Evidence map›Paper›PMID 41269345›Full record

ArticleCancer immunology, immunotherapy : CII2025

Early trajectory of inflammatory cytokines following tarlatamab administration in three advanced SCLC patients.

Takuma Imakita, Kohei Fujita, Yuki Yamamoto, Osamu Kanai, Yuta Okada, Shogo Toyama, Takanori Ito, Issei Oi, Kiminobu Tanizawa

Abstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

9 authors.

Takuma Imakita *Division of Respiratory Medicine, Center for Respiratory Diseases, National Hospital Organization Kyoto Medical Center, 1-1, Fukakusa-Mukaihata, Fushimi, Kyoto, Japan.
Kohei Fujita *Division of Respiratory Medicine, Center for Respiratory Diseases, National Hospital Organization Kyoto Medical Center, 1-1, Fukakusa-Mukaihata, Fushimi, Kyoto, Japan. kfujita.acd@gmail.com.
Yuki YamamotoDivision of Respiratory Medicine, Center for Respiratory Diseases, National Hospital Organization Kyoto Medical Center, 1-1, Fukakusa-Mukaihata, Fushimi, Kyoto, Japan.
Osamu KanaiDivision of Respiratory Medicine, Center for Respiratory Diseases, National Hospital Organization Kyoto Medical Center, 1-1, Fukakusa-Mukaihata, Fushimi, Kyoto, Japan.
Yuta OkadaDivision of Respiratory Medicine, Center for Respiratory Diseases, National Hospital Organization Kyoto Medical Center, 1-1, Fukakusa-Mukaihata, Fushimi, Kyoto, Japan.
Shogo ToyamaDivision of Respiratory Medicine, Center for Respiratory Diseases, National Hospital Organization Kyoto Medical Center, 1-1, Fukakusa-Mukaihata, Fushimi, Kyoto, Japan.
Takanori ItoDivision of Respiratory Medicine, Center for Respiratory Diseases, National Hospital Organization Kyoto Medical Center, 1-1, Fukakusa-Mukaihata, Fushimi, Kyoto, Japan.
Issei OiDivision of Respiratory Medicine, Center for Respiratory Diseases, National Hospital Organization Kyoto Medical Center, 1-1, Fukakusa-Mukaihata, Fushimi, Kyoto, Japan.
Kiminobu TanizawaDivision of Respiratory Medicine, Center for Respiratory Diseases, National Hospital Organization Kyoto Medical Center, 1-1, Fukakusa-Mukaihata, Fushimi, Kyoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tarlatamab, a bispecific T-cell engager (BiTE), effectively activates the immune system but often causes cytokine release syndrome (CRS). To understand the early in vivo cytokine dynamics of post-BiTE therapy, we analyzed serum from three SCLC patients before and after tarlatamab administration using the Bio-Plex Pro Human Cytokine Screening Panel, 48-Plex. CRS occurred once in case 1, twice in case 2, and not at all in case 3. During the initial CRS in cases 1 and 2, IL-6, IL-1Ra, IL-10, granulocyte colony-stimulating factor, MIG, and IP-10 increased from baseline. Of these, MIG and IP-10 were also elevated during the second CRS episode in case 2. Some cytokines (hepatocyte growth factor, IFN-α2, IFN-γ, IL-2Rα, MIP-1α, MCP-1, and TRAIL) rose during CRS in either case 1 or 2 but showed little change in the other. RANTES decreased during CRS in case 1, yet increased and remained high in case 2, and stayed elevated in case 3. This cytokine profiling highlights the complex pathophysiology of CRS and the involvement of diverse cytokine networks beyond the IL-6 axis. These findings may guide future biomarker development, disease classification, and therapeutic strategies beyond IL-6 inhibition, advancing personalized CRS management.

Indexed as

Antibodies, BispecificCytokine Release SyndromeCytokinesLung NeoplasmsSmall Cell Lung CarcinomaAgedHumansMaleAntibodies, BispecificCytokinesBispecific T-cell engager (BiTE)Cytokine release syndrome (CRS)Inflammatory cytokinesSmall-cell lung cancer (SCLC)Tarlatamab

Identifiers

PMID41269345
PMCPMC12638590

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.