Evidence map›Paper›PMID 42189883›Full record

Observational studyClinical cancer research : an official journal of the American Association for Cancer Research2026

Sequential Immune Activation of Effector T Cells as Biomarkers of Response to Durvalumab in Patients with Locally Advanced NSCLC.

Atsuto Mouri, Hirotsugu Kenmotsu, Hiroshi Kagamu, Koichi Azuma, Ryota Saito, Hiroaki Akamatsu, Kimio Yonesaka, Mikiko Kakegawa, Hiromi Nagashima, Satoshi Takahashi and 10 more

Abstract readObservational Study
In one paragraph

Observational study in Clinical cancer research : an official journal of the American Association for Cancer Research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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

20 authors.

Atsuto MouriDepartment of Respiratory Medicine, International Medical Center, Saitama Medical University, Hidaka, Japan.ORCID 0000-0001-8704-8151
Hirotsugu KenmotsuDivision of Thoracic Oncology, Shizuoka Cancer Center, Sunto-gun, Japan.ORCID 0000-0003-0590-9259
Hiroshi KagamuDepartment of Respiratory Medicine, International Medical Center, Saitama Medical University, Hidaka, Japan.ORCID 0000-0003-4523-8517
Koichi AzumaDivision of Respirology, Neurology and Rheumatology, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan.ORCID 0000-0001-5040-5856
Ryota SaitoDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.ORCID 0009-0007-6476-6741
Hiroaki AkamatsuInternal Medicine III, Wakayama Medical University, Wakayama, Japan.ORCID 0000-0001-5856-5512
Kimio YonesakaDepartment of Medical Oncology, Kindai University Faculty of Medicine, Osaka-Sayama, Japan.ORCID 0000-0002-0816-5315
Mikiko KakegawaDepartment of Respiratory Medicine, Kitasato University School of Medicine, Sagamihara, Japan.ORCID 0009-0004-3605-4569
Hiromi NagashimaDepartment of Respiratory Medicine, Iwate Medical University School of Medicine, Yahaba-cho, Japan.ORCID 0000-0003-1271-1152
Satoshi TakahashiDepartment of Thoracic Surgery, Tokyo Medical University Hospital, Shinjuku-ku, Japan.ORCID 0009-0006-0733-6094
Masaki FujitaDepartment of Respiratory Medicine, Fukuoka University Hospital, Fukuoka, Japan.ORCID 0000-0003-1209-1272
Noriko YanagitaniDepartment of Thoracic Medical Oncology, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Koto-ku, Japan.ORCID 0009-0000-9922-1214
Kiichiro NinomiyaCenter for Comprehensive Genomic Medicine, Okayama University Hospital, Kita-ku, Japan.ORCID 0000-0002-2134-2865
Yasuhiko NishiokaDepartment of Respiratory Medicine and Rheumatology, Graduate School of Biomedical Sciences, Tokushima University, Tokushima, Japan.ORCID 0000-0001-6311-1654
Keita MoriDepartment of Biostatistics, Clinical Research Support Center, Shizuoka Cancer Center, Sunto-gun, Japan.ORCID 0000-0002-5473-1488
Shigehisa KitanoDepartment of Advanced Medical Development, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Koto-ku, Japan.ORCID 0000-0002-4041-8298
Koji TamadaDepartment of Immunology, Yamaguchi University Graduate School of Medicine, Ube, Japan.ORCID 0000-0002-3098-2565
Nobuyuki YamamotoInternal Medicine III, Wakayama Medical University, Wakayama, Japan.ORCID 0000-0002-7342-0853
Akihiko GemmaDepartment of Pulmonary Medicine and Oncology, Graduate School of Medicine, Nippon Medical School, Bunkyo-ku, Japan.ORCID 0000-0003-0762-2737
Tetsuya MitsudomiDivision of Thoracic Surgery, Izumi City General Hospital, Izumi, Japan.ORCID 0000-0001-9860-8505

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeDurvalumab therapy following concurrent chemoradiotherapy (cCRT) improves progression-free survival (PFS) in patients with unresectable locally advanced non-small cell lung cancer. In this prospective observational study, we evaluated the changes in peripheral blood immune cell counts to elucidate the immunologic mechanisms underlying cCRT and durvalumab therapy. EXPERIMENTAL

designPeripheral blood mononuclear cell (PBMC) samples were collected at four time points: before cCRT, after cCRT, at the start of durvalumab, and 8 weeks after the start of durvalumab, and analyzed by multicolor flow cytometry.

resultsOf the 149 enrolled patients, 115 received durvalumab consolidation therapy after cCRT. The median PFS in the overall population was 24.2 months, and the 3-year PFS rate was 38.9%. PBMC analysis showed an increased effector fraction of CD4+ T cells before and after cCRT but no change in CD8+ T cells. Following durvalumab therapy, the effector fraction ratio of CD8+ T cells (CD62Llow CD8+ T cells) increased and positively correlated with increased CD62Llow CD4+ T cells during cCRT. Patients whose proportion of CD62Llow CD4+ T cells exceeded the threshold for cCRT had better PFS than those below the threshold. Patients whose CD62Llow CD8+ T-cell proportion exceeded the threshold after durvalumab therapy showed prolonged PFS compared with those below the threshold.

conclusionscCRT promotes an increase in effector CD4+ T cells, and the subsequent increase in CD8+ T cells following durvalumab therapy prolongs PFS. Peripheral blood effector-type CD4+ and CD8+ T cells are potential biomarkers for evaluating the immune status of patients and predicting treatment efficacy.

Indexed as

Antibodies, MonoclonalAntineoplastic Agents, ImmunologicalBiomarkers, TumorCarcinoma, Non-Small-Cell LungLung NeoplasmsLymphocyte ActivationAdultAgedAged, 80 and overCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesChemoradiotherapyFemaleHumansMaleMiddle AgedAntibodies, MonoclonalAntineoplastic Agents, ImmunologicalBiomarkers, Tumordurvalumab

Identifiers

PMID42189883
PMCPMC13530998

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.