Evidence map›Paper›PMID 27283896›Full record

ArticleOncotarget2016

PNT2258, a novel deoxyribonucleic acid inhibitor, induces cell cycle arrest and apoptosis via a distinct mechanism of action: a new class of drug for non-Hodgkin's lymphoma.

Abdul Shukkur Ebrahim, Mustapha Kandouz, Allison Liddane, Hussam Sabbagh, Yuning Hou, Chunying Li, Ayad Al-Katib

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Molecularly targeted therapy and immunotherapy in leukemias.Journal of hematology & oncology · 2026
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  4. Tumor biomarkers for diagnosis, prognosis and targeted therapy.Signal transduction and targeted therapy · 2024
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  7. Review
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  9. Article
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  11. Article
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  14. Article
  15. Review
  16. Review
  17. Treatment of Richter's Syndrome.Current treatment options in oncology · 2017
    Review
  18. Review
  19. Unintended target effect of anti-BCL-2 DNAi.Cancer management and research · 2017
    Article
  20. Article
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

7 authors at 1 institution in 1 country.

Abdul Shukkur EbrahimLymphoma Research Lab, Wayne State University, Detroit, MI, 48201-USA.
Mustapha KandouzDepartment of Pathology, Wayne State University, Detroit, MI, 48201-USA.
Allison LiddaneLymphoma Research Lab, Wayne State University, Detroit, MI, 48201-USA.
Hussam SabbaghLymphoma Research Lab, Wayne State University, Detroit, MI, 48201-USA.
Yuning HouDepartment of Biochemistry and Molecular Biology, Wayne State University, Detroit, MI, 48201-USA.
Chunying LiDepartment of Biochemistry and Molecular Biology, Wayne State University, Detroit, MI, 48201-USA.
Ayad Al-KatibLymphoma Research Lab, Wayne State University, Detroit, MI, 48201-USA.
Wayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current therapy for BCL-2-associated tumors such as Non-Hodgkin Lymphomas (NHL) is inadequate. The DNAi PNT2258, a 24 base single-stranded phosphodiester DNA oligodeoxynucleotide (PNT100) encapsulated in a protective liposome, was precisely designed to treat cancers that over-express BCL-2. PNT2258 strongly inhibited BCL-2 promoter activity, confirming its predicted mechanism of action. BCL-2 mRNA and protein expression were significantly downregulated in a follicular small cleaved cell lymphoma (WSU-FSCCL) cell line. 2.5μM PNT2258 induced an initial S- phase arrest followed by a gradual increase in the sub-G0 (apoptosis) compartment and a reciprocal progressive decrease of the S phase. Terminal deoxynucleotidyl transferase (TdT)-positive populations and cleaved caspase-3 and PARP were also increased. The data are consistent with the idea that BCL-2 inhibition by PNT2258 activates apoptotic pathways in WSU-FSCCL cells. This is the first report to address the distinct mechanism of action underlying the anti-BCL-2 functions of PNT2258. Growth inhibition in two other cell lines, WSU-DLCL2 and WSU-WM, supports broad applicability of BCL-2 DNAi to treatment of B-cell NHL.

Indexed as

ApoptosisCaspase 3Cell Cycle CheckpointsCell Line, TumorCell SurvivalGene Expression Regulation, NeoplasticGene SilencingHumansLiposomesLymphoma, Non-HodgkinOligodeoxyribonucleotidesPromoter Regions, GeneticProto-Oncogene Proteins c-bcl-2RNA, MessengerS PhaseTranslocation, GeneticCASP3 protein, humanCaspase 3LiposomesOligodeoxyribonucleotidesPNT100Proto-Oncogene Proteins c-bcl-2RNA, MessengerapoptosisDNAinon-Hodgkin’s lymphomaPNT2258WSU-FSCCL

Identifiers

PMID27283896
PMCPMC5173141
OpenAlexW2415624398

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.