Evidence map›Paper›PMID 35141027›Full record

ArticleAmerican journal of cancer research2022

Guanosine primes acute myeloid leukemia for differentiation via guanine nucleotide salvage synthesis.

Hanying Wang, Xin He, Zheng Li, Hongchuan Jin, Xian Wang, Ling Li

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 50% 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

6 citing papers in PubMed, 3 citations in OpenAlex.

  1. Targeting IMPDH to inhibit SAMHD1 inCell cycle (Georgetown, Tex.) · 2026
    Article
  2. Translational pediatrics · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. 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

6 authors at 2 institutions in 2 countries.

Hanying WangDepartment of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University Hangzhou 310016, Zhejiang, China.
Xin HeDepartment of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, Beckman Research Institute, City of Hope National Medical Center Duarte, CA 91010, USA.
Zheng LiDepartment of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, Beckman Research Institute, City of Hope National Medical Center Duarte, CA 91010, USA.
Hongchuan JinLaboratory of Cancer Biology, Key Lab of Biotherapy in Zhejiang Province, Cancer Center of Zhejiang University, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University Hangzhou 310016, Zhejiang, China.
Xian WangDepartment of Medical Oncology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University Hangzhou 310016, Zhejiang, China.
Ling LiDepartment of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, Beckman Research Institute, City of Hope National Medical Center Duarte, CA 91010, USA.
City Of Hope National Medical Center · USSir Run Run Shaw Hospital · CN

Funding

Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI John Charles Williams · 1985 to 2026
$86.3M
NCI NIH HHS P30 CA033572
6 · The paper itself

Abstract

Differentiation arrest represents a distinct hallmark of acute myeloid leukemia (AML). Identification of differentiation-induction agents that are effective across various subtypes remains an unmet challenge. GTP biosynthesis is elevated in several types of cancers, considered to support uncontrolled tumor growth. Here we report that GTP overload by supplementation of guanosine, the nucleoside precursor of GTP, poises AML cells for differentiation and growth inhibition. Transcriptome profiling of guanosine-treated AML cells reveals a myeloid differentiation pattern. Importantly, the treatment compromises leukemia progression in AML xenograft models. Mechanistically, GTP overproduction requires sequential metabolic conversions executed by the purine salvage biosynthesis pathway including the involvement of purine nucleoside phosphorylase (PNP) and hypoxanthine phosphoribosyltransferase 1 (HPRT1). Taken together, our study offers novel metabolic insights tethering GTP homeostasis to myeloid differentiation and provides an experimental basis for further clinical investigations of guanosine or guanine nucleotides in the treatment of AML patients.

Indexed as

Acute myeloid leukemiaguanosine 5’-triphosphateHPRT1myeloid differentiationPNP

Identifiers

PMID35141027
PMCPMC8822274
OpenAlexW4211266942

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.