Evidence map›Paper›PMID 18757333›Full record

ReviewJournal of clinical oncology : official journal of the American Society of Clinical Oncology2008

Expanding circle of inhibition: small-molecule inhibitors of Bcl-2 as anticancer cell and antiangiogenic agents.

Benjamin D Zeitlin, Isaac J Zeitlin, Jacques E Nör

Open access · greenAbstract readReview
In one paragraph

Review in Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 80 citations in OpenAlex.

  1. Ro 08-2750 increases radiation-induced cytotoxicity in DLBCL by dysregulating the DNA damage response.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026
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  7. Natural Agents Targeting Mitochondria in Cancer.International journal of molecular sciences · 2020
    Review
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  19. Impact of biomarkers expression before and after portal vein embolization on recurrence after two-stage hepatectomy for colorectal liver metastases.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2012
    Article
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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

3 authors at 2 institutions in 2 countries.

Benjamin D ZeitlinDepartment of Restorative Sciences, University of Michigan School of Dentistry, University of Michigan, Ann Arbor, MI 48109-1078, USA.
Isaac J Zeitlin
Jacques E Nör
University of Michigan–Ann Arbor · USUniversity of Strathclyde · GB

Funding

Therapeutic Potential and Mechanism of Action of Potent Small Molecule InhibitorsP50CA097248 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NOR, JACQUES EDUARDO · 2002 to 2013
$25.3M
Bcl-2 /CXC Chemokines in Head /Neck Tumor AngiogenesisR01DE015948 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NOR, JACQUES EDUARDO · 2004 to 2008
$1.9M
Therapeutic Inhibition of Bcl-2 and Head & Neck Tumor AngiogenesisR01DE016586 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NOR, JACQUES EDUARDO · 2005 to 2009
$1.7M
Neovascular Regression for Oral Cancer TherapyR01DE014601 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI NOR, JACQUES EDUARDO · 2002 to 2006
$1.3M
NCI NIH HHS P50 CA097248NIDCR NIH HHS R01 DE014601NIDCR NIH HHS R01 DE015948NIDCR NIH HHS R01 DE016586NIDCR NIH HHS R01-DE14601NIDCR NIH HHS R01-DE15948NIDCR NIH HHS R01-DE16586
6 · The paper itself

Abstract

The specific targeting of diseases, particularly cancer, is a primary aim in drug development, as specificity reduces unwelcome effects on healthy tissue and increases drug efficacy at the target site. Drug specificity can be increased by improving the delivery system or by selecting drugs with affinity for a molecular ligand specific to the disease state. The role of the prosurvival Bcl-2 protein in maintaining the normal balance between apoptosis and cellular survival has been recognized for more than a decade. Bcl-2 is vital during development, much less so in adults. It has also been noted that some cancers evade apoptosis and obtain a survival advantage through aberrant expression of Bcl-2. The new and remarkably diverse class of drugs, small-molecule inhibitors of Bcl-2 (molecular weight approximately 400 to 800 Daltons), is examined herein. We present the activities of these compounds along with clinical observations, where available. The effects of Bcl-2 inhibition on attenuation of tumor cell growth are discussed, as are studies revealing the potential for Bcl-2 inhibitors as antiangiogenic agents. Despite an enormous body of work published for the Bcl-2 family of proteins, we are still learning exactly how this group of molecules interacts and indeed what they do. The small-molecule inhibitors of Bcl-2, in addition to their therapeutic potential, are proving to be an important investigative tool for understanding the function of Bcl-2.

Indexed as

Angiogenesis InhibitorsAntineoplastic AgentsApoptosisChemistry, PharmaceuticalFemaleGene Expression Regulation, NeoplasticHumansLigandsMaleModels, BiologicalModels, ChemicalNeovascularization, PathologicProto-Oncogene Proteins c-bcl-2Angiogenesis InhibitorsAntineoplastic AgentsLigandsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID18757333
PMCPMC2654265
OpenAlexW1992672293

What OpenQuestion holds

Textmetadata
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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.