Evidence map›Paper›PMID 26219913›Full record

ArticleMolecular pharmacology2015

Suppression of Cytosolic NADPH Pool by Thionicotinamide Increases Oxidative Stress and Synergizes with Chemotherapy.

Philip M Tedeschi, HongXia Lin, Murugesan Gounder, John E Kerrigan, Emine Ercikan Abali, Kathleen Scotto, Joseph R Bertino

Open access · bronzeAbstract read
In one paragraph

Article in Molecular pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

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  12. The Invasive AnemoneMetabolites · 2023
    Article
  13. lncRNAActa biochimica et biophysica Sinica · 2023
    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

7 authors at 1 institution in 1 country.

Philip M TedeschiDepartments of Pharmacology and Medicine, Rutgers Cancer Institute of New Jersey (P.M.T., H.L., M.G., J.E.K., K.S., J.R.B.), and Department of Biochemistry (E.E.A.), Rutgers University, New Brunswick, New Jersey.
HongXia LinDepartments of Pharmacology and Medicine, Rutgers Cancer Institute of New Jersey (P.M.T., H.L., M.G., J.E.K., K.S., J.R.B.), and Department of Biochemistry (E.E.A.), Rutgers University, New Brunswick, New Jersey.
Murugesan GounderDepartments of Pharmacology and Medicine, Rutgers Cancer Institute of New Jersey (P.M.T., H.L., M.G., J.E.K., K.S., J.R.B.), and Department of Biochemistry (E.E.A.), Rutgers University, New Brunswick, New Jersey.
John E KerriganDepartments of Pharmacology and Medicine, Rutgers Cancer Institute of New Jersey (P.M.T., H.L., M.G., J.E.K., K.S., J.R.B.), and Department of Biochemistry (E.E.A.), Rutgers University, New Brunswick, New Jersey.
Emine Ercikan AbaliDepartments of Pharmacology and Medicine, Rutgers Cancer Institute of New Jersey (P.M.T., H.L., M.G., J.E.K., K.S., J.R.B.), and Department of Biochemistry (E.E.A.), Rutgers University, New Brunswick, New Jersey.
Kathleen ScottoDepartments of Pharmacology and Medicine, Rutgers Cancer Institute of New Jersey (P.M.T., H.L., M.G., J.E.K., K.S., J.R.B.), and Department of Biochemistry (E.E.A.), Rutgers University, New Brunswick, New Jersey.
Joseph R BertinoDepartments of Pharmacology and Medicine, Rutgers Cancer Institute of New Jersey (P.M.T., H.L., M.G., J.E.K., K.S., J.R.B.), and Department of Biochemistry (E.E.A.), Rutgers University, New Brunswick, New Jersey bertinoj@cinj.rutgers.edu.
Rutgers, The State University of New Jersey · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
UMDNJ TRAINING GRANT IN BIOTECHNOLOGYT32GM008339 · NIGMS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI YARMUSH, MARTIN L · 1989 to 2019
$6.1M
NCI NIH HHS P30 CA072720NIGMS NIH HHS T32 GM008339NIGMS NIH HHS T32-GM8339
6 · The paper itself

Abstract

NAD(+) kinase (NADK) is the only known cytosolic enzyme that converts NAD(+) to NADP(+), which is subsequently reduced to NADPH. The demand for NADPH in cancer cells is elevated as reducing equivalents are required for the high levels of nucleotide, protein, and fatty acid synthesis found in proliferating cells as well as for neutralizing high levels of reactive oxygen species (ROS). We determined whether inhibition of NADK activity is a valid anticancer strategy alone and in combination with chemotherapeutic drugs known to induce ROS. In vitro and in vivo inhibition of NADK with either small-hairpin RNA or thionicotinamide inhibited proliferation. Thionicotinamide enhanced the ROS produced by several chemotherapeutic drugs and produced synergistic cell kill. NADK inhibitors alone or in combination with drugs that increase ROS-mediated stress may represent an efficacious antitumor combination and should be explored further.

Indexed as

AnimalsAntineoplastic AgentsCytosolDrug SynergismHumansMaleMiceMice, Inbred NODMice, SCIDNADPNiacinamideOxidative StressTumor Cells, CulturedXenograft Model Antitumor AssaysAntineoplastic AgentsNADPNiacinamidethionicotinamide

Identifiers

PMID26219913
PMCPMC4576680
OpenAlexW2217992775

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.