Evidence map›Paper›PMID 27043233›Full record

ReviewJournal of cancer research and clinical oncology2016

Hematologic malignancies: newer strategies to counter the BCL-2 protein.

Abdul Shukkur Ebrahim, Hussam Sabbagh, Allison Liddane, Ali Raufi, Mustapha Kandouz, Ayad Al-Katib

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cancer research and clinical oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  7. Effects of Different Levels ofAntioxidants (Basel, Switzerland) · 2025
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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

6 authors at 1 institution in 1 country.

Abdul Shukkur EbrahimDepartment of Internal Medicine-Lymphoma Research Lab, Wayne State University and School of Medicine, 8229 Scott Hall, 540 E. Canfield, Detroit, MI, 48201, USA.
Hussam SabbaghDepartment of Internal Medicine-Lymphoma Research Lab, Wayne State University and School of Medicine, 8229 Scott Hall, 540 E. Canfield, Detroit, MI, 48201, USA.
Allison LiddaneDepartment of Internal Medicine-Lymphoma Research Lab, Wayne State University and School of Medicine, 8229 Scott Hall, 540 E. Canfield, Detroit, MI, 48201, USA.
Ali RaufiDepartment of Internal Medicine-Lymphoma Research Lab, Wayne State University and School of Medicine, 8229 Scott Hall, 540 E. Canfield, Detroit, MI, 48201, USA.
Mustapha KandouzDepartment of Pathology, Wayne State University, Detroit, MI, 48201, USA.
Ayad Al-KatibDepartment of Internal Medicine-Lymphoma Research Lab, Wayne State University and School of Medicine, 8229 Scott Hall, 540 E. Canfield, Detroit, MI, 48201, USA. alkatib@med.wayne.edu.ORCID http://orcid.org/0000-0002-5684-948X
Wayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionBCL-2 is the founding member of the BCL-2 family of apoptosis regulatory proteins that either induce (pro-apoptotic) or inhibit (anti-apoptotic) apoptosis. The anti-apoptotic BCL-2 is classified as an oncogene, as damage to the BCL-2 gene has been shown to cause a number of cancers, including lymphoma. Ongoing research has demonstrated that disruption of BCL-2 leads to cell death. BCL-2 is also known to be involved in the development of resistance to chemotherapeutic agents, further underscoring the importance of targeting the BCL-2 gene in cancer therapeutics. Thus, numerous approaches have been developed to block or modulate the production of BCL-2 at the RNA level using antisense oligonucleotides or at the protein level with BCL-2 inhibitors, such as the novel ABT737.

methodsIn this article, we briefly review previous strategies to target the BCL-2 gene and focus on a new approach to silence DNA, DNA interference (DNAi). RESULTS AND

conclusionDNA interference is aimed at blocking BCL-2 gene transcription. Evaluations of this technology in preclinical and early clinical studies are very encouraging and strongly support further development of DNAi as cancer therapeutics. A pilot phase II clinical trial in patients with relapsed or refractory non-Hodgkin lymphoma, PNT2258 demonstrated clinical benefit in 11 of 13 patients with notable responses in diffuse large B cell lymphoma and follicular lymphoma. By targeting the DNA directly, the DNAi technology promises to be more effective compared with other gene-interference strategies that target the RNA or protein but leaves the dysregulated DNA functional.

Indexed as

Genes, bcl-2AnimalsAntineoplastic AgentsHematologic NeoplasmsHumansMolecular Targeted TherapyProto-Oncogene Proteins c-bcl-2Small Molecule LibrariesAntineoplastic AgentsProto-Oncogene Proteins c-bcl-2Small Molecule LibrariesAntisense oligonucleotidesBCL-2DNA interferenceNon-Hodgkin lymphomaSmall-molecule inhibitors

Identifiers

PMID27043233
PMCPMC11819263
OpenAlexW2340251168

What OpenQuestion holds

Textmetadata
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.