Evidence map›Paper›PMID 40612871›Full record

ArticleOncology research2025

Immune landscape of neoadjuvant chemoradiotherapy: involvement of MAL, a T-cell differentiation protein.

Kosei Nakajima, Yoshinori Ino

Abstract read
In one paragraph

Article in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

2 authors.

Kosei NakajimaDivision of Molecular Pathology, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, 104-0045, Tokyo Japan.
Yoshinori InoDivision of Molecular Pathology, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, 104-0045, Tokyo Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Neoadjuvant/preoperative therapy (NAT) involves the administration of chemotherapy, with or without radiation, prior to surgical resection. This approach is commonly used for locally advanced tumors to reduce tumor volume, improve resectability, and minimize the need for extensive surgical procedures. While NAT has been shown to be effective in inducing local anti-tumor immunity in potentially resectable solid tumors, the underlying molecular mechanisms remain poorly understood. Methods: Cohort samples from pancreatic cancer patients who underwent NAT (n = 26) and those who did not (n = 20) were analyzed. Changes in the immune microenvironment induced by NAT were assessed using stratified bioinformatic approaches, including heatmap analysis of immune-related genes selected via Gene Ontology, Gene Set Enrichment Analysis (GSEA) with the immunologic signature database, and Ingenuity Pathway Analysis (IPA). Findings were further validated through immunohistochemical analysis. Results: A comprehensive, stratified evaluation integrating pathological and bioinformatic approaches revealed that NAT induced the upregulation of 212 genes, including DC-SIGN (CD209), and activated 13 immune-associated pathways, such as T-cell receptor (TCR) signaling. Additionally, NAT promoted an increased shift toward CD8 (+) T-cell populations through the upregulation of MAL (T-cell differentiation protein). Immunohistochemical analysis further confirmed a significant accumulation of DC-SIGN (+) dendritic cells and MAL (+) lymphocytes in NAT-treated patients. Conclusions: NAT enhances anti-tumor immunity by promoting CD8 (+) T-cell generation through the activation of DC-SIGN (+) dendritic cells and MAL (+) lymphocytes. This study is the first to report an increase in MAL (+) lymphocytes following NAT. Given its potential significance, further investigation in other solid tumors treated with NAT is warranted.

Indexed as

Pancreatic NeoplasmsAgedCD8-Positive T-LymphocytesChemoradiotherapyFemaleHumansLectins, C-TypeMaleMiddle AgedNeoadjuvant TherapyTumor MicroenvironmentLectins, C-TypeAnti-tumor immunityNeoadjuvant/preoperative therapy (NAT)T-cell differentiation

Identifiers

PMID40612871
PMCPMC12215608

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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.