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

Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Treatment Resistent Cancers02:56

Treatment Resistent Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.

También podría leer

Artículos Relacionados

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

Ordenar por
Same author

A lncRNA-mediated metabolic rewiring of cell senescence.

Cell reports·2025
Same author

The lncRNA DUBR is regulated by CTCF and coordinates chromatin landscape and gene expression in hematopoietic cells.

Nucleic acids research·2025
Same author

Author Correction: Uncovering functional lncRNAs by scRNA-seq with ELATUS.

Nature communications·2025
Same author

Uncovering functional lncRNAs by scRNA-seq with ELATUS.

Nature communications·2024
Same author

Novel protocol for the transcriptomic analysis of endothelial extracellular vesicles in atherosclerosis.

Clinica e investigacion en arteriosclerosis : publicacion oficial de la Sociedad Espanola de Arteriosclerosis·2024
Same author

YTHDC1 m<sup>6</sup>A-dependent and m<sup>6</sup>A-independent functions converge to preserve the DNA damage response.

The EMBO journal·2024

Video Experimental Relacionado

Updated: Jun 14, 2026

Potentiation of Anticancer Antibody Efficacy by Antineoplastic Drugs: Detection of Antibody-drug Synergism Using the Combination Index Equation
15:04

Potentiation of Anticancer Antibody Efficacy by Antineoplastic Drugs: Detection of Antibody-drug Synergism Using the Combination Index Equation

Published on: January 19, 2019

Un "contro potenciador" en la supresión de tumores

Francesco P Marchese1, Maite Huarte1

  • 1University of Navarra, Center for Applied Medical Research (CIMA), Pamplona 31008, Spain; Institute of Health Research of Navarra (IdiSNA), Pamplona 31008, Spain.

Cell
|June 2, 2018
PubMed
Resumen

Los investigadores descubrieron un nuevo mecanismo que regula la expresión del gen MYC. Un elemento de ADN dentro del gen PVT1 actúa como competidor de los promotores y potenciadores, lo que sugiere que puede funcionar como supresor de tumores.

Más Videos Relacionados

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells
09:04

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

Videos de Experimentos Relacionados

Last Updated: Jun 14, 2026

Potentiation of Anticancer Antibody Efficacy by Antineoplastic Drugs: Detection of Antibody-drug Synergism Using the Combination Index Equation
15:04

Potentiation of Anticancer Antibody Efficacy by Antineoplastic Drugs: Detection of Antibody-drug Synergism Using the Combination Index Equation

Published on: January 19, 2019

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
07:02

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells
09:04

Analysis of Human T Cell Activity in an Allogeneic Co-Culture Setting of Pre-Treated Tumor Cells

Published on: March 7, 2025

Área de la Ciencia:

  • Biología del cáncer
  • La genómica
  • Biología molecular

Sus antecedentes:

  • El papel del genoma no codificante en el cáncer es cada vez más reconocido.
  • La expresión del gen MYC es crítica en el desarrollo y la progresión del cáncer.

Objetivo del estudio:

  • Para aclarar un nuevo mecanismo de regulación para la expresión MYC.
  • Para investigar la función de un elemento específico de ADN dentro del gen PVT1.

Principales métodos:

  • Análisis de la regulación genética.
  • Investigando las interacciones promotor-potenciador.
  • Estudios funcionales de los elementos del ADN.

Principales resultados:

  • Un elemento de ADN dentro del gen PVT1 regula la expresión de MYC.
  • Este elemento funciona como un competidor promotor y potenciador.
  • El elemento muestra potencial como supresor de tumores.

Conclusiones:

  • Se ha identificado un nuevo mecanismo para la regulación de MYC que involucra la secuencia promotora del gen PVT1.
  • Este elemento regulador actúa como un competidor promotor y potenciador.
  • Los hallazgos sugieren un potencial papel supresor de tumores para este elemento de ADN.