Evidence map›Paper›PMID 31671773›Full record

ArticleCancers2019

SL-BioDP: Multi-Cancer Interactive Tool for Prediction of Synthetic Lethality and Response to Cancer Treatment.

Xiang Deng, Shaoli Das, Kristin Valdez, Kevin Camphausen, Uma Shankavaram

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 24 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

5 authors at 3 institutions in 1 country.

Xiang DengBioinformatics core facility, Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. dengx@mail.nih.gov.
Shaoli DasBioinformatics core facility, Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. shaoli.das@nih.gov.
Kristin ValdezBioinformatics core facility, Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. kristin.valdez@nih.gov.
Kevin CamphausenBioinformatics core facility, Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. camphauk@mail.nih.gov.
Uma ShankavaramBioinformatics core facility, Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. uma@mail.nih.gov.
National Cancer Institute · USNational Institutes of Health · USLeidos (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synthetic lethality exploits the phenomenon that a mutation in a cancer gene is often associated with new vulnerability which can be uniquely targeted therapeutically, leading to a significant increase in favorable outcome. DNA damage and survival pathways are among the most commonly mutated networks in human cancers. Recent data suggest that synthetic lethal interactions between a tumor defect and a DNA repair pathway can be used to preferentially kill tumor cells. We recently published a method, DiscoverSL, using multi-omic cancer data, that can predict synthetic lethal interactions of potential clinical relevance. Here, we apply the generality of our models in a comprehensive web tool called Synthetic Lethality Bio Discovery Portal (SL-BioDP) and extend the cancer types to 18 cancer genome atlas cohorts. SL-BioDP enables a data-driven computational approach to predict synthetic lethal interactions from hallmark cancer pathways by mining cancer's genomic and chemical interactions. Our tool provides queries and visualizations for exploring potentially targetable synthetic lethal interactions, shows Kaplan-Meier plots of clinical relevance, and provides in silico validation using short hairpin RNA (shRNA) and drug efficacy data. Our method would thus shed light on mechanisms of synthetic lethal interactions and lead to the discovery of novel anticancer drugs.

Indexed as

bioinformaticscancerDNA repair pathwaysynthetic lethalityweb application

Identifiers

PMID31671773
PMCPMC6895978
OpenAlexW2982352208

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.