Evidence map›Paper›PMID 30230653›Full record

ReviewCancer science2018

Optimizing poly (ADP-ribose) polymerase inhibition through combined epigenetic and immunotherapy.

Thiru Prasanna, Fan Wu, Kum Kum Khanna, Desmond Yip, Laeeq Malik, Jane E Dahlstrom, Sudha Rao

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Thiru PrasannaHealth Research Institute, Faculty of ESTeM, University of Canberra, Canberra, ACT, Australia.
Fan WuHealth Research Institute, Faculty of ESTeM, University of Canberra, Canberra, ACT, Australia.
Kum Kum KhannaQIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Desmond YipDepartment of Medical Oncology, The Canberra Hospital, Canberra, ACT, Australia.
Laeeq MalikDepartment of Medical Oncology, The Canberra Hospital, Canberra, ACT, Australia.
Jane E DahlstromANU Medical School, Australian National University, Canberra, ACT, Australia.
Sudha RaoHealth Research Institute, Faculty of ESTeM, University of Canberra, Canberra, ACT, Australia.ORCID http://orcid.org/0000-0001-9547-947X
Australian National University · AUUniversity of Canberra · AUQIMR Berghofer Medical Research Institute · AU

Funding

National Health and Medical Research Council APP1068065University of Canberra
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with poor survival outcomes. Currently, there are no targeted therapies available for TNBCs despite remarkable progress in targeted and immune-directed therapies for other solid organ malignancies. Poly (ADP-ribose) polymerase inhibitors (PARPi) are effective anticancer drugs that produce good initial clinical responses, especially in homologous recombination DNA repair-deficient cancers. However, resistance is the rule rather than the exception, and recurrent tumors tend to have an aggressive phenotype associated with poor survival. Many efforts have been made to overcome PARPi resistance, mostly by targeting genes and effector proteins participating in homologous recombination that are overexpressed during PARPi therapy. Due to many known and unknown compensatory pathways, genes, and effector proteins, overlap and shared resistance are common. Overexpression of programmed cell death-ligand 1 (PD-L1) and cancer stem cell (CSC) sparing are novel PARPi resistance hypotheses. Although adding programmed cell death-1 (PD-1)/PD-L1 inhibitors to PARPi might improve immunogenic cell death and be crucial for durable responses, they are less likely to target the CSC population that drives recurrent tumor growth. Lysine-specific histone demethylase-1A and histone deacetylase inhibitors have shown promising activity against CSCs. Combining epigenetic drugs such as lysine-specific histone demethylase-1A inhibitors or histone deacetylase inhibitors with PARPi/anti-PD-1/PD-L1 is a novel, potentially synergistic strategy for priming tumors and overcoming resistance. Furthermore, such an approach could pave the way for the identification of new upstream epigenetic and genetic signatures.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsB7-H1 AntigenClinical Trials as TopicDrug Resistance, NeoplasmEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHistone Deacetylase InhibitorsHomologous RecombinationHumansImmunotherapyNeoplastic Stem CellsPoly(ADP-ribose) Polymerase InhibitorsTriple Negative Breast NeoplasmsUp-RegulationB7-H1 AntigenCD274 protein, humanHistone Deacetylase InhibitorsPoly(ADP-ribose) Polymerase Inhibitorscancer stem cellimmune checkpoint inhibitorlysine-specific histone demethylase-1Apoly (ADP-ribose) polymerase inhibitortriple-negative breast cancer

Identifiers

PMID30230653
PMCPMC6215877
OpenAlexW2891045304

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.