Evidence map›Paper›PMID 33142831›Full record

ArticleCancers2020

An Aptamer for Broad Cancer Targeting and Therapy.

Bethany Powell Gray, Xirui Song, David S Hsu, Christina Kratschmer, Matthew Levy, Ashley P Barry, Bruce A Sullenger

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The effects of doxorubicin loaded aptamer S3-linked DNA tetrahedrons on nasopharyngeal carcinoma.Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale · 2023
    Article
  5. Article
  6. Article
  7. Aptamer-based Advances in Skin Cancer Research.Current medicinal chemistry · 2023
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
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 3 institutions in 1 country.

Bethany Powell GrayDepartment of Surgery, Duke Cancer Institute, Duke University School of Medicine, Durham, NC 27710, USA.
Xirui SongDepartment of Surgery, Duke Cancer Institute, Duke University School of Medicine, Durham, NC 27710, USA.
David S HsuDepartment of Medical Oncology, Duke Cancer Institute, Center for Genomics and Computational Biology, Duke University Medical Center, Durham, NC 27710, USA.
Christina KratschmerDepartment of Biochemistry, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Matthew LevyDepartment of Biochemistry, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Ashley P BarryResearch and Development Division, b3 bio, Inc., Durham, NC 27709, USA.
Bruce A SullengerDepartment of Surgery, Duke Cancer Institute, Duke University School of Medicine, Durham, NC 27710, USA.
Duke University · USAlbert Einstein College of Medicine · USDuke Medical Center · US

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI JOHN N. NORTON · 1985 to 2026
$174.8M
Division of Cancer Prevention, National Cancer Institute P30-CA014236U.S. Department of Defense PC111812P2/W81XWH-12-1-0262U.S. Department of Defense PC131874
6 · The paper itself

Abstract

Recent advances in chemotherapy treatments are increasingly targeted therapies, with the drug conjugated to an antibody able to deliver it directly to the tumor. As high-affinity chemical ligands that are much smaller in size, aptamers are ideal for this type of drug targeting. Aptamer-highly toxic drug conjugates (ApTDCs) based on the E3 aptamer, selected on prostate cancer cells, target and inhibit prostate tumor growth in vivo. Here, we observe that E3 also broadly targets numerous other cancer types, apparently representing a universal aptamer for cancer targeting. Accordingly, ApTDCs formed by conjugation of E3 to the drugs monomethyl auristatin E (MMAE) or monomethyl auristatin F (MMAF) efficiently target and kill a range of different cancer cells. Notably, this targeting extends to both patient-derived explant (PDX) cancer cell lines and tumors, with the E3 MMAE and MMAF conjugates inhibiting PDX cell growth in vitro and with the E3 aptamer targeting PDX colorectal tumors in vivo.

Indexed as

aptameraptamer-drug conjugateaptamer highly toxic drug conjugatecancerdrug targeting

Identifiers

PMID33142831
PMCPMC7694147
OpenAlexW3095296017

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.