Evidence map›Paper›PMID 33824345›Full record

ArticleNature communications2021

Ferroptosis response segregates small cell lung cancer (SCLC) neuroendocrine subtypes.

Christina M Bebber, Emily S Thomas, Jenny Stroh, Zhiyi Chen, Ariadne Androulidaki, Anna Schmitt, Michaela N Höhne, Lukas Stüker, Cleidson de Pádua Alves, Armin Khonsari and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 1% of its field
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

101 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Programmed cell death in lung cancer: mechanisms, immune responses, and therapeutics.Apoptosis : an international journal on programmed cell death · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. An atlas of ferroptosis-induced secretomes.Cell death and differentiation · 2025
    Article
  19. Article
  20. Review

41 more citing papers are in PubMed but not listed here.

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

21 authors at 5 institutions in 2 countries.

Christina M BebberDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-7841-7493
Emily S ThomasDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-4563-8695
Jenny StrohDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Zhiyi ChenDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Ariadne AndroulidakiDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Anna SchmittCECAD Cluster of Excellence, University of Cologne, Cologne, Germany.
Michaela N HöhneCECAD Cluster of Excellence, University of Cologne, Cologne, Germany.
Lukas StükerDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Cleidson de Pádua AlvesDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Armin KhonsariDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Marcel A DammertDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Fatma ParmaksizDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Hannah L TumbrinkDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
Filippo BeleggiaClinic I for Internal Medicine, Medical Faculty, University Hospital of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0003-0234-7094
Martin L SosDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-2868-100X
Jan RiemerCECAD Cluster of Excellence, University of Cologne, Cologne, Germany.
Julie GeorgeDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-4272-3683
Susanne BrodesserCECAD Cluster of Excellence, University of Cologne, Cologne, Germany.
Roman K ThomasDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany.
H Christian ReinhardtDepartment of Hematology and Stem Cell Transplantation, University Hospital Essen, University Duisburg-Essen, German Cancer Consortium (DKTK partner site Essen), Essen, Germany.
Silvia von KarstedtDepartment of Translational Genomics, Medical Faculty, University of Cologne, Cologne, Germany. s.vonkarstedt@uni-koeln.de.ORCID http://orcid.org/0000-0002-7816-5919
University of Cologne · DEEssen University Hospital · DEGerman Cancer Research Center · DETH Köln - University of Applied Sciences · DEUniversity Hospital Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of TP53 and RB1 in treatment-naïve small cell lung cancer (SCLC) suggests selective pressure to inactivate cell death pathways prior to therapy. Yet, which of these pathways remain available in treatment-naïve SCLC is unknown. Here, through systemic analysis of cell death pathway availability in treatment-naïve SCLC, we identify non-neuroendocrine (NE) SCLC to be vulnerable to ferroptosis through subtype-specific lipidome remodeling. While NE SCLC is ferroptosis resistant, it acquires selective addiction to the TRX anti-oxidant pathway. In experimental settings of non-NE/NE intratumoral heterogeneity, non-NE or NE populations are selectively depleted by ferroptosis or TRX pathway inhibition, respectively. Preventing subtype plasticity observed under single pathway targeting, combined treatment kills established non-NE and NE tumors in xenografts, genetically engineered mouse models of SCLC and patient-derived cells, and identifies a patient subset with drastically improved overall survival. These findings reveal cell death pathway mining as a means to identify rational combination therapies for SCLC.

Indexed as

FerroptosisAnimalsAntioxidantsApoptosisBiomarkers, TumorCell Line, TumorCell SurvivalHumansLipid MetabolismMaleMiceMice, NudeModels, BiologicalNecroptosisNeuroendocrine TumorsPhospholipid Hydroperoxide Glutathione PeroxidaseAntioxidantsBiomarkers, TumorPhospholipid Hydroperoxide Glutathione PeroxidasePhospholipidsThioredoxins

Identifiers

PMID33824345
PMCPMC8024350
OpenAlexW3148185623

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.