tumorales TP53, CDKN2A, CDKN1A, RB1, CDK2AP1, ATM, ERCC2, BRCA1, CCND1, STK11, PDLIM2, PTEN, ARID1A, ASCL4, CUL3, EP300, KEAP1, KMT2D, NF1, NOTCH1, RASA1, ETD2 y SMARCA4. El conocimiento de la genética molecular del cáncer pulmonar es importante para la identificación de biomarcadores diagnósticos y pronósticos más eficaces y para el diseño de fármacos diana sobre genes específicos(AU)

Introduction: Lung cancer is a serious global health problem due to its high prevalence and mortality. Lung carcinogenesis involves oncogenes and tumor suppressor genes which interact in complex manners with environmental factors, paving the way for the cancerous transformation. Objective: Describe the main genes involved in lung cancer. Methods: References were searched for in the databases PubMed Central, Annual Reviews and SciELO. Particular attention was paid to original papers, bibliographic reviews, systematic reviews and meta-analyses published in the last five years. Data analysis and integration: Lung carcinogenesis involves the oncogenes JUN, FOS, ABL1, BRAF, RAF1, GNAS, KRAS, NRAS, HRAS, CSF 1R, MYC, EGFR, MET, ALK, CCNE1, DDR2, ERBB3, FGFR1, MDM2, ROS1, SOX2 and TP63, and the tumor suppressor genes TP53, CDKN2A, CDKN1A, RB1, CDK2AP1, ATM, ERCC2, BRCA1, CCND1, STK11, PDLIM2, PTEN, ARID1A, ASCL4, CUL3, EP300, KEAP1, KMT2D, NF1, NOTCH1, RASA1, ETD2 and SMARCA4. Knowledge about the molecular genetics of lung cancer is important to identify more efficient diagnostic and prognostic biomarkers and to design targeted drugs for specific genes(AU)

Caracterización molecular del glioblastoma multiforme de un paciente con larga sobrevida / Molecular characterization of glioblastoma multiforme in a patient with long survival

RESUMEN El glioblastoma multiforme (GBM) es un tumor del sistema nervioso central con alta tasa de recambio celular, infiltración, degradación de la matriz extracelular y resistencia al tratamiento resectivo y quimioterapéutico. La sobrevida general no suele ser superior a los dos años. Sin embargo, en los últimos años se han dilucidado mejor los mecanismos moleculares que sustentan su comportamiento y que, potencialmente, podrían modularse con la terapia. A continuación se presenta el caso de un adulto joven, de 20 años, con diagnóstico de glioblastoma multiforme frontal derecho a los 13 años. El tratamiento incluyó cirugía resectiva, quimioterapia y dieta cetogénica. La caracterización genética del tumor se analiza en el contexto clínico del paciente.

SUMMARY Glioblastoma multiforme is a very aggressive central nervous system tumor with a high celular replacement, local infiltration, degradation of the extracellular matrix and resistance to surgery and chemotherapeutical agents. General survival used to be less than 2 years. However, research in the last years has shown the molecular mechanisms underlying behavior and potentially be a therapeutical targets. We show an adult with 20 years old diagnosed with glioblastoma multiforme when he was 13 years, whose treatment involved resective surgery, chemoterapy and ketogenic diet. Genetic characterization was performed and analyzed in the context of the clinical pathway.

Cyclin-dependent kinases-based synthetic lethality: Evidence, concept, and strategy

Synthetic lethality is a proven effective antitumor strategy that has attracted great attention. Large-scale screening has revealed many synthetic lethal genetic phenotypes, and relevant small-molecule drugs have also been implemented in clinical practice. Increasing evidence suggests that CDKs, constituting a kinase family predominantly involved in cell cycle control, are synthetic lethal factors when combined with certain oncogenes, such as

Mechanism of action of forkhead box transcription factors in hepatocellular carcinoma and their prospects as treatment targets / 临床肝胆病杂志

Hepatocellular carcinoma (HCC) is one of the most common malignant cancers and has high incidence and mortality rates and poor prognosis. Forkhead box (FOX) transcription factor family can regulate cell growth, differentiation, and tissue development and plays an important role in tumor. This article reviews the association of the molecular expression of the FOX family with the development, progression, and prognosis of HCC and analyzes the mechanism of action of FOX in the progression of HCC. It is pointed out that FOX family is expected to become a new target for HCC treatment.

The effect of PM2.5 on oncogene expression in HBE cells / 中华劳动卫生职业病杂志

Objective@#To study the effect of particulate matter 2.5 (PM2.5) on oncogene expression in human bronchial epithelial (HBE) cells.@*Methods@#HBE cells were selected as the study subjects, and PM2.5 treatment group (10 μg/ml and 50 μg/ml) , negative control group and positive control group (10 μmol/L Cr6+) were set. CCK8 assay was used to test the IC50 value of PM2.5. HBE cells were treated with PM2.5 for 24 h at 10 μg/ml and 50 μg/ml, additionally, cells were treated with blank as negative control, 10 μmol/L Cr6+ as a positive control for 24 h. After the treatment, mRNA expression of oncogenes including c-myc, c-fos, k-ras and p53 were detected by fluorescent quantitative RT-PCR, the protein expression of oncogenes were detected with western blot.@*Results@#The IC50 value of PM2.5 in HBE cells is 70.12 μg/ml. The qRT-PCR data showed that compared with the control group, the expression level of c-myc gene increased by respectively 500.1%、780.7%、305.3% after exposure to 10、50 μg/ml PM2.5 and positive control group; c-fos gene increased respectively 34.0%、76.7%、131.3% after exposure to 10、50 μg/ml PM2.5 and positive control group; k-ras gene increased respectively 50.3%、107.0%、49.7% after exposure to 10、50 μg/ml PM2.5 and positive control group; p53 gene decreased by 28.3%、28.7%、59.7% after exposure to 10、50 μg/ml PM2.5 and positive control group. The western blot results showed that compared with the control group, c-myc protein increased respectively 29.7%、77.3% after exposure to 50 μg/ml PM2.5 and positive control group; c-fos protein increased respectively 200.3%、137.0% after exposure to 50 μg/ml PM2.5 and positive control group; k-ras protein increased respectively 106.3%、130.3%、116.7% after exposure to 10、50 μg/ml PM2.5 and positive control group; p53 protein decreased by 43.7%、53.3%、52.1% after exposure to 10、50 μg/ml PM2.5 and positive control group.@*Conclusion@#PM2.5 could promote the expression of oncogenes in HBE cells, the carcinogenicity of haze might be related to promotion of oncogenes expression induced by PM2.5.

Predictive value of 18F-FDG PET/CT related metabolic parameters for Kras mutation in colorectal cancer patients / 中华核医学与分子影像杂志

Objective To explore the predictive value of 18F-fluorodeoxyglucose (FDG) PET/CT related metabolic parameters for Kras mutation in colorectal cancer (CRC) patients.Methods Retrospective analysis was conducted in 150 patients (105 males,45 females,median age:63 years) with CRC who underwent 18F-FDG PET/CT in Changhai Hospital of Navy Medical University between November 2011 and August 2017.The primary tumors were removed by surgery and patients received genetic testing within 1 month after PET/CT.18F-FDG PET/CT related metabolic parameters were measured,including maximum standardized uptake value (SUVmax),metabolic tumor volume (MTV;including MTV2.5,MTV20％,MTV30％,MTV40％,MTV50％),total lesion glycolysis (TLG;including TLG2.5,TLG20％,TLG30％,TLG40％,TLG50％).Logistic regression analysis and receiver operating characteristic (ROC) curve analysis were used to analyze the data.Results There were 78 Kras-mutated type patients and 72 wild-type patients.Logistic regression analysis showed that SUVmax (odds ratio (OR) =1.176,95％ CI:1.043-1.327) and MTV2.5 (OR =1.125,95 ％ CI:1.002-1.263) were predictors of Kras mutation.With SUVmax =15.5 and MTV2.5 =23.79 cm3 as the cut-off value,the prediction accuracies of Kras mutation were 67.33％(101/150) and 65.33％(98/150),respectively.The accuracies of SUVmax and MTV2.5 for predicting Kras mutation were higher in recta or sigmoid colon cancers (70.79％(63/89) and 68.54％(61/89)).Conclusion SUVmax and MTV2.5 can predict Kras mutation in CRC patients,but there is a significant gap of predictive efficiency between PET/CT and gene detection.

Biological function and regulatory mechanism of epithelial-mesenchymal transition-related long non-coding RNAs in liver cancer / 临床肝胆病杂志

Liver cancer has a high degree of malignancy, and many oncogenes and tumor suppressor genes play an important regulatory role in the development and progression of liver cancer. Epithelial-mesenchymal transition (EMT) is a biological process in which epithelial cells transform into mesenchymal cells, which can increase the migration and invasion abilities of tumor cells. Long non-coding RNAs (lncRNAs) can regulate EMT process in various ways. This article reviews the research advances in the main biological functions and regulatory mechanisms of EMT-related lncRNAs in liver cancer.

Biological function and regulatory mechanism of epithelial-mesenchymal transition-related long non-coding RNAs in liver cancer / 临床肝胆病杂志

Liver cancer has a high degree of malignancy, and many oncogenes and tumor suppressor genes play an important regulatory role in the development and progression of liver cancer. Epithelial-mesenchymal transition (EMT) is a biological process in which epithelial cells transform into mesenchymal cells, which can increase the migration and invasion abilities of tumor cells. Long non-coding RNAs (lncRNAs) can regulate EMT process in various ways. This article reviews the research advances in the main biological functions and regulatory mechanisms of EMT-related lncRNAs in liver cancer.

β-carotene Inhibits Expression of c-Myc and Cyclin E in Helicobacter pylori-infected Gastric Epithelial Cells

BACKGROUND: Helicobacter pylori infection is a major risk factor in the development of gastric cancer. H. pylori infection of gastric epithelial cells increases the levels of reactive oxygen species (ROS), activates oncogenes, and leads to β-catenin-mediated hyper-proliferation. β-Carotene reduces ROS levels, inhibits oxidant-mediated activation of inflammatory signaling and exhibits anticancer properties. The present study was carried out to determine if β-carotene inhibits H. pylori-induced cell proliferation and the expression of oncogenes c-myc and cyclin E by reducing the levels of β-catenin and phosphorylated glycogen synthase kinase 3β (p-GSK3β). METHODS: Gastric epithelial AGS cells were pre-treated with β-carotene (5 and 10 μM) for 2 hours prior to H. pylori infection and cultured for 6 hours (for determination of the levels of p-GSK3β, GSK3β, and β-catenin) and 24 hours (for determination of cell viability and protein levels of c-myc and cyclin E). Cell viability was determined by the MTT assay and protein levels were determined via western blot-based analysis. RESULTS: β-Carotene inhibited H. pylori-induced increases in the percentage of viable cells, phosphorylated GSK3β (p-GSK3β), and the levels of β-catenin, c-myc and cyclin E. CONCLUSIONS: β-Carotene inhibits H. pylori-induced hyper-proliferation of gastric epithelial cells by suppressing β-catenin signaling and oncogene expression.

The Roles of miRNAs in Medulloblastoma: A Systematic Review

Medulloblastoma is considered one of the most threatening malignant brain tumors with an extremely high mortality rate in children. In the medulloblastoma, there are several genes and mutations found to work in an unregulated manner that works together to push the cells into a cancerous state. With the discovery of non-coding RNAs such as microRNAs (miRNAs), it has been shown that a different layer of gene regulations may be disrupted which would cause cancer. This fact led scientists to put their focus on the role of miRNAs in cancer. A mature miRNA contains a seed sequence which gives the miRNA to identify and attach to the interest mRNA; this attachment may lead degradation of mRNA or suppress of translation of the mRNA. The expression of miRNAs in medulloblastoma shows that some of these non-coding RNAs are overexpressed (OncomiRs) which help cells to proliferate and keep their stemness features. On the other hand, there are other forms of these miRNAs which normally inhibit cell proliferation and promote cell differentiation (tumor suppressor). These are down-regulated during cancer progression. In this systematic review, we attempted to gather several important studies on miRNAs’ role in medulloblastoma tumors and the importance of these non-coding RNAs in the future study of cancer.

KIF11 Functions as an Oncogene and Is Associated with Poor Outcomes from Breast Cancer / Journal of the Korean Cancer Association, 대한암학회지

PURPOSE: The study aimed to search and identify genes that were differentially expressed in breast cancer, and their roles in cancer growth and progression. MATERIALS AND METHODS: The Gene Expression Omnibus (Oncomine) and The Cancer Genome Atlas databases (https://cancergenome.nih.gov/) were screened for genes that were expressed differentially in breast cancer and were closely related to a poor prognosis. Gene expressions were verified by quantitative real-time polymerase chain reaction, and genes were knocked down by a lentivirus-based system. Cell growth and motility were evaluated and in vivo nude mice were used to confirm the in vitro roles of genes. Markers of epithelial-to-mesenchymal transition and the associations of KIF11 with the classical cancer signaling pathways were detected by Western blot. RESULTS: A series of genes expressed differentially in patients with breast cancer. The prognosis associated with high KIF11 expression was poor, and the expression of KIF11 increased significantly in high stage and malignant tumor cells. Inhibiting KIF11 expression in lentivirus-suppressed cells revealed that KIF11 inhibition significantly reduced cell viability and colony formation, inhibited migration and invasion, but promoted apoptosis. The sizes and weights of KIF11-inhibited tumors in nude mice were significantly lower than in the negative controls. Western blot showed that E-cadherin in breast cancer was significantly upregulated in KIF-inhibited cells and tumor tissues, whereas N-cadherin and vimentin were significantly down-regulated. BT549 and MDA231 cells with KIF11 knockdown exhibited decreased ERK, AMPK, AKT, and CREB phosphorylation. CONCLUSION: KIF11 acts as a potential oncogene that regulates the development and progression of breast cancer.

Gliomas malignos: biología molecular y detalles oncogenéticos / Wicked gliomas: molecular biology and oncogenetics detail

RESUMEN La biología de los gliomas malignos se asocia con el balance de la expresión de las proteínas que controlan de manera positiva o negativa el ciclo celular, la proliferación, la motilidad, la neoformación vascular y el reconocimiento del sistema inmune. La frecuencia de las alteraciones genéticas que están presentes en GBM2 y GBM1 son diferentes así como la edad de los pacientes en la que se presentan. Mientras que los GBM1 suelen aparecer en edades más tardías, alrededor de los 60-70 años, los GBM2 suelen presentarse en edades más tempranas, 40-50 años. En la génesis del glioblastoma existen alteraciones moleculares a nivel de genes supresores de tumores, oncogenes y genes reparadores de ADN (AU).

ABSTRACT The glioblastoma it is the primary wicked tumor of the central nervous system more common in adults and it invariably associates to a bad presage. The biology of the wicked gliomas associates with the balance of the expression of the proteins that they control of positive way or negative the cellular cycle, the proliferation, the motility, the vascular neoformation and the recognition of the immune system. The frequency of the genetic alterations that they are present in GBM2 and GBM1 is different. While the GBM1 usually appears in later ages, around the 60-70 years, the GBM2 usually presents in earlier ages, 40-50 years. In the genesis of the glioblastoma exist molecular alterations at level of suppressive genes of tumors (GST), oncogenes and reparative genes of DNA (AU).

Revisión sistemática: estrategias virales para la inducción de cáncer "virus de Epstein-Barr: latencia y mecanismos asociados a la oncogénesis viral" / Viral strategies for cancer induction "Epstein-Barr virus: latency and mechanisms associated with viral oncogenesis"

Resumen La infección crónica con virus oncogénicos es responsable de aproximadamente el 20% de todos los cánceres reportados en humanos, este proceso de oncogénesis viral presenta una naturaleza compleja, multietapa y multifactorial. Un ejemplo de ello es el Virus de Epstein- Barr (EBV), un herpesvirus que infecta de manera latente a más del 90% de la población. Aunque la infección a menudo cursa de manera asintomática, el EBV es capaz de modificar su expresión genómica estableciendo diferentes fases de latencia, alterando así el metabolismo de sus células blanco, como son los linfocitos B y las células epiteliales, proceso que resulta determinante en la aparición y desarrollo de diferentes patologías que van desde la mononucleosis infecciosa hasta procesos oncológicos como el linfoma de Burkitt, el cáncer gástrico o el cáncer nasofaríngeo.

Abstract Chronic infection with oncogenic viruses is responsible for approximately 20% of all cancers worldwide in humans, this viral transformation represents a complex, multistage and multifactorial process. An example is the Epstein-Barr virus (EBV), a herpesvirus that latently infects over 90% of the population. Although the infection often courses asymptomatically, EBV is able to modify its genomic expression by establishing different latency phases, thus altering the B lymphocytes and epithelial cells metabolism, a determinant process in the appearance and development of different pathologies ranging from infectious mononucleosis to oncological processes such as Burkitt's lymphoma, gastric cancer and nasopharyngeal cancer.