Evidence map›Paper›PMID 29202181›Full record

ArticleNucleic acids research2018

Targeted nanocomplex carrying siRNA against MALAT1 sensitizes glioblastoma to temozolomide.

Sang-Soo Kim, Joe B Harford, Manish Moghe, Antonina Rait, Kathleen F Pirollo, Esther H Chang

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. LncRNA-Mediated TPI1 and PKM2 Promote Self-Renewal and Chemoresistance in GBM.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

17 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Sang-Soo KimDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA.
Joe B HarfordSynerGene Therapeutics, Inc., Potomac, MD 20854, USA.
Manish MogheDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA.
Antonina RaitDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA.
Kathleen F PirolloDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA.
Esther H ChangDepartment of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057, USA.
Georgetown University Medical Center · USGeorgetown University · USAllogene Therapeutics (United States) · US

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI MARCUS S NOEL · 1990 to 2026
$71.5M
NCI NIH HHS P30 CA051008
6 · The paper itself

Abstract

Intrinsic therapeutic resistance especially in cancer stem cells (CSCs) together with extensive tumor cell infiltration and restricted permeation of the blood-brain barrier (BBB) by drugs may all contribute to the treatment failure in patients with glioblastoma multiforme (GBM). Accumulating evidence suggests that long non-coding RNA (lncRNA), metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a role in tumor cell infiltration and therapeutic resistance of GBM. Using our tumor-targeted nanocomplex, we have modulated the expression of MALAT1 and investigated its impact on GBM cells. Importantly, our nanocomplex is able to target CSCs that are considered to be the prime culprits in therapeutic resistance and recurrence of GBM. Attenuation of MALAT1 by RNA interference significantly lowered the growth, motility and stemness of GBM cells. In addition, silencing of MALAT1 clearly improved the sensitivity of GBM cells to chemotherapeutic agents including the current first-line therapy of GBM [temozolomide (TMZ)]. In animal models of GBM, tumor involution with a modest but statistically significant survival benefit was achieved with concurrent treatment of TMZ and nanocomplex-mediated silencing of MALAT1. These results suggest that combining standard TMZ treatment with lncRNA-targeting therapies using our nanocomplex could substantially enhance the very poor prognosis for GBM patients.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntineoplastic Agents, AlkylatingBrain NeoplasmsCell Line, TumorDrug Resistance, NeoplasmFemaleGlioblastomaHumansLiposomesMiceMice, NudeMolecular Targeted TherapyNanostructuresNeoplastic Stem CellsReceptors, TransferrinAntineoplastic Agents, AlkylatingLiposomesMALAT1 long non-coding RNA, humanReceptors, TransferrinRNA, Long NoncodingRNA, Small InterferingSingle-Chain AntibodiesTemozolomide

Identifiers

PMID29202181
PMCPMC5815062
OpenAlexW2773307196

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.