{"id":6408,"date":"2015-11-02T17:57:18","date_gmt":"2015-11-03T01:57:18","guid":{"rendered":"https:\/\/vermont.salk.edu\/?post_type=disclosure&#038;p=6408"},"modified":"2024-01-30T15:50:53","modified_gmt":"2024-01-30T23:50:53","slug":"molecular-brake-stifles-human-lung-cancer","status":"publish","type":"disclosure","link":"https:\/\/www.salk.edu\/es\/news-release\/molecular-brake-stifles-human-lung-cancer\/","title":{"rendered":"El \u201cfreno\u201d molecular sofoca el c\u00e1ncer de pulm\u00f3n en humanos"},"content":{"rendered":"<p>LA JOLLA\u2013Cient\u00edficos del Instituto Salk descubrieron una mol\u00e9cula cuya mutaci\u00f3n conduce al crecimiento agresivo de un tipo com\u00fan y mortal de c\u00e1ncer de pulm\u00f3n. <a href=\"https:\/\/www.salk.edu\/es\/ra\/cancer.html\/\">c\u00e1ncer<\/a> en humanos.<\/p>\n<p>Esta enzima, llamada EphA2, normalmente vigila un gen responsable del crecimiento de tejidos. Pero cuando EphA2 se muta, el equipo de Salk descubri\u00f3, los sistemas celulares pueden descontrolarse y desarrollar tumores r\u00e1pidamente. El nuevo trabajo, publicado la semana del 2 de noviembre de 2015 en <em>PNAS<\/em>, sugiere que EphA2 podr\u00eda ser un nuevo objetivo para un subconjunto de c\u00e1ncer de pulm\u00f3n, que afecta tanto a no fumadores como a fumadores, y es la principal causa de muertes relacionadas con el c\u00e1ncer en todo el mundo.<\/p>\n<div class=\"imageCaption530\">\n<img decoding=\"async\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2015\/01\/2129-EphA2-verma.jpg\" alt=\"\" \/>\n<p>Cient\u00edficos de Salk descubren una mol\u00e9cula en humanos llamada EphA2 que act\u00faa como supresora de tumores en ciertos tipos de c\u00e1ncer de pulm\u00f3n. Esta imagen muestra tejido pulmonar normal de rat\u00f3n (izquierda) y pulmones con tumores resultantes de una mutaci\u00f3n KRAS (centro). Cuando se elimina EphA2, la mutaci\u00f3n KRAS resulta en muchos m\u00e1s tumores y de mayor tama\u00f1o durante el mismo per\u00edodo de tiempo (derecha).<\/p>\n<p><a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2015\/02\/2129-EphA2-verma.jpg\" target=\"_blank\" rel=\"noopener\">Haga clic aqu\u00ed<\/a> para obtener una imagen en alta resoluci\u00f3n.<\/p>\n<p>Imagen: Cortes\u00eda del Instituto Salk de Estudios Biol\u00f3gicos<\/p>\n<\/div>\n<p>\u201cA veces, hay cientos de mutaciones en los genes de los tumores de un paciente, pero no se sabe si son impulsoras de la enfermedad o subproductos\u201d, dice el autor principal. <a href=\"https:\/\/www.salk.edu\/es\/faculty\/verma.html\/\">Inder Verma<\/a>, profesor de gen\u00e9tica y titular de la C\u00e1tedra Irwin y Joan Jacobs de Ciencias Ejemplares de la Vida en Salk. \u201cEncontramos una nueva forma de identificar genes supresores de tumores y comprender c\u00f3mo podr\u00edan ser el objetivo de terapias\u201d.\u201d<\/p>\n<p>Dos mutaciones gen\u00e9ticas en particular son conocidas por estimular el crecimiento de tumores humanos: KRAS y p53. Aunque ambos genes han sido estudiados exhaustivamente, son dif\u00edciles de tratar terap\u00e9uticamente, por lo que el equipo Salk decidi\u00f3 buscar genes que pudieran controlar KRAS y p53 en su lugar.<\/p>\n<p>Los investigadores se enfocaron en los 4.700 genes del genoma humano relacionados con la se\u00f1alizaci\u00f3n celular, espec\u00edficamente, genes que tienen la capacidad de disminuir el crecimiento y la proliferaci\u00f3n celular. Luego, el equipo adapt\u00f3 una t\u00e9cnica de cribado gen\u00e9tico para probar de manera r\u00e1pida y eficiente el efecto de estos miles de genes en el desarrollo de tumores. En modelos animales, el equipo de Salk descubri\u00f3 que 16 de estos genes de se\u00f1alizaci\u00f3n celular produc\u00edan mol\u00e9culas que ten\u00edan un efecto significativo en los tumores relacionados con KRAS y p53.<\/p>\n<p>De estas 16 mol\u00e9culas, una destac\u00f3 especialmente: la enzima EphA2, descubierta originalmente en el laboratorio de otro cient\u00edfico de Salk, <a href=\"https:\/\/www.salk.edu\/es\/faculty\/hunter.html\/\">Tony Hunter<\/a>. Anteriormente, la importancia de EphA2 en el c\u00e1ncer de pulm\u00f3n no estaba clara, pero el equipo descubri\u00f3 que su ausencia hac\u00eda que los tumores asociados a KRAS crecieran de forma mucho m\u00e1s agresiva.<\/p>\n<p>\u201cCon una mutaci\u00f3n en KRAS, un tumor se forma en 300 d\u00edas. Pero sin EphA2, la mutaci\u00f3n KRAS conduce a tumores en la mitad de tiempo, de 120 a 150 d\u00edas\u201d, afirma Verma, quien tambi\u00e9n es Profesor de Biolog\u00eda Molecular de la American Cancer Society. \u201cEsta mol\u00e9cula EphA2 tiene un enorme efecto en la restricci\u00f3n del crecimiento del c\u00e1ncer cuando KRAS est\u00e1 mutado\u201d. KRAS mutado es un culpable com\u00fan en aproximadamente entre el 10 y el 20 por ciento de todos los c\u00e1nceres, particularmente el c\u00e1ncer de colon y el c\u00e1ncer de pulm\u00f3n humano.<\/p>\n<div class=\"imageCaption530\">\n<img decoding=\"async\" src=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2015\/01\/2129-Yifeng-Xia_Eugene-Ke_Narayana-Yeddula_Inder-Verma.jpg\" alt=\"\" \/>\n<p>De izquierda a derecha: los investigadores de Salk Yifeng Xia, Eugene Ke, Narayana Yeddula e Inder Verma<\/p>\n<p><a href=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2015\/02\/2129-Yifeng-Xia_Eugene-Ke_Narayana-Yeddula_Inder-Verma.jpg\" target=\"_blank\" rel=\"noopener\">Haga clic aqu\u00ed<\/a> para obtener una imagen en alta resoluci\u00f3n.<\/p>\n<p>Imagen: Cortes\u00eda del Instituto Salk de Estudios Biol\u00f3gicos<\/p>\n<\/div>\n<p>\u201cDado que la activaci\u00f3n de EphA2 llev\u00f3 a la supresi\u00f3n tanto de la se\u00f1alizaci\u00f3n celular como de la proliferaci\u00f3n celular, creemos que la enzima podr\u00eda servir como un posible objetivo farmacol\u00f3gico en el adenocarcinoma de pulm\u00f3n dependiente de KRAS\u201d, dice Narayana Yeddula, asociada de investigaci\u00f3n de Salk y primera autora del art\u00edculo.<\/p>\n<p>Un proyecto nacional de 10 a\u00f1os llamado The Cancer Genome Atlas mape\u00f3 los genomas de cientos de pacientes con m\u00e1s de 20 tipos de c\u00e1ncer diferentes y descubri\u00f3 varias mutaciones gen\u00e9ticas relacionadas, aunque el papel de estas mutaciones no se ha entendido bien en el c\u00e1ncer de pulm\u00f3n (especialmente el adenocarcinoma, que representa casi una cuarta parte de todos los c\u00e1nceres de pulm\u00f3n). A partir de los datos del Cancer Genome Atlas, el equipo de Salk descubri\u00f3 que las alteraciones gen\u00e9ticas de EphA2 se detectaron en 54 de 230 pacientes con adenocarcinoma. El equipo tambi\u00e9n descubri\u00f3, sorprendentemente, que la p\u00e9rdida de EphA2 activaba una v\u00eda com\u00fanmente asociada con el c\u00e1ncer (denominada Hedgehog) que promueve el crecimiento tumoral.<\/p>\n<p>\u201cCuriosamente, entre los pacientes humanos con c\u00e1ncer de pulm\u00f3n y mutaciones en EphA2, alrededor del 8 por ciento de los pacientes tienen en realidad una alta expresi\u00f3n de EphA2. Por lo tanto, en algunos casos, EphA2 no est\u00e1 suprimiendo tumores y puede depender del contexto. Por ello, necesitamos evaluar cuidadosamente la funci\u00f3n de la mol\u00e9cula al dise\u00f1ar nuevas terapias\u201d, a\u00f1ade Yifeng Xia, investigadora del personal de Salk involucrada en el trabajo.<\/p>\n<p>Otros autores del art\u00edculo fueron Eugene Ke del Instituto Salk y Joep Beumer del Instituto Salk y del Instituto Hubrecht en los Pa\u00edses Bajos.<\/p>\n<p>Este trabajo fue apoyado en parte por un <a href=\"http:\/\/nih.gov\" target=\"_blank\" rel=\"noopener\">NIH<\/a> subvenci\u00f3n Salk Cancer Center Core, <a href=\"http:\/\/www.ipsen.com\/en\/\" target=\"_blank\" rel=\"noopener\">Ipsen<\/a>, la <a href=\"http:\/\/www.hnberger.org\/\" target=\"_blank\" rel=\"noopener\">Fundaci\u00f3n H.N. and Frances C. Berger<\/a>, y el <a href=\"http:\/\/helmsleytrust.org\/\" target=\"_blank\" rel=\"noopener\">Fundaci\u00f3n Ben\u00e9fica Leona M. y Harry B. Helmsley<\/a>.<\/p>","protected":false},"featured_media":6409,"template":"","faculty":[115],"disease-research":[46,164],"class_list":["post-6408","disclosure","type-disclosure","status-publish","has-post-thumbnail","hentry","faculty-inder-verma","disease-research-cancer-biology","disease-research-lung-cancer"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.3 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Molecular &quot;brake&quot; stifles human lung cancer - Salk Institute for Biological Studies<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.salk.edu\/es\/news-release\/molecular-brake-stifles-human-lung-cancer\/\" \/>\n<meta property=\"og:locale\" content=\"es_MX\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Molecular &quot;brake&quot; stifles human lung cancer - Salk Institute for Biological Studies\" \/>\n<meta property=\"og:description\" content=\"LA JOLLA\u2013Scientists at the Salk Institute have uncovered a molecule whose mutation leads to the aggressive growth of a common and deadly type of lung cancer in humans.\" \/>\n<meta property=\"og:url\" content=\"https:\/\/www.salk.edu\/es\/news-release\/molecular-brake-stifles-human-lung-cancer\/\" \/>\n<meta property=\"og:site_name\" content=\"Salk Institute for Biological Studies\" \/>\n<meta property=\"article:modified_time\" content=\"2024-01-30T23:50:53+00:00\" \/>\n<meta property=\"og:image\" content=\"https:\/\/www.salk.edu\/wp-content\/uploads\/2015\/11\/2129.jpg\" \/>\n\t<meta property=\"og:image:width\" content=\"180\" \/>\n\t<meta property=\"og:image:height\" content=\"179\" \/>\n\t<meta property=\"og:image:type\" content=\"image\/jpeg\" \/>\n<meta name=\"twitter:card\" content=\"summary_large_image\" \/>\n<meta name=\"twitter:label1\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data1\" content=\"5 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/www.salk.edu\\\/news-release\\\/molecular-brake-stifles-human-lung-cancer\\\/\",\"url\":\"https:\\\/\\\/www.salk.edu\\\/news-release\\\/molecular-brake-stifles-human-lung-cancer\\\/\",\"name\":\"Molecular \\\"brake\\\" stifles human lung cancer - Salk Institute for Biological Studies\",\"isPartOf\":{\"@id\":\"https:\\\/\\\/www.salk.edu\\\/#website\"},\"primaryImageOfPage\":{\"@id\":\"https:\\\/\\\/www.salk.edu\\\/news-release\\\/molecular-brake-stifles-human-lung-cancer\\\/#primaryimage\"},\"image\":{\"@id\":\"https:\\\/\\\/www.salk.edu\\\/news-release\\\/molecular-brake-stifles-human-lung-cancer\\\/#primaryimage\"},\"thumbnailUrl\":\"https:\\\/\\\/www.salk.edu\\\/wp-content\\\/uploads\\\/2015\\\/11\\\/2129.jpg\",\"datePublished\":\"2015-11-03T01:57:18+00:00\",\"dateModified\":\"2024-01-30T23:50:53+00:00\",\"breadcrumb\":{\"@id\":\"https:\\\/\\\/www.salk.edu\\\/news-release\\\/molecular-brake-stifles-human-lung-cancer\\\/#breadcrumb\"},\"inLanguage\":\"es-MX\",\"potentialAction\":[{\"@type\":\"ReadAction\",\"target\":[\"https:\\\/\\\/www.salk.edu\\\/news-release\\\/molecular-brake-stifles-human-lung-cancer\\\/\"]}]},{\"@type\":\"ImageObject\",\"inLanguage\":\"es-MX\",\"@id\":\"https:\\\/\\\/www.salk.edu\\\/news-release\\\/molecular-brake-stifles-human-lung-cancer\\\/#primaryimage\",\"url\":\"https:\\\/\\\/www.salk.edu\\\/wp-content\\\/uploads\\\/2015\\\/11\\\/2129.jpg\",\"contentUrl\":\"https:\\\/\\\/www.salk.edu\\\/wp-content\\\/uploads\\\/2015\\\/11\\\/2129.jpg\",\"width\":180,\"height\":179},{\"@type\":\"BreadcrumbList\",\"@id\":\"https:\\\/\\\/www.salk.edu\\\/news-release\\\/molecular-brake-stifles-human-lung-cancer\\\/#breadcrumb\",\"itemListElement\":[{\"@type\":\"ListItem\",\"position\":1,\"name\":\"Home\",\"item\":\"https:\\\/\\\/www.salk.edu\\\/\"},{\"@type\":\"ListItem\",\"position\":2,\"name\":\"Molecular &#8220;brake&#8221; 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