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

Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

15.5K
Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
15.5K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

3.4K
No description available
3.4K
Tumor Progression02:07

Tumor Progression

7.8K
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...
7.8K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

7.4K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
7.4K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

4.3K
No description available
4.3K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

6.3K
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...
6.3K

También podría leer

Artículos Relacionados

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

Ordenar por
Same author

Advancements in extracellular vesicle research.

Extracellular vesicle·2026
Same author

A New Filter for Isolation of Circulating Tumor Cells by Only Blood Filtration.

Methods in molecular biology (Clifton, N.J.)·2026
Same author

Anti-PD-1 plus anti-CTLA-4 blockade overcomes immune exclusion in NSCLC brain metastases by enhancing CD8<sup>+</sup> T cell responses and promoting tertiary lymphoid structure formation.

Nature communications·2026
Same author

Real-time, automated, standardized, and transparent analysis of microfluidic nanoparticle data with RPS<sub>PASS</sub>.

bioRxiv : the preprint server for biology·2026
Same author

Impact of Pathological Lymphovascular Invasion of Lung Adenocarcinoma after Induction Chemoradiotherapy.

Annals of thoracic and cardiovascular surgery : official journal of the Association of Thoracic and Cardiovascular Surgeons of Asia·2026
Same author

Initial chemotherapy decreases transfusion dependence and enables definitive therapy in metastatic thymoma complicated by pure red cell aplasia: A case report.

Oncology letters·2026

Video Experimental Relacionado

Updated: Mar 29, 2026

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
10:21

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma

Published on: September 20, 2024

948

Las mutaciones somáticas afectan a las vías clave en el adenocarcinoma pulmonar.

Li Ding1, Gad Getz, David A Wheeler

  • 1The Genome Center at Washington University, Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63108, USA.

Nature
|October 25, 2008
PubMed
Resumen

Los investigadores descubrieron más de 1.000 mutaciones somáticas en 188 adenocarcinomas pulmonares, identificando 26 genes con mutaciones frecuentes que probablemente estén involucrados en el desarrollo del cáncer. Estos hallazgos ofrecen nuevos objetivos moleculares para el tratamiento del cáncer de pulmón.

Más Videos Relacionados

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
09:38

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Published on: August 11, 2017

9.3K
Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
11:15

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

25.2K

Videos de Experimentos Relacionados

Last Updated: Mar 29, 2026

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
10:21

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma

Published on: September 20, 2024

948
Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
09:38

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Published on: August 11, 2017

9.3K
Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
11:15

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

25.2K

Área de la Ciencia:

  • Oncología Oncología.
  • Genética La genética.
  • Biología Molecular Biología Molecular

Sus antecedentes:

  • Comprender la base genética del cáncer requiere analizar grandes colecciones de tumores.
  • El adenocarcinoma pulmonar es una causa importante de mortalidad relacionada con el cáncer, lo que requiere conocimientos genéticos más profundos.

Objetivo del estudio:

  • Para identificar las mutaciones somáticas en los adenocarcinomas pulmonares primarios.
  • Descubrir genes con frecuencia mutados en el adenocarcinoma pulmonar y su posible papel en la carcinogénesis.
  • Para correlacionar los perfiles mutacionales con las características clínicas y los defectos de reparación del ADN.

Principales métodos:

  • Secuenciación completa del ADN de 623 genes relacionados con el cáncer en 188 adenocarcinomas pulmonares primarios.
  • Análisis estadístico para identificar genes significativamente mutados.
  • Integración de datos con una matriz de polimorfismo de un solo nucleótido y datos de matriz de expresión génica.

Principales resultados:

  • Se identificaron más de 1.000 mutaciones somáticas en las muestras.
  • 26 genes, incluidas las tirosinacinasas (ERBB4, EPHA3, KDR, NTRK), fueron frecuentemente mutados.
  • Se encontraron mutaciones somáticas en genes supresores de tumores conocidos (NF1, APC, RB1, ATM) y otros genes (PTPRD, LRP1B).
  • Los perfiles mutacionales se correlacionan con las características clínicas, el estado de fumar y los defectos de reparación del ADN.

Conclusiones:

  • El estudio identificó las principales vías de señalización involucradas en el desarrollo del adenocarcinoma pulmonar.
  • Los genes con mutaciones frecuentes representan objetivos moleculares potenciales para nuevas terapias contra el cáncer de pulmón.
  • Las alteraciones genéticas proporcionan información sobre la patogénesis del adenocarcinoma pulmonar.