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

The Tumor Microenvironment02:17

The Tumor Microenvironment

8.1K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
8.1K
The Tumor Microenvironment02:17

The Tumor Microenvironment

3.1K
3.1K
Tumor Immunotherapy01:27

Tumor Immunotherapy

2.2K
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.
2.2K
Abnormal Proliferation02:23

Abnormal Proliferation

5.4K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.4K

You might also read

Related Articles

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

Sort by
Same author

Case Report: Long-term maternal and neonatal outcomes after nivolumab therapy in metastatic tonsillar sarcomatoid squamous cell carcinoma.

Frontiers in immunology·2026
Same author

​EuroNet-PHL-LP1: Complete resection or low-dose chemo for pediatric low-risk nodular lymphocyte-predominant Hodgkin lymphoma.

Blood advances·2026
Same author

Systemic and Local Adiposity in the Bone Marrow Microenvironment Associated With Improved Prognosis in Hodgkin Lymphoma: Imaging and Molecular Analysis.

International journal of cancer·2026
Same author

Immunity and coagulation.

Journal of translational medicine·2026
Same author

High BRAF variant allele frequency predicts poor outcomes in metastatic melanoma patients treated with BRAF/MEK inhibitors.

Journal of translational medicine·2025
Same author

Progressive T cell defects correlate with disease outcome in high-count monoclonal B-cell lymphocytosis.

Leukemia·2025

Related Experiment Video

Updated: Mar 30, 2026

Studying the Effects of Tumor-Secreted Paracrine Ligands on Macrophage Activation using Co-Culture with Permeable Membrane Supports
07:44

Studying the Effects of Tumor-Secreted Paracrine Ligands on Macrophage Activation using Co-Culture with Permeable Membrane Supports

Published on: November 28, 2019

8.3K

Tumor microenvironment (TME)-driven immune suppression in B cell malignancy.

Nicole S Nicholas1, Benedetta Apollonio1, Alan G Ramsay1

  • 1Department of Haemato-Oncology, Division of Cancer Studies, Faculty of Life Sciences & Medicine, King's College London, London, UK.

Biochimica Et Biophysica Acta
|November 12, 2015
PubMed
Summary

Immunotherapy shows promise for lymphoid cancers, but many patients don't respond. This review explores how the tumor microenvironment (TME) in chronic lymphocytic leukemia (CLL) and diffuse large B-cell lymphoma (DLBCL) promotes immune evasion, hindering treatment effectiveness.

Keywords:
CLLCTLA-4DLBCLImmune checkpoint blockadeImmune evasionLenalidomidePD-1PD-L1T cells

More Related Videos

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

1.9K
Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model
07:49

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model

Published on: April 13, 2015

21.1K

Related Experiment Videos

Last Updated: Mar 30, 2026

Studying the Effects of Tumor-Secreted Paracrine Ligands on Macrophage Activation using Co-Culture with Permeable Membrane Supports
07:44

Studying the Effects of Tumor-Secreted Paracrine Ligands on Macrophage Activation using Co-Culture with Permeable Membrane Supports

Published on: November 28, 2019

8.3K
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

1.9K
Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model
07:49

Evaluation of Tumor-infiltrating Leukocyte Subsets in a Subcutaneous Tumor Model

Published on: April 13, 2015

21.1K

Area of Science:

  • Immunology and Oncology
  • Tumor Microenvironment (TME) Research

Background:

  • Immunotherapy, including immune checkpoint blockade and immunomodulatory drugs, can induce anti-tumor T cell responses and durable regressions in cancer patients.
  • Despite immunotherapy's potential, a significant portion of patients do not achieve a clinical response, necessitating a deeper understanding of treatment resistance mechanisms.
  • Lymphoid malignancies possess inherent immune sensitivity, suggesting they should be responsive to immunotherapy; however, complex interactions within the TME often lead to immune evasion.

Purpose of the Study:

  • To review the contributions of the tumor microenvironment (TME) to immune evasion in lymphoid malignancies.
  • To focus on the immune checkpoint network and TME-driven mechanisms in chronic lymphocytic leukemia (CLL) and diffuse large B-cell lymphoma (DLBCL).
  • To highlight emerging therapeutic strategies aimed at re-educating the TME to promote anti-tumorigenic effects.

Main Methods:

  • Literature review focusing on the role of the tumor microenvironment in immune evasion within lymphoid cancers.
  • Analysis of immune checkpoint expression and activity as modulated by TME components.
  • Examination of therapeutic strategies targeting TME reprogramming for enhanced anti-cancer immunity.

Main Results:

  • Malignant cells establish complex interdependencies with reprogrammed immune and stromal cells within the TME.
  • These TME-driven associations are critical for promoting tumor progression and facilitating immune evasion by suppressing anti-tumor immune responses.
  • Specific focus on chronic lymphocytic leukemia (CLL) and diffuse large B-cell lymphoma (DLBCL) reveals distinct TME-mediated immune suppression pathways.

Conclusions:

  • The tumor microenvironment plays a pivotal role in mediating resistance to immunotherapy in lymphoid malignancies like CLL and DLBCL.
  • Understanding and targeting TME-driven immune evasion mechanisms is crucial for improving patient responses to immunotherapy.
  • Reprogramming the TME offers a promising therapeutic avenue to enhance anti-tumor immunity and achieve durable cancer regressions.