Evidence map›Paper›PMID 27158638›Full record

ArticleCancer cell & microenvironment

Temozolomide resistance and tumor recurrence: Halting the Hedgehog.

Jessian L Munoz, Vivian Rodriguez-Cruz, Nykia D Walker, Steven J Greco, Pranela Rameshwar

Open access · greenAbstract read
In one paragraph

Article in Cancer cell & microenvironment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Trial
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  8. PTB-AS, a Novel Natural Antisense Transcript, Promotes Glioma Progression by Improving PTBP1 mRNA Stability with SND1.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
  9. Article
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  11. Exosome mediated multidrug resistance in cancer.American journal of cancer research · 2018
    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

5 authors at 2 institutions in 1 country.

Jessian L MunozDepartment of Medicine-Hematology/Oncology, Rutgers New Jersey Medical School, Newark, NJ, USA.
Vivian Rodriguez-CruzDepartment of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences-SUNY University of Buffalo, Buffalo, NY, USA.
Nykia D WalkerDepartment of Medicine-Hematology/Oncology, Rutgers New Jersey Medical School, Newark, NJ, USA; Rutgers Graduate School of Biomedical Sciences, Newark, NJ, USA.
Steven J GrecoDepartment of Medicine-Hematology/Oncology, Rutgers New Jersey Medical School, Newark, NJ, USA.
Pranela RameshwarDepartment of Medicine-Hematology/Oncology, Rutgers New Jersey Medical School, Newark, NJ, USA; Rutgers Graduate School of Biomedical Sciences, Newark, NJ, USA.
Rutgers New Jersey Medical SchoolRutgers, The State University of New Jersey · US

Funding

BREAST CANCER/BONE MARROW STROMAL INTERACTIONSR01CA089868 · NCI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI RAMESHWAR, PRANELA · 2000 to 2003
$873k
NCI NIH HHS R01 CA089868
6 · The paper itself

Abstract

Chemotherapy with Temozolomide (TMZ), radiation and surgery are the primary methods to treat Glioblastoma Multiforme (GBM), the most common adult intracranial tumor with dismal outcome. GBM resistance to therapy is the main reason of poor patient outcomes. Thus, methods to overcome the resistance are an area of extensive research. This highlight focuses on three recently published articles on the mechanism of resistance and possible therapeutic intervention, including RNA treatment with stem cells. We showed a crucial role of the developmental Sonic Hedgehog (SHH) pathway in the acquisition and maintenance of TMZ resistance. SHH signaling caused TMZ resistance in GBM cells through an increase in the multiple drug resistance gene (MDR1). The SHH receptor, Patched-1 (PTCH1), negatively regulate SHH signaling. In GBM, miR-9 suppressed PTCH1 levels, resulting in the activation of SHH pathway. Thus, SHH signaling is independent of the ligand in resistant GBM cells. MiR-9 was also increased in chemoresistance CD133+ GBM cells. A potential method to reverse resistance was tested by delivering the anti-miR in bone marrow-derived Mesenchymal Stem Cells (MSCs). The anti-miR-9 was transferred into the resistant GBM cells through exosomes and gap junctional intercellular communication. We also review on-going clinical trials with inhibitor of SHH signaling, and also discuss drug delivery by cell therapy for GBM. While GBM treatment has proven to be a challenge, there are a number of novel approaches we are currently developing to manage this malignancy.

Indexed as

exosomeglioblastomamiR-9sonic hedgehogstem celltemozolomide

Identifiers

PMID27158638
PMCPMC4856152
OpenAlexW1578018089

What OpenQuestion holds

Textmetadata
LicenceTDM
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.