Jove
Visualize
Contáctanos
JoVE
x logofacebook logolinkedin logoyoutube logo
ACERCA DE JoVE
Visión GeneralLiderazgoBlogCentro de Ayuda JoVE
AUTORES
Proceso de PublicaciónConsejo EditorialAlcance y PolíticasRevisión por ParesPreguntas FrecuentesEnviar
BIBLIOTECARIOS
TestimoniosSuscripcionesAccesoRecursosConsejo Asesor de BibliotecasPreguntas Frecuentes
INVESTIGACIÓN
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchivo
EDUCACIÓN
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualCentro de Recursos para ProfesoresSitio de Profesores
Términos y Condiciones de Uso
Política de Privacidad
Políticas

Videos de Conceptos Relacionados

Epigenetic Regulation01:37

Epigenetic Regulation

3.4K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
3.4K
Epigenetic Regulation01:46

Epigenetic Regulation

32.1K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
32.1K
Gene-Environment Interactions01:20

Gene-Environment Interactions

841
Gene expression is a dynamic process that is significantly influenced by environmental factors. This interaction underlies the complex nature of biological development and the phenotypic differences observed among individuals, even among those with identical genetic makeups. Factors such as radiation, temperature, behavior, nutrition, and stress play pivotal roles in determining how genes are expressed. The concept of the reaction range is central to understanding this interaction. It posits...
841
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

1.7K
Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
1.7K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

5.5K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
5.5K
Cancer Prevention02:59

Cancer Prevention

7.2K
Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
Some...
7.2K

También podría leer

Artículos Relacionados

Artículos vinculados a este trabajo por autores compartidos, revista y gráfico de citas.

Ordenar por
Same author

L1CAM signaling through planar cell polarity drives SOX2 expression and lung adenocarcinoma metastasis.

Nature communications·2026
Same author

Hierarchical classification of immune cell transcriptomes at population-scale.

bioRxiv : the preprint server for biology·2026
Same author

GATA4 loss promotes mutant <i>Kras</i>-driven pancreatic ductal adenocarcinoma in the absence of canonical precursor lesions.

bioRxiv : the preprint server for biology·2026
Same author

Plasma signals of lung tumor promotion for molecular cancer prevention.

Cell·2026
Same author

Scalable genotyping in fixed transcriptomes resolves clonal heterogeneity via single-cell sequencing.

bioRxiv : the preprint server for biology·2026
Same author

Immune Checkpoint Therapy Drives Maturation of a Cellular Neighborhood Nucleated by T Cell-APC Triads Enabling Spatially Compartmentalized Tumor Immunity.

bioRxiv : the preprint server for biology·2026

Video Experimental Relacionado

Updated: Nov 18, 2025

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
08:14

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia

Published on: July 25, 2017

15.5K

Un programa epigenético inducido por el entorno genético inicia la tumorigénesis

Direna Alonso-Curbelo1, Yu-Jui Ho1, Cassandra Burdziak2,3

  • 1Cancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Nature
|February 4, 2021
PubMed
Resumen

El daño tisular y las mutaciones de Kras crean rápidamente un estado epigenético único en las células pancreáticas, impulsando el desarrollo temprano del cáncer. Este interruptor molecular, que involucra a la interleucina 33, explica cómo los factores genéticos y ambientales inician el cáncer de páncreas.

Más Videos Relacionados

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
10:41

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues

Published on: April 5, 2018

10.6K
Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA
04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA

Published on: December 19, 2019

14.9K

Videos de Experimentos Relacionados

Last Updated: Nov 18, 2025

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
08:14

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia

Published on: July 25, 2017

15.5K
An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
10:41

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues

Published on: April 5, 2018

10.6K
Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA
04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA

Published on: December 19, 2019

14.9K

Área de la Ciencia:

  • En el campo de la oncología
  • La epigenética
  • Biología molecular

Sus antecedentes:

  • El daño tisular es un factor de riesgo conocido para el cáncer, pero los mecanismos subyacentes siguen sin estar claros.
  • En el cáncer de páncreas, la pancreatitis y las mutaciones en el gen Kras aceleran la formación de tumores.
  • La comprensión de las interacciones entre genes y entorno es crucial para la investigación de la iniciación del cáncer.

Objetivo del estudio:

  • Para investigar cómo las mutaciones de Kras y el daño tisular interactúan para promover el cáncer de páncreas.
  • Identificar los primeros cambios moleculares y epigenéticos que impulsan la transformación neoplásica.
  • Para aclarar el papel de las vías de señalización específicas, como la interleucina 33, en la iniciación del cáncer.

Principales métodos:

  • Se utilizaron modelos autóctonos de cáncer de páncreas en ratones.
  • Genómica integrada, ensayos de cromatina de una sola célula y perturbaciones funcionales.
  • Se analizaron los cambios espaciotemporales en el epitelio pancreático después de la lesión y la mutación de Kras.

Principales resultados:

  • La mutación de Kras y el daño tisular inducen un estado distinto de cromatina en el epitelio pancreático, diferenciando la neoplasia de la regeneración.
  • Este cambio de cromatina de "acinar a neoplasia" ocurre dentro de las 48 horas de la lesión, desregulando los genes clave asociados con el cáncer.
  • La interleucina 33 se activa rápidamente después de la lesión y coopera con el Kras mutante para impulsar la reprogramación epigenética y la transformación neoplásica.

Conclusiones:

  • Las interacciones entre genes y entornos establecen rápidamente programas de regulación genética que comprometen a las células al desarrollo neoplásico.
  • Se proporciona un marco molecular para comprender cómo los factores genéticos y ambientales inician el cáncer de páncreas.
  • El estudio destaca el papel crítico de las alteraciones epigenéticas en el desarrollo temprano del cáncer.