Cancer is a disease caused by the uncontrolled growth of cells that escape the body’s natural defenses. One way cancer protects itself is by taking advantage of certain immune cells called regulatory T cells, or Tregs. Normally, Tregs help prevent autoimmune diseases by controlling the immune system. But inside tumors, they behave differently. Instead of defending the body, they suppress the immune cells that could attack the cancer.
Many cancer treatments aim to activate the immune system to fight tumors more effectively. However, the presence of Tregs within the tumor makes this difficult. These cells act like bodyguards for the cancer, blocking the immune response that might otherwise slow or stop tumor growth.
Researchers have tried to eliminate Tregs by targeting a protein called CD25, found on their surface. However, earlier efforts often failed because these treatments also interfere with interleukin-2 (IL-2), a molecule that is essential for other immune cells to function. Blocking IL-2 weakens the entire immune response, limiting the treatment’s effectiveness.
To overcome this challenge, scientists recently developed a new antibody called 2B010. This study, titled “A novel anti-human CD25 mAb with preferential reactivity to activated T regulatory cells depletes them from the tumor microenvironment,” was published in Oncotarget (Volume 16).
Full blog - https://www.oncotarget.org/2025/11/19/new-antibody-removes-tregs-to-boost-immune-response-against-cancer/
Paper DOI - https://doi.org/10.18632/oncotarget.28752
Correspondence to - Ethan M. Shevach - eshevach@Niaid.NIH.gov
Abstract video - https://www.youtube.com/watch?v=2NJcGsI7WXA
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Keywords - cancer, Treg, CD25, TME, mAb, GVHD
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Cancer is a disease caused by the uncontrolled growth of cells that escape the body’s natural defenses. One way cancer protects itself is by taking advantage of certain immune cells called regulatory T cells, or Tregs. Normally, Tregs help prevent autoimmune diseases by controlling the immune system. But inside tumors, they behave differently. Instead of defending the body, they suppress the immune cells that could attack the cancer.
Many cancer treatments aim to activate the immune system to fight tumors more effectively. However, the presence of Tregs within the tumor makes this difficult. These cells act like bodyguards for the cancer, blocking the immune response that might otherwise slow or stop tumor growth.
Researchers have tried to eliminate Tregs by targeting a protein called CD25, found on their surface. However, earlier efforts often failed because these treatments also interfere with interleukin-2 (IL-2), a molecule that is essential for other immune cells to function. Blocking IL-2 weakens the entire immune response, limiting the treatment’s effectiveness.
To overcome this challenge, scientists recently developed a new antibody called 2B010. This study, titled “A novel anti-human CD25 mAb with preferential reactivity to activated T regulatory cells depletes them from the tumor microenvironment,” was published in Oncotarget (Volume 16).
Full blog - https://www.oncotarget.org/2025/11/19/new-antibody-removes-tregs-to-boost-immune-response-against-cancer/
Paper DOI - https://doi.org/10.18632/oncotarget.28752
Correspondence to - Ethan M. Shevach - eshevach@Niaid.NIH.gov
Abstract video - https://www.youtube.com/watch?v=2NJcGsI7WXA
Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28752
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Keywords - cancer, Treg, CD25, TME, mAb, GVHD
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Amivantamab Monotherapy in Rare EGFR-Mutated Advanced NSCLC
Oncotarget
5 minutes 27 seconds
3 months ago
Amivantamab Monotherapy in Rare EGFR-Mutated Advanced NSCLC
Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality. While the development of targeted therapies has improved outcomes for many patients with EGFR-mutated NSCLC, those with rare EGFR variants often face limited treatment options, especially when the disease involves the central nervous system (CNS).
A recent research paper, titled “Durable complete response in leptomeningeal disease of EGFR mutated non-small cell lung cancer to amivantamab, an EGFR-MET receptor bispecific antibody, after progressing on osimertinib” published in Volume 16 of Oncotarget, describes a patient with NSCLC harboring two uncommon EGFR mutations—G719A and A289V—who experienced a prolonged and clinically significant response to amivantamab monotherapy, after prior treatments had failed.
Full blog - https://www.oncotarget.org/2025/08/26/amivantamab-monotherapy-in-rare-egfr-mutated-advanced-nsclc/
Paper DOI - https://doi.org/10.18632/oncotarget.28730
Correspondence to - Young Kwang Chae - young.chae@northwestern.edu
Video short - https://www.youtube.com/watch?v=UEiCz834a8c
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Keywords - cancer, amivantamab, monotherapy, rare EGFR mutation, NSCLC, leptomeningeal disease
About Oncotarget
Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.
Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
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Oncotarget
Cancer is a disease caused by the uncontrolled growth of cells that escape the body’s natural defenses. One way cancer protects itself is by taking advantage of certain immune cells called regulatory T cells, or Tregs. Normally, Tregs help prevent autoimmune diseases by controlling the immune system. But inside tumors, they behave differently. Instead of defending the body, they suppress the immune cells that could attack the cancer.
Many cancer treatments aim to activate the immune system to fight tumors more effectively. However, the presence of Tregs within the tumor makes this difficult. These cells act like bodyguards for the cancer, blocking the immune response that might otherwise slow or stop tumor growth.
Researchers have tried to eliminate Tregs by targeting a protein called CD25, found on their surface. However, earlier efforts often failed because these treatments also interfere with interleukin-2 (IL-2), a molecule that is essential for other immune cells to function. Blocking IL-2 weakens the entire immune response, limiting the treatment’s effectiveness.
To overcome this challenge, scientists recently developed a new antibody called 2B010. This study, titled “A novel anti-human CD25 mAb with preferential reactivity to activated T regulatory cells depletes them from the tumor microenvironment,” was published in Oncotarget (Volume 16).
Full blog - https://www.oncotarget.org/2025/11/19/new-antibody-removes-tregs-to-boost-immune-response-against-cancer/
Paper DOI - https://doi.org/10.18632/oncotarget.28752
Correspondence to - Ethan M. Shevach - eshevach@Niaid.NIH.gov
Abstract video - https://www.youtube.com/watch?v=2NJcGsI7WXA
Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28752
Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/
Keywords - cancer, Treg, CD25, TME, mAb, GVHD
To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us:
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