Evidence map›Paper›PMID 32974194›Full record

ReviewFrontiers in oncology2020

Targeting Base Excision Repair in Cancer: NQO1-Bioactivatable Drugs Improve Tumor Selectivity and Reduce Treatment Toxicity Through Radiosensitization of Human Cancer.

Colton L Starcher, S Louise Pay, Naveen Singh, I-Ju Yeh, Snehal B Bhandare, Xiaolin Su, Xiumei Huang, Erik A Bey, Edward A Motea, David A Boothman

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. European journal of biology · 2023
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
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

10 authors.

Colton L StarcherDepartment of Biochemistry and Molecular Biology, IU Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN, United States.
S Louise PayDepartment of Biochemistry and Molecular Biology, IU Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN, United States.
Naveen SinghDepartment of Biochemistry and Molecular Biology, IU Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN, United States.
I-Ju YehDepartment of Biochemistry and Molecular Biology, IU Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN, United States.
Snehal B BhandareDepartment of Biochemistry and Molecular Biology, IU Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN, United States.
Xiaolin SuDepartment of Biochemistry and Molecular Biology, IU Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN, United States.
Xiumei HuangDepartment of Radiation Oncology, IU Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN, United States.
Erik A BeyDepartment of Biochemistry and Molecular Biology, IU Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN, United States.
Edward A MoteaDepartment of Biochemistry and Molecular Biology, IU Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN, United States.
David A BoothmanDepartment of Biochemistry and Molecular Biology, IU Simon Cancer Center, Indiana University School of Medicine, Indianapolis, IN, United States.

Funding

RPRD1B/Kub5/Hera, an RNA Pol II determinant that controls PARPi & IR sensitivityR01CA210489 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MOTEA, EDWARD AYSON · 2016 to 2020
$1.8M
Tumor-selective radiosensitization of NSCLC using NQO1 bioactivatable drugsR01CA224493 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI HUANG, XIUMEI · 2018 to 2022
$1.8M
NCI NIH HHS R01 CA210489NCI NIH HHS R01 CA224493
6 · The paper itself

Abstract

Ionizing radiation (IR) creates lethal DNA damage that can effectively kill tumor cells. However, the high dose required for a therapeutic outcome also damages healthy tissue. Thus, a therapeutic strategy with predictive biomarkers to enhance the beneficial effects of IR allowing a dose reduction without losing efficacy is highly desirable. NAD(P)H:quinone oxidoreductase 1 (NQO1) is overexpressed in the majority of recalcitrant solid tumors in comparison with normal tissue. Studies have shown that NQO1 can bioactivate certain quinone molecules (e.g., ortho-naphthoquinone and β-lapachone) to induce a futile redox cycle leading to the formation of oxidative DNA damage, hyperactivation of poly(ADP-ribose) polymerase 1 (PARP1), and catastrophic depletion of NAD

Indexed as

abasic sitesbase excision repairdouble-strand break repairionizing radiationNQO1PARP1 hyperactivationsynergyβ-lapachone

Identifiers

PMID32974194
PMCPMC7468503

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.