Evidence map›Paper›PMID 29535912›Full record

ReviewTranslational lung cancer research2018

Targeting DNA damage repair in small cell lung cancer and the biomarker landscape.

Triparna Sen, Carl M Gay, Lauren Averett Byers

Open access · hybridAbstract readReview
In one paragraph

Review in Translational lung cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

86 citing papers in PubMed, 134 citations in OpenAlex.

  1. Trial
  2. Article
  3. Programmed cell death in lung cancer: mechanisms, immune responses, and therapeutics.Apoptosis : an international journal on programmed cell death · 2026
    Review
  4. Article
  5. Article
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  7. Article
  8. Review
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  12. Article
  13. Review
  14. Article
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  16. Article
  17. Emerging Nanomedicine Approaches in Targeted Lung Cancer Treatment.International journal of molecular sciences · 2024
    Review
  18. Article
  19. Review
  20. Review

26 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

3 authors at 1 institution in 1 country.

Triparna SenDepartment of Thoracic and Head & Neck Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Carl M GayDepartment of Thoracic and Head & Neck Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
Lauren Averett ByersDepartment of Thoracic and Head & Neck Medical Oncology, University of Texas, MD Anderson Cancer Center, Houston, TX, USA.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
TRAINING FOR ACADEMIC ONCOLOGY/HEMATOLOGYT32CA009666 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Michael Davies, Courtney DiNardo · 1994 to 2026
$9.8M
Therapeutic strategies for targeting PARP1 in small cell lung cancerR01CA207295 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Lauren Averett Byers · 2016 to 2026
$3.7M
NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA207295NCI NIH HHS T32 CA009666
6 · The paper itself

Abstract

Small cell lung cancer (SCLC) is an aggressive malignancy that accounts for 14% of all lung cancer diagnoses. Despite decades of active research, treatment options for SCLC are limited and resistance to the few Food and Drug Administration (FDA) approved therapies develops rapidly. With no approved targeted agents to date, new therapeutic strategies are desperately needed. SCLC is characterized by high mutation burden, ubiquitous loss of TP53 and RB1, mutually exclusive amplification of MYC family members, thereby, high genomic instability. Studies in the past few years have demonstrated the potential of targeting the DNA damage response (DDR) pathway as a promising therapeutic strategy for SCLC. Inhibitors targeting DDR proteins have shown promise in preclinical models, and are under clinical investigation as single agents and in combination with cytotoxic therapies. Recent efforts to expand the therapeutic arsenal toward SCLC have focused in part on immune checkpoint inhibitors, such as agents targeting the receptor-ligand pair programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1). Clinical trials have confirmed activity of these agents in extensive stage (ES)-SCLC. However, while several patients had dramatic responses, overall response rates to immune checkpoint blockade (ICB) remain poor. As a result, there is an urgent need to develop rational combination therapies to enhance response rates to immunotherapy in SCLC. Identification of predictive biomarkers for patient stratification, identifying effective combinations to overcome adaptive resistance to DDR-targeted therapies and identifying strategies to enhance response to immunotherapy are areas of active investigation in SCLC.

Indexed as

biomarkersDNA damage response (DDR)immunotherapysmall cell lung cancer (SCLC)

Identifiers

PMID29535912
PMCPMC5835589
OpenAlexW2785870654

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.