Evidence map›Paper›PMID 41281945›Full record

ReviewCancer drug resistance (Alhambra, Calif.)2025

Targeting tumor-draining lymph node to overcome resistance to cancer immunotherapy: an update.

Jianan Lu, Jiangnan Yu, Tuo Xu, Yina Li, Shuxian Chen, Qian Zhou, Lei Wang

Abstract readReview
In one paragraph

Review in Cancer drug resistance (Alhambra, Calif.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Jianan LuThese authors contributed equally.
Jiangnan YuThese authors contributed equally.
Tuo XuInternational Cancer Center, Department of Immunology, Shenzhen University Medical School, Shenzhen 518054, Guangdong, China.
Yina LiInternational Cancer Center, Department of Immunology, Shenzhen University Medical School, Shenzhen 518054, Guangdong, China.
Shuxian ChenInternational Cancer Center, Department of Immunology, Shenzhen University Medical School, Shenzhen 518054, Guangdong, China.
Qian ZhouInternational Cancer Center, Department of Immunology, Shenzhen University Medical School, Shenzhen 518054, Guangdong, China.
Lei WangInternational Cancer Center, Department of Immunology, Shenzhen University Medical School, Shenzhen 518054, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune checkpoint inhibitor (ICI) resistance often stems from intratumoral T cell dysfunction. This review focuses on both tumor-intrinsic and tumor-draining lymph node (TDLN)-centric resistance mechanisms. We detail how specific defects within TDLNs - such as impaired dendritic cell migration and the establishment of immunosuppressive niches - initiate and perpetuate systemic immune dysfunction, ultimately leading to ICI resistance. To counter these challenges, we summarize the following TDLN-targeted strategies: (1) remodeling the TDLN immunosuppressive microenvironment to restore effective antigen presentation; (2) expanding the pool of progenitor exhausted T (Tpex) cells, with a focus on their primary reservoir in TDLNs; and (3) developing adoptive cell therapies using TDLN-derived Tpex cells to generate a robust, personalized antitumor response. By repositioning TDLNs as a central therapeutic target, recent findings suggest strategies aiming to overcome resistance at its source and improve ICI clinical outcomes.

Indexed as

Immune checkpoint inhibitorimmunotherapy resistancetumor-draining lymph nodetumor microenvironment

Identifiers

PMID41281945
PMCPMC12635989

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.