Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...

You might also read

Related Articles

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

Sort by
Same author

Isocitrate Dehydrogenase-1 Mutation Status and Dynamic Subcortical Motor Mapping Using Ultrasonic Aspirator Stimulation.

Operative neurosurgery (Hagerstown, Md.)·2026
Same author

Ibrutinib with Venetoclax in Patients with Relapsed/Refractory Chronic Lymphocytic Leukemia: A Phase II Study.

Blood cancer discovery·2026
Same author

Influence of Ether-Functionalized Pyrrolidinium Ionic Liquids on Properties and Li<sup>+</sup> Cation Solvation in Solvate Ionic Liquids.

The journal of physical chemistry. C, Nanomaterials and interfaces·2025
Same author

CLL cell-derived exosomes alter the immune and hematopoietic systems.

Leukemia·2025
Same author

The mutational landscape and functional effects of noncoding ultraconserved elements in human cancers.

Science advances·2025
Same author

A pilot study of lower doses of ibrutinib: patient body weight does not correlate with plasma ibrutinib levels during therapy.

Leukemia & lymphoma·2025

Related Experiment Video

Updated: May 8, 2026

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation
09:02

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation

Published on: November 26, 2018

Targeting inflammatory pathways in chronic lymphocytic leukemia.

Uri Rozovski1, Michael J Keating, Zeev Estrov

  • 1Department of Leukemia, Unit 428, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, United States.

Critical Reviews in Oncology/Hematology
|August 15, 2013
PubMed
Summary

Chronic inflammation is implicated in the development and progression of chronic lymphocytic leukemia (CLL). Targeting inflammatory pathways with drugs like ibrutinib shows promise for treating this leukemia.

Keywords:
CLLChronic lymphocytic leukemiaExperimental therapyInflammation

More Related Videos

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
09:52

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

Published on: December 4, 2018

From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia
10:18

From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia

Published on: October 19, 2014

Related Experiment Videos

Last Updated: May 8, 2026

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation
09:02

Immunoglobulin Gene Sequence Analysis In Chronic Lymphocytic Leukemia: From Patient Material To Sequence Interpretation

Published on: November 26, 2018

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
09:52

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

Published on: December 4, 2018

From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia
10:18

From a 2DE-Gel Spot to Protein Function: Lesson Learned From HS1 in Chronic Lymphocytic Leukemia

Published on: October 19, 2014

Area of Science:

  • Hematology
  • Oncology
  • Immunology

Background:

  • Chronic lymphocytic leukemia (CLL) pathobiology is not fully understood despite advances.
  • Chronic inflammation is increasingly recognized as a factor in CLL initiation and progression.

Purpose of the Study:

  • To review the role of chronic inflammation in chronic lymphocytic leukemia (CLL).
  • To discuss the therapeutic implications of targeting inflammatory pathways in CLL.

Main Methods:

  • Literature review of studies on inflammation in CLL.
  • Analysis of clinical trial data for anti-inflammatory and immunomodulatory agents in CLL.

Main Results:

  • Evidence suggests chronic inflammation, cytokine production, and pro-inflammatory signaling pathways contribute to CLL.
  • Glucocorticoids and non-steroidal anti-inflammatory drugs show anti-tumor activity in CLL.
  • Tyrosine kinase inhibitors (e.g., ibrutinib) and lenalidomide yield significant responses in relapsed/refractory CLL.

Conclusions:

  • Chronic inflammation plays a significant pathophysiological role in CLL.
  • Inhibitors of pro-inflammatory pathways and immunomodulatory agents are effective in CLL treatment.
  • Ongoing research into novel agents offers hope for effective CLL therapies and potential cures.