Evidence map›Paper›PMID 26873719›Full record

ReviewFamilial cancer2016

Hereditary cancer syndromes: utilizing DNA repair deficiency as therapeutic target.

Gaurav Goyal, Tiffany Fan, Peter Todd Silberstein

Open access · hybridAbstract readReview
In one paragraph

Review in Familial cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Functional validation of somatic variability inCancer biology & therapy · 2025
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  6. Review
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  8. Article
  9. Genomic profiling in oncology clinical practice.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Review
  10. Review
  11. Cancer Genetic Counseling-Current Practice and Future Challenges.Cold Spring Harbor perspectives in medicine · 2020
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. 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

3 authors at 3 institutions in 1 country.

Gaurav GoyalDepartment of Internal Medicine, CHI Health Creighton University Medical Center, Omaha, NE, USA.
Tiffany FanClass of 2017, Creighton University School of Medicine, Omaha, NE, USA.
Peter Todd SilbersteinDivision of Hematology/Oncology, CHI Health Creighton University Medical Center and VA Nebraska-Western Iowa Health Care System, Omaha, NE, USA. PeterSilberstein@creighton.edu.
CHI Health · USCHI Health Creighton University Medical Center - Bergan Mercy · USCreighton University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human cells have numerous repair mechanisms to counteract various insults incurred on the DNA. Any mutation in these repair mechanisms can lead to accumulation of DNA errors and carcinogenesis. This review aims to discuss the therapeutic options in the two most common DNA repair deficient cancer syndromes, namely Lynch syndrome (hereditary non-polyposis colorectal cancer) and breast cancer susceptibility gene (BRCA) associated ovarian and breast cancer. Deficiency in DNA repair mechanisms renders these tumors with increased sensitivity to platinum agents. There has been increasing amount of information on the utility of the defects in DNA repair as targets for cancer therapy in these syndromes. Novel therapies like poly (ADP-ribose) polymerase (PARP) inhibitors are one of such example where the induction of double stranded breaks in DNA leads to tumoricidal effect in patients with homologous DNA repair deficiency. Interestingly, patients with DNA repair deficiencies tend to have a more favorable prognosis than sporadic malignancies. In microsatellite high colorectal cancer patients, this has been attributed to increased recruitment of CD8+ T lymphocytes in tumor microenvironment. However, these tumors are able to limit the host immune response by activation of immune checkpoints that seem like attractive targets of therapy in the future.

Indexed as

Antineoplastic AgentsBRCA1 ProteinBRCA2 ProteinClinical Trials as TopicColorectal Neoplasms, Hereditary NonpolyposisDNA RepairDNA Repair EnzymesFemaleHereditary Breast and Ovarian Cancer SyndromeHumansMolecular Targeted TherapyMutationPlatinum CompoundsPoly(ADP-ribose) Polymerase InhibitorsAntineoplastic AgentsBRCA1 ProteinBRCA2 ProteinDNA Repair EnzymesPlatinum CompoundsPoly(ADP-ribose) Polymerase InhibitorsBRCADNA repairHereditary cancerLynch syndromeMicrosatellite highPARP

Identifiers

PMID26873719
PMCPMC4901091
OpenAlexW2257104660

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.