Evidence map›Paper›PMID 32639661›Full record

ReviewCancer science2020

Synthetic lethality strategies: Beyond BRCA1/2 mutations in pancreatic cancer.

Yunlong Hu, Mingzhou Guo

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Epigenetic silencingCancer biology & therapy · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Exploration of targeted anti-tumor therapy · 2026
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Molecular insights into immune evasion and therapeutic paradigms in pancreatic cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025
    Article
  15. Review
  16. Epigenetic silencingCancer biology & therapy · 2024
    Article
  17. Article
  18. Review
  19. Methylation ofJournal of translational internal medicine · 2024
    Article
  20. 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

2 authors at 1 institution in 1 country.

Yunlong HuDepartment of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing, China.
Mingzhou GuoDepartment of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing, China.ORCID https://orcid.org/0000-0002-9445-9984
Chinese PLA General Hospital · CN

Funding

Beijing Science Foundation of China 7171008National Key Research and Development Programme of China 2018YFA0208902National Key Research and Development Programme of China 2020YFC2002705National Key Scientific Instrument Special Programme of China 2011YQ03013405National Natural Science Foundation of China 81672138National Science Foundation of China U1604281
6 · The paper itself

Abstract

Cancer cells are often characterized by abnormalities in DNA damage response including defects in cell cycle checkpoints and/or DNA repair. Synthetic lethality between DNA damage repair (DDR) pathways has provided a paradigm for cancer therapy by targeting DDR. The successful example is that cancer cells with BRCA1/2 mutations are sensitized to poly(adenosine diphosphate [ADP]-ribose)polymerase (PARP) inhibitors. Beyond the narrow scope of defects in the BRCA pathway, "BRCAness" provides more opportunities for synthetic lethality strategy. In human pancreatic cancer, frequent mutations were found in cell cycle and DDR genes, including P16, P73, APC, MLH1, ATM, PALB2, and MGMT. Combined DDR inhibitors and chemotherapeutic agents are under preclinical or clinical trials. Promoter region methylation was found frequently in cell cycle and DDR genes. Epigenetics joins the Knudson's "hit" theory and "BRCAness." Aberrant epigenetic changes in cell cycle or DDR regulators may serve as a new avenue for synthetic lethality strategy in pancreatic cancer.

Indexed as

Synthetic Lethal MutationsAnimalsBRCA1 ProteinBRCA2 ProteinCell CycleChemoradiotherapyDisease SusceptibilityDNA DamageDNA RepairEpigenesis, GeneticGene Expression RegulationHumansPancreatic NeoplasmsPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesSignal TransductionBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanPoly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) Polymerasescell cycleDNA damage repairepigeneticspancreatic cancersynthetic lethality

Identifiers

PMID32639661
PMCPMC7469842
OpenAlexW3041739046

What OpenQuestion holds

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LicenceCC BY-NC
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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.