Evidence map›Paper›PMID 33020173›Full record

ReviewMolecular cancer research : MCR2021

Exploiting Replication Stress as a Novel Therapeutic Intervention.

Jeffrey C Martin, Tamara J Hoegel, Miranda L Lynch, Anna Woloszynska, Thomas Melendy, Joyce E Ohm

Abstract readReview
In one paragraph

Review in Molecular cancer research : MCR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Molecularly Defined Subsets of Ewing Sarcoma Tumors Differ in Their Responses to IGF1R and WEE1 Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  9. Targeting replication stress in cancer therapy.Nature reviews. Drug discovery · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. 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

6 authors.

Jeffrey C MartinDepartment of Cancer Genetics and Genomics, Roswell Park Comprehensive Cancer Center, Buffalo, New York.
Tamara J HoegelDepartment of Pediatric Hematology and Oncology, Roswell Park Comprehensive Cancer Center, Buffalo, New York.
Miranda L LynchHauptman-Woodward Medical Research Institute, Buffalo, New York.ORCID https://orcid.org/0000-0001-8604-4431
Anna WoloszynskaDepartment of Pharmacology and Therapeutics, Roswell Park Comprehensive Cancer Center, Buffalo, New York.
Thomas MelendyDepartment of Microbiology and Immunology, State University of New York at Buffalo, Buffalo, New York.ORCID https://orcid.org/0000-0003-1558-6262
Joyce E OhmDepartment of Cancer Genetics and Genomics, Roswell Park Comprehensive Cancer Center, Buffalo, New York. joyce.ohm@roswellpark.org.ORCID https://orcid.org/0000-0002-7390-8701

Funding

Environmental toxins and stem cell epigenetic remodelingR01ES022030 · NIEHS · UNIVERSITY OF NORTH DAKOTA · PI OHM, JOYCE ELLEN · 2012 to 2016
$1.6M
NIEHS NIH HHS R01 ES022030
6 · The paper itself

Abstract

Ewing sarcoma is an aggressive pediatric tumor of the bone and soft tissue. The current standard of care is radiation and chemotherapy, and patients generally lack targeted therapies. One of the defining molecular features of this tumor type is the presence of significantly elevated levels of replication stress as compared with both normal cells and many other types of cancers, but the source of this stress is poorly understood. Tumors that harbor elevated levels of replication stress rely on the replication stress and DNA damage response pathways to retain viability. Understanding the source of the replication stress in Ewing sarcoma may reveal novel therapeutic targets. Ewing sarcomagenesis is complex, and in this review, we discuss the current state of our knowledge regarding elevated replication stress and the DNA damage response in Ewing sarcoma, one contributor to the disease process. We will also describe how these pathways are being successfully targeted therapeutically in other tumor types, and discuss possible novel, evidence-based therapeutic interventions in Ewing sarcoma. We hope that this consolidation will spark investigations that uncover new therapeutic targets and lead to the development of better treatment options for patients with Ewing sarcoma. IMPLICATIONS: This review uncovers new therapeutic targets in Ewing sarcoma and highlights replication stress as an exploitable vulnerability across multiple cancers.

Indexed as

HumansMutationOncogene Proteins, FusionSarcoma, EwingOncogene Proteins, Fusion

Identifiers

PMID33020173
PMCPMC7864862

What OpenQuestion holds

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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.