Evidence map›Paper›PMID 38673926›Full record

ArticleInternational journal of molecular sciences2024

Duocarmycin SA Reduces Proliferation and Increases Apoptosis in Acute Myeloid Leukemia Cells In Vitro.

William A Chen, Terry G Williams, Leena So, Natalie Drew, Jie Fang, Pedro Ochoa, Nhi Nguyen, Yasmeen Jawhar, Jide Otiji, Penelope J Duerksen-Hughes and 7 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. 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

17 authors at 3 institutions in 1 country.

William A ChenDepartment of Pharmaceutical Sciences, School of Pharmacy, Loma Linda University, Shryock Hall 24745 Stewart Street, Loma Linda, CA 92350, USA.ORCID 0000-0002-0557-9504
Terry G WilliamsDepartment of Pharmaceutical Sciences, School of Pharmacy, Loma Linda University, Shryock Hall 24745 Stewart Street, Loma Linda, CA 92350, USA.
Leena SoDepartment of Pharmaceutical Sciences, School of Pharmacy, Loma Linda University, Shryock Hall 24745 Stewart Street, Loma Linda, CA 92350, USA.
Natalie DrewDepartment of Pharmaceutical Sciences, School of Pharmacy, Loma Linda University, Shryock Hall 24745 Stewart Street, Loma Linda, CA 92350, USA.
Jie FangDepartment of Surgery, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
Pedro OchoaDepartment of Basic Sciences, School of Medicine, Loma Linda University, 11175 Campus Street, Loma Linda, CA 92350, USA.
Nhi NguyenDepartment of Pharmaceutical Sciences, School of Pharmacy, Loma Linda University, Shryock Hall 24745 Stewart Street, Loma Linda, CA 92350, USA.
Yasmeen JawharDepartment of Pharmaceutical Sciences, School of Pharmacy, Loma Linda University, Shryock Hall 24745 Stewart Street, Loma Linda, CA 92350, USA.
Jide OtijiDepartment of Pharmaceutical Sciences, School of Pharmacy, Loma Linda University, Shryock Hall 24745 Stewart Street, Loma Linda, CA 92350, USA.
Penelope J Duerksen-HughesDepartment of Basic Sciences, School of Medicine, Loma Linda University, 11175 Campus Street, Loma Linda, CA 92350, USA.ORCID 0000-0002-0998-2157
Mark E ReevesDepartment of Basic Sciences, School of Medicine, Loma Linda University, 11175 Campus Street, Loma Linda, CA 92350, USA.
Carlos A CasianoDepartment of Basic Sciences, School of Medicine, Loma Linda University, 11175 Campus Street, Loma Linda, CA 92350, USA.ORCID 0000-0002-7320-4333
Hongjian JinCenter for Applied Bioinformatics, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.
Sinisa DovatDepartments of Pediatrics, Biochemistry and Molecular Biology, and Pharmacology, Penn State Cancer Institute, 400 University Drive, Hershey, PA 17033, USA.
Jun YangDepartment of Surgery, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA.ORCID 0000-0002-4233-3220
Kristopher E BoyleDepartment of Pharmaceutical Sciences, School of Pharmacy, Loma Linda University, Shryock Hall 24745 Stewart Street, Loma Linda, CA 92350, USA.
Olivia L Francis-BoyleDepartment of Pharmaceutical Sciences, School of Pharmacy, Loma Linda University, Shryock Hall 24745 Stewart Street, Loma Linda, CA 92350, USA.ORCID 0000-0001-6930-967X
Loma Linda University · USSt. Jude Children's Research Hospital · USPenn State Milton S. Hershey Medical Center · US

Funding

EXPLORE AND TARGET THE EPIGENETIC VULNERABILITY OF PAX3-FOXO1-DRIVEN RHABDOMYOSARCOMAR01CA266600 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Xiang Chen, Jun Yang · 2022 to 2026
$3.4M
Novel targeted therapy to reduce health disparities in pediatric leukemiaR01CA278226 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI Sinisa Dovat · 2023 to 2026
$2.1M
NCI NIH HHS R01 CA266600NCI NIH HHS R01 CA278226
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is a hematological malignancy that is characterized by an expansion of immature myeloid precursors. Despite therapeutic advances, the prognosis of AML patients remains poor and there is a need for the evaluation of promising therapeutic candidates to treat the disease. The objective of this study was to evaluate the efficacy of duocarmycin Stable A (DSA) in AML cells in vitro. We hypothesized that DSA would induce DNA damage in the form of DNA double-strand breaks (DSBs) and exert cytotoxic effects on AML cells within the picomolar range. Human AML cell lines Molm-14 and HL-60 were used to perform 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT), DNA DSBs, cell cycle, 5-ethynyl-2-deoxyuridine (EdU), colony formation unit (CFU), Annexin V, RNA sequencing and other assays described in this study. Our results showed that DSA induced DNA DSBs, induced cell cycle arrest at the G2M phase, reduced proliferation and increased apoptosis in AML cells. Additionally, RNA sequencing results showed that DSA regulates genes that are associated with cellular processes such as DNA repair, G2M checkpoint and apoptosis. These results suggest that DSA is efficacious in AML cells and is therefore a promising potential therapeutic candidate that can be further evaluated for the treatment of AML.

Indexed as

ApoptosisCell ProliferationDuocarmycinsLeukemia, Myeloid, AcuteAntineoplastic AgentsCell Cycle CheckpointsCell Line, TumorDNA Breaks, Double-StrandedDNA DamageHL-60 CellsHumansAntineoplastic AgentsDuocarmycinsacute myeloid leukemiaapoptosischemotherapyDNA alkylationDNA double-strand breakduocarmycin SA

Identifiers

PMID38673926
PMCPMC11050052
OpenAlexW4394821886

What Socratic 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 Socratic graph.