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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
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We began analyzing https://www.nature.com/articles/s41420-025-02415-x, but it redirected us to https://www.nature.com/articles/s41420-025-02415-x. The analysis below is for the second page.

Title[redir]:
Ferroptosis: CD8+T cells’ blade to destroy tumor cells or poison for self-destruction | Cell Death Discovery
Description:
Ferroptosis represents an emerging, iron-dependent form of cell death driven by lipid peroxidation. In recent years, it has garnered significant attention in the realm of cancer immunotherapy, particularly in studies involving immune checkpoint inhibitors. This form of cell death not only enhances our comprehension of the tumor microenvironment but is also considered a promising therapeutic strategy to address tumor resistance, investigate immune activation mechanisms, and facilitate the development of cancer vaccines. The combination of immunotherapy with ferroptosis provides innovative targets and fresh perspectives for advancing cancer treatment. Nevertheless, tumor cells appear to possess a wider array of ferroptosis evasion strategies compared to CD8+T cells, which have been conclusively shown to be more vulnerable to ferroptosis. Furthermore, ferroptosis in the TME can create a favorable environment for tumor survival and invasion. Under this premise, both inducing tumor cell ferroptosis and inhibiting T cell ferroptosis will impact antitumor immunity to some extent, and even make the final result run counter to our therapeutic purpose. This paper systematically elucidates the dual-edged sword role of ferroptosis in the antitumor process of T cells, briefly outlining the complexity of ferroptosis within the TME. It explores potential side effects associated with ferroptosis-inducing therapies and critically considers the combined application of ferroptosis-based therapies with ICIs. Furthermore, it highlights the current challenges faced by this combined therapeutic approach and points out future directions for development.

Matching Content Categories {📚}

  • Science
  • Health & Fitness
  • Education

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Doi.org Make Money? {💸}

We see no obvious way the site makes money.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Doi.org could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

cells, ferroptosis, pubmed, article, google, scholar, cancer, tumor, cell, cas, central, immune, cdt, antitumor, lipid, immunotherapy, death, immunity, levels, effects, pathway, chen, peroxidation, treatment, therapy, zhang, expression, function, nature, tme, role, therapeutic, activation, dcs, gpx, wang, ferroptotic, microenvironment, accumulation, activity, resistance, iron, liu, mechanisms, targeting, response, induce, promoting, nat, zhao,

Topics {✒️}

nature portfolio privacy policy open-label keynote-021 study editing long-chain acyl-coa synthetases wnt/β-catenin-mitf pathway advertising unrestrained proliferative nature peroxisome proliferator-activated receptor-gamma barnawi io atf4-chop-chac1 signaling pathway anti-pd-l1 immunotherapy-activated cd8+ pd-1/pd-l1 checkpoint inhibitors social media jama netw open cell-mediated anti-tumor immunity lactate-mediated ampk-scd1 activity reprints middle calcium-independent phospholipase a2β pd-1/pd-l1 bockade dual-edged sword role gcn2-eif2α-atf4 pathway myeloid-derived suppressor cells limiting nf-κb recruitment triple-negative breast cancer nature pd-1/pd-l1 inhibitors significant research gap kras-mutant lung adenocarcinoma jak1-stat1 signaling pathway anti-tumor immune responses mitochondrial iron-sulfur cluster current antitumor research fatty acid oxidation oxidized low-density lipoprotein author information authors small-cell lung cancer important research topic p53-independent tumor suppression image-guided drug delivery jak-stat1-irf1 pathway resist ferroptosis-inducing therapies personal data received official approval ros/acetyl-p53 pathway real-time treatment monitoring inducing epithelial-mesenchymal transformation data protection vhl-defective ccrcc cells

Questions {❓}

  • Can tumor cells be specifically induced to undergo ferroptosis without affecting normal antitumor immune cells?
  • How can ferroptosis be utilized to reverse the immunosuppressive microenvironment and protect the antitumor effects of immune cells?
  • How can we design standardized and reasonable clinical translation experiments based on the atypia and heterogeneity of tumors, and explore reliable biomarkers to predict patients’ responses to ferroptosis-combined immunotherapy?
  • How can we minimize the toxic and side effects caused by derivatives of ferroptotic cancer cells?

Schema {🗺️}

WebPage:
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         description:Ferroptosis represents an emerging, iron-dependent form of cell death driven by lipid peroxidation. In recent years, it has garnered significant attention in the realm of cancer immunotherapy, particularly in studies involving immune checkpoint inhibitors. This form of cell death not only enhances our comprehension of the tumor microenvironment but is also considered a promising therapeutic strategy to address tumor resistance, investigate immune activation mechanisms, and facilitate the development of cancer vaccines. The combination of immunotherapy with ferroptosis provides innovative targets and fresh perspectives for advancing cancer treatment. Nevertheless, tumor cells appear to possess a wider array of ferroptosis evasion strategies compared to CD8+T cells, which have been conclusively shown to be more vulnerable to ferroptosis. Furthermore, ferroptosis in the TME can create a favorable environment for tumor survival and invasion. Under this premise, both inducing tumor cell ferroptosis and inhibiting T cell ferroptosis will impact antitumor immunity to some extent, and even make the final result run counter to our therapeutic purpose. This paper systematically elucidates the dual-edged sword role of ferroptosis in the antitumor process of T cells, briefly outlining the complexity of ferroptosis within the TME. It explores potential side effects associated with ferroptosis-inducing therapies and critically considers the combined application of ferroptosis-based therapies with ICIs. Furthermore, it highlights the current challenges faced by this combined therapeutic approach and points out future directions for development.
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      headline:Ferroptosis: CD8+T cells’ blade to destroy tumor cells or poison for self-destruction
      description:Ferroptosis represents an emerging, iron-dependent form of cell death driven by lipid peroxidation. In recent years, it has garnered significant attention in the realm of cancer immunotherapy, particularly in studies involving immune checkpoint inhibitors. This form of cell death not only enhances our comprehension of the tumor microenvironment but is also considered a promising therapeutic strategy to address tumor resistance, investigate immune activation mechanisms, and facilitate the development of cancer vaccines. The combination of immunotherapy with ferroptosis provides innovative targets and fresh perspectives for advancing cancer treatment. Nevertheless, tumor cells appear to possess a wider array of ferroptosis evasion strategies compared to CD8+T cells, which have been conclusively shown to be more vulnerable to ferroptosis. Furthermore, ferroptosis in the TME can create a favorable environment for tumor survival and invasion. Under this premise, both inducing tumor cell ferroptosis and inhibiting T cell ferroptosis will impact antitumor immunity to some extent, and even make the final result run counter to our therapeutic purpose. This paper systematically elucidates the dual-edged sword role of ferroptosis in the antitumor process of T cells, briefly outlining the complexity of ferroptosis within the TME. It explores potential side effects associated with ferroptosis-inducing therapies and critically considers the combined application of ferroptosis-based therapies with ICIs. Furthermore, it highlights the current challenges faced by this combined therapeutic approach and points out future directions for development.
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         Immune cell death
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         Cell Cycle Analysis
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      name:Cancer Center, the First Hospital of Jilin University, Changchun, Jilin, China

Social Networks {👍}(1)

External Links {🔗}(809)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.js
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
  • zita.ns.cloudflare.com

CDN Services {📦}

  • Crossref

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