Evidence map›Paper›PMID 19966933›Full record

ArticleAmerican journal of translational research2009

Overcoming cancer therapy resistance by targeting inhibitors of apoptosis proteins and nuclear factor-kappa B.

Yao Dai, Theodore S Lawrence, Liang Xu

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 84 citations in OpenAlex.

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  11. 15-Deoxy-ΔJournal of cancer prevention · 2020
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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 1 country.

Yao DaiDepartment of Radiation Oncology and Comprehensive Cancer Center, University of Michigan Medical School Ann Arbor, MI 48109, USA.
Theodore S Lawrence
Liang Xu
Radiation Oncology Associates · USUniversity of Michigan–Ann Arbor · US

Funding

Tumor-targeted silencing of Bcl-2/Bcl-xL by the self-assembled siRNA-nanovectorsR01CA121830 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI XU, LIANG · 2006 to 2010
$1.9M
Tumor targeted RNAi by novel nanovectors for molecular therapy of prostate cancerR21CA128220 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI XU, LIANG · 2007 to 2008
$225k
NCI NIH HHS R01 CA121830NCI NIH HHS R21 CA128220
6 · The paper itself

Abstract

Chemo- or radioresistance markedly impairs the efficacy of cancer therapy and involves anti-apoptotic signal transduction pathways that prevent cell death. In resistant cancer cells, both inhibitors of apoptosis proteins (IAPs) and nuclear factor-kappa B (NF-kappaB) play a pivotal role in preventing apoptosis triggered by a variety of stresses, facilitating them as potential targets in cancer treatment. Furthermore, mounting evidences have established the crosstalks between IAPs (eg. XIAP, cIAP-1, cIAP-2) and proteins involved in NF-kappaB signaling (eg. TRAF2, RIP1, TAB1). Second mitochondria-derived activator of caspases (Smac) is a mitochondrial protein that released into cytoplasm upon apoptotic stimuli. As Smac functions as an endogenous IAP inhibitor, small molecule Smac-mimetics are believed to neutralize IAPs function that results in liberating caspase activity and promoting apoptosis. Moreover, recent studies show that Smac-mimetics may kill cancer cells in a different manner, which involves inducing ubiquitination of cIAPs, regulating NF-kappaB signaling and facilitating TNFalpha-triggered, caspase-8-mediated apoptosis in a certain cancer cell types. In other cancer cells that are resistant to TNFalpha or chemo/radiotherapy, Smac-mimetic IAP-inhibitors can enhance ionizing radiation or tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, indicating the potential role of Smac-mimetics in overcoming acquired therapy-resistance. Such findings provide important impetus for utilizing IAP-inhibitors as novel adjuvant therapy for the TNFalpha-resistant, NF-kappaB constitutively active cancers that account for the majority of patients who are refractory to current therapeutic approaches.

Indexed as

Chemoresistanceinhibitors of apoptosis proteinsNF-κBsmall molecule inhibitors

Identifiers

PMID19966933
PMCPMC2776288
OpenAlexW2165021123

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.