Evidence map›Paper›PMID 38347838›Full record

ReviewFrontiers in oncology2024

Targeting the DNA damage response in hematological malignancies.

Sanjay De Mel, Ainsley Ryan Lee, Joelle Hwee Inn Tan, Rachel Zi Yi Tan, Li Mei Poon, Esther Chan, Joanne Lee, Yen Lin Chee, Satish R Lakshminarasappa, Patrick William Jaynes and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
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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

11 authors at 3 institutions in 1 country.

Sanjay De MelDepartment of Haematology-Oncology, National University Cancer Institute, Singapore, National University Health System, Singapore, Singapore.
Ainsley Ryan LeeDepartment of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Joelle Hwee Inn TanDepartment of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Rachel Zi Yi TanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Li Mei PoonDepartment of Haematology-Oncology, National University Cancer Institute, Singapore, National University Health System, Singapore, Singapore.
Esther ChanDepartment of Haematology-Oncology, National University Cancer Institute, Singapore, National University Health System, Singapore, Singapore.
Joanne LeeDepartment of Haematology-Oncology, National University Cancer Institute, Singapore, National University Health System, Singapore, Singapore.
Yen Lin CheeDepartment of Haematology-Oncology, National University Cancer Institute, Singapore, National University Health System, Singapore, Singapore.
Satish R LakshminarasappaDepartment of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Patrick William JaynesCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Anand D JeyasekharanDepartment of Haematology-Oncology, National University Cancer Institute, Singapore, National University Health System, Singapore, Singapore.
National University of Singapore · SGNational University Health System · SGNational University Cancer Institute, Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of the DNA damage response (DDR) plays a critical role in the pathogenesis and progression of many cancers. The dependency of certain cancers on DDR pathways has enabled exploitation of such through synthetically lethal relationships e.g., Poly ADP-Ribose Polymerase (PARP) inhibitors for BRCA deficient ovarian cancers. Though lagging behind that of solid cancers, DDR inhibitors (DDRi) are being clinically developed for haematological cancers. Furthermore, a high proliferative index characterize many such cancers, suggesting a rationale for combinatorial strategies targeting DDR and replicative stress. In this review, we summarize pre-clinical and clinical data on DDR inhibition in haematological malignancies and highlight distinct haematological cancer subtypes with activity of DDR agents as single agents or in combination with chemotherapeutics and targeted agents. We aim to provide a framework to guide the design of future clinical trials involving haematological cancers for this important class of drugs.

Indexed as

clinical trialscombination therapyDNA damagehaematologic malignanciesinhibitors

Identifiers

PMID38347838
PMCPMC10859481
OpenAlexW4391320716

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.