Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Targeted Cancer Therapies

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...

Combination Therapies and Personalized Medicine

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...

Treatment Resistent Cancers

Treatment Resistent Cancers

Treatment Resistant Cancers

Treatment Resistant 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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Cellular therapy in mantle cell lymphoma: recommendations from the EBMT practice harmonisation and guidelines committee.

Bone marrow transplantation·2026

Same author

Spatial and multi-omic profiling reveals pericyte-derived CCL19 as a key prognostic factor in CNS lymphoma.

HemaSphere·2026

Same author

A Phase Ib Trial of Copanlisib in Combination with Venetoclax in Patients with Relapsed or Refractory B-Cell Non-Hodgkin Lymphoma-SAKK 66/18 Trial.

Cancers·2026

Same author

High-risk single-refractory and double-refractory chronic lymphocytic leukemia: feasibility and impact of alloHCT.

Blood advances·2026

Same author

Treatment intensification does not improve outcomes beyond rituximab-based therapy in primary mediastinal B-cell lymphoma: a multicenter retrospective analysis.

Leukemia & lymphoma·2026

Same author

Prognostic impact of bone marrow iron and serum ferritin in patients with myelodysplastic syndromes.

Annals of hematology·2026

Search research articles

Related Experiment Video

Updated: Mar 29, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

BRAF inhibitor therapy in HCL.

Sascha Dietrich¹, Thorsten Zenz²

¹Department of Translational Oncology, National Center for Tumor Diseases (NCT) and German Cancer Research Center (DKFZ), Im Neuenheimer Feld 460, 69120 Heidelberg, Germany; Department of Medicine V, Heidelberg University Medical Center, Heidelberg, Germany; Genome Biology Unit, European Molecular Biology Laboratory, Heidelberg, Germany.

Best Practice & Research. Clinical Haematology

|November 29, 2015

Summary

Targeted therapy for hairy cell leukemia (HCL) is advancing due to the BRAF V600E mutation. Inhibiting BRAF offers a promising, tumor-specific treatment strategy for HCL patients.

Keywords:

BRAF V600E BRAF inhibitor Dabrafenib Hairy cell leukemia MEK Vemurafenib

More Related Videos

Kinase Inhibitor Screening In Self-assembled Human Protein Microarrays

Kinase Inhibitor Screening In Self-assembled Human Protein Microarrays

Published on: October 23, 2019

Neutrophil Isolation and Analysis to Determine their Role in Lymphoma Cell Sensitivity to Therapeutic Agents

Neutrophil Isolation and Analysis to Determine their Role in Lymphoma Cell Sensitivity to Therapeutic Agents

Published on: March 25, 2016

Related Experiment Videos

Last Updated: Mar 29, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Kinase Inhibitor Screening In Self-assembled Human Protein Microarrays

Kinase Inhibitor Screening In Self-assembled Human Protein Microarrays

Published on: October 23, 2019

Neutrophil Isolation and Analysis to Determine their Role in Lymphoma Cell Sensitivity to Therapeutic Agents

Neutrophil Isolation and Analysis to Determine their Role in Lymphoma Cell Sensitivity to Therapeutic Agents

Published on: March 25, 2016

Area of Science:

Oncology
Molecular Biology
Cancer Therapeutics

Background:

Classical hairy cell leukemia (HCL) is increasingly understood at a molecular level.
The BRAF V600E mutation is identified in the majority of HCL cases.
This mutation provides a specific target for novel therapeutic interventions.

Purpose of the Study:

To summarize the discovery and biological significance of BRAF V600E in HCL.
To review the current clinical evidence supporting BRAF inhibitors in HCL treatment.
To discuss ongoing and future clinical trials focused on BRAF inhibition in HCL.

Main Methods:

Literature review of studies on BRAF V600E in HCL.
Analysis of clinical trial data for BRAF inhibitors in HCL.
Exploration of the MEK/ERK signaling pathway's role in HCL pathogenesis.

Main Results:

The BRAF V600E mutation is a key driver in most classical HCL cases.
BRAF inhibitors have demonstrated significant clinical activity in HCL.
Targeting the MEK/ERK pathway is a viable therapeutic strategy.

Conclusions:

BRAF V600E mutation identification enables targeted therapy in HCL.
BRAF inhibition represents a highly effective and specific treatment approach for HCL.
Further clinical trials are warranted to optimize BRAF-targeted treatments in HCL.