INTERNATIONAL CANCER GENOME CONSORTIUM

Este es el proyecto global en el que participa el INMEGEN. El ICGC es uno de los dos proyectos más grandes a nivel mundial (el oro es el TCGA). México es el único país latinoamericano en participar. En él están 13 países y 390 grupos de investigación.

ICGC Goal: To obtain a comprehensive description of genomic, transcriptomic and epigenomic changes in 50 different tumor types and/or subtypes which are of clinical and societal importance across the globe.

!Al final esperamos tener 18000 tumores secuenciados!

 

Pueden echarle un vistazo en icgc.org

 

Curso

Elsevier y el Instituto Nacional de Medicina Genómica tienen el honor de invitarle a participar y a convocar a personas interesadas en recibir un Taller para Autores y Editores.

El Taller para Autores está dirigido a científicos de todas las edades y disciplinas que quieran obtener guías de ¿Cómo publicar un artículo científico para revistas internacionales?. Y el taller para Editores está dirigido a personas que editan revistas científicas de todas las áreas de investigación para proveerles guías sobre la Profesionalización de las revistas científicas en la era de la información.

Día:
lunes 26 de marzo 2012

Lugar:
Instituto Nacional de Medicina Genómica (INMEGEN nueva sede)

Dirección:
Periférico Sur No. 4809 Col. Arenal Tepepan, Delegación Tlalpan México, D.F. C.P. 14610
Entrada SÓLO por: Arenal S/N esquina Xochimaltzin. Ver Mapa

Horarios:
Taller para Autores: de 9:00 a 13:30 horas 
Taller para Editores: de 16:00 a 19:30 horas

Entrada Gratuita. Cupo Limitado

Ver la agenda detallada del evento.

Favor de reservar su lugar AQUÍ ó con la Lic. Ana Laura Pavón al teléfono 5350-1900 ext.1933 o al correo electrónico alpavon@inmegen.gob.mx.

Antiangiogenic therapy and Cancer Stem Cells

Antiangiogenic agents increase breast cancer stem cells via the generation of tumor hypoxia [Medical Sciences]

de Conley, S. J., Gheordunescu, E., Kakarala, P., Newman, B., Korkaya, H., Heath, A. N., Clouthier, S. G., Wicha, M. S.

Antiangiogenic therapy has been thought to hold significant potential for the treatment of cancer. However, the efficacy of such treatments, especially in breast cancer patients, has been called into question, as recent clinical trials reveal only limited effectiveness of antiangiogenic agents in prolonging patient survival. New research using preclinical models further suggests that antiangiogenic agents actually increase invasive and metastatic properties of breast cancer cells. We demonstrate that by generating intratumoral hypoxia in human breast cancer xenografts, the antiangiogenic agents sunitinib and bevacizumab increase the population of cancer stem cells. In vitro studies revealed that hypoxia-driven stem/progenitor cell enrichment is primarily mediated by hypoxia-inducible factor 1α. We further show that the Akt/β-catenin cancer stem cell regulatory pathway is activated in breast cancer cells under hypoxic conditions in vitro and in sunitinib-treated mouse xenografts. These studies demonstrate that hypoxia-driven cancer stem cell stimulation limits the effectiveness of antiangiogenic agents, and suggest that to improve patient outcome, these agents might have to be combined with cancer stem cell-targeting drugs.

Algunos Webcast para publicar

http://www.elsevier.com/wps/find/authorsview.authors/trainingwebcasts

CNN

Entrevista

Microarreglos no tan exactos

Concerning the Affymetrix™ human genotyping array, we detected 25 differences (5 in different chromosomes), of which 10 (40%) were in different genes. These 25 discrepancies lead to 61,916 SNPs being in a different genomic order, with 89% being less or equal than 2 indexes away (Data S5). By checking manually a subset of those alignment discrepancies, we found that the Affymetrix™ mismappings were due to their hit not being perfect, having one or more extra SNPs on the SNP flanking sequence, or having less flanking sequence aligned. With the Illumina's™ human beadchip, 271 SNPs have different genomic positions (with 22 on different chromosomes), of which 59 (22%) are on different genes. The 271 discrepancies lead to 131,378 SNPs being in a different genomic order, although 98% are less or equal than two indexes away (Data S6). By checking manually a subset of those alignment discrepancies, we found that the Illumina™ mismappings were due to their hit not being perfect, having one or more extra SNPs on the SNP flanking sequence, or having less flanking sequence aligned.


Fuente
Fadista J , Bendixen C , 2012 Genomic Position Mapping Discrepancies of Commercial SNP Chips. PLoS ONE 7(2): e31025. doi:10.1371/journal.pone.0031025