Evidence map›Paper›PMID 29927979›Full record

ArticlePloS one2018

A novel epigenetic modulating agent sensitizes pancreatic cells to a chemotherapy agent.

Manjusha Thakar, Yue Hu, Michael Morreale, Lane Lerner, Wan Ying Lin, Rupashree Sen, Yi Cai, Enusha Karunasena, Maya Thakar, Soren Saggi and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

  1. Targeting one-carbon metabolism for cancer immunotherapy.Clinical and translational medicine · 2024
    Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Gene Therapy for Pancreatic Diseases: Current Status.International journal of molecular sciences · 2018
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Manjusha ThakarDepartment of Surgical Oncology, Johns Hopkins University, Baltimore, MD, United States of America.ORCID 0000-0002-3934-8640
Yue HuDepartment of Surgical Oncology, Johns Hopkins University, Baltimore, MD, United States of America.
Michael MorrealeDepartment of Surgical Oncology, Johns Hopkins University, Baltimore, MD, United States of America.ORCID 0000-0003-3610-9641
Lane LernerDepartment of Surgical Oncology, Johns Hopkins University, Baltimore, MD, United States of America.
Wan Ying LinDepartment of Surgical Oncology, Johns Hopkins University, Baltimore, MD, United States of America.
Rupashree SenDepartment of Oncology, Johns Hopkins University, Baltimore, MD, United States of America.
Yi CaiDepartment of Oncology, Johns Hopkins University, Baltimore, MD, United States of America.
Enusha KarunasenaDepartment of Oncology, Johns Hopkins University, Baltimore, MD, United States of America.
Maya ThakarDepartment of Surgical Oncology, Johns Hopkins University, Baltimore, MD, United States of America.
Soren SaggiDepartment of Surgical Oncology, Johns Hopkins University, Baltimore, MD, United States of America.
Harold KeerAstex Pharmaceuticals, Incorporated, Pleasanton, CA, United States of America.
Nita AhujaDepartment of Surgical Oncology, Johns Hopkins University, Baltimore, MD, United States of America.
Johns Hopkins University · USAstex Pharmaceuticals

Funding

(PQD3)Molecular Profiles associated with Long-Term Survival in pancreas CancerR01CA185357 · NCI · YALE UNIVERSITY · PI AHUJA, NITA, EASWARAN, HARIHARAN · 2014 to 2017
$1.8M
NCI NIH HHS R01 CA185357
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is expected to be the second leading cause of cancer mortality by 2030. PDAC remains resistant to the majority of systemic chemotherapies. In this paper, we explore if epigenetic sensitization can improve chemotherapy response in PDAC. Multiple PDAC cell lines were tested with serial concentrations of the epigenetic modulators 5-azacitidine (Aza) and guadecitabine (SGI-110). Guadecitabine was effective at inhibiting the expression of DNA Methyltransferase 1 (DNMT1) and in decreasing cell viability at nanomolar concentrations. We also report that guadecitabine has increased efficacy following a delay period or as we reference, a 'rest period'. Sensitization with guadecitabine improved response to the chemotherapeutic agent-Irinotecan- as measured by decreased cell viability and accompanied by an increase in caspase activity. Additional studies are needed to understand the mechanism of action.

Indexed as

Antineoplastic AgentsAzacitidineCarcinoma, Pancreatic DuctalCell Line, TumorCell SurvivalDNA (Cytosine-5-)-Methyltransferase 1Epigenesis, GeneticHumansIrinotecanPancreasPancreatic NeoplasmsTopoisomerase I InhibitorsAntineoplastic AgentsAzacitidineDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanguadecitabineIrinotecanTopoisomerase I Inhibitors

Identifiers

PMID29927979
PMCPMC6013229
OpenAlexW2809379238

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.