Evidence map›Paper›PMID 33801569›Full record

ArticleCancers2021

Bone Marrow Homeostasis Is Impaired via JAK/STAT and Glucocorticoid Signaling in Cancer Cachexia Model.

Jinyeong Yu, Sanghyuk Choi, Aran Park, Jungbeom Do, Donghyun Nam, Youngjae Kim, Jinok Noh, Kil Yeon Lee, Chi Hoon Maeng, Ki-Sook Park

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07237464 (A Randomized, Double-Blind, Placebo-Controlled, Dose-Escalation Phase I Trial to Evaluate the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, and Immunogenicity of GB18 Following Single Subcutaneous Injection in Healthy Adult Participants), which is not on this map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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.

NCT07237464 phase1recruitingnot on this mapstarted 2025, after this paper: background citation

A Randomized, Double-Blind, Placebo-Controlled, Dose-Escalation Phase I Trial to Evaluate the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, and Immunogenicity of GB18 Following Single Subcutaneous Injection in Healthy Adult Participants

TypeinterventionalSponsorShenzhen Kexing Pharmaceutical Co., Ltd.Ran2025 to 2026Enrolled36ConditionsCancer Cachexia (CC), Cancer Cachexia, Cancer Cachexia SyndromeArmsGB18 injection, Placebo
3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 9 citations in OpenAlex.

  1. Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026
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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

10 authors at 2 institutions in 1 country.

Jinyeong YuGraduate School of Biotechnology, Kyung Hee University, Yongin 17104, Korea.
Sanghyuk ChoiGraduate School of Biotechnology, Kyung Hee University, Yongin 17104, Korea.
Aran ParkGraduate School of Biotechnology, Kyung Hee University, Yongin 17104, Korea.
Jungbeom DoDepartment of Biomedical Science and Technology, Graduate School, Kyung Hee University, Seoul 02447, Korea.
Donghyun NamDepartment of Biomedical Science and Technology, Graduate School, Kyung Hee University, Seoul 02447, Korea.
Youngjae KimDepartment of Biomedical Science and Technology, Graduate School, Kyung Hee University, Seoul 02447, Korea.
Jinok NohDepartment of Biomedical Science and Technology, Graduate School, Kyung Hee University, Seoul 02447, Korea.
Kil Yeon LeeDepartment of Surgery, College of Medicine, Kyung Hee University, Seoul 02447, Korea.
Chi Hoon MaengDepartment of Internal Medicine, College of Medicine, Kyung Hee University, Seoul 02447, Korea.
Ki-Sook ParkDepartment of Biomedical Science and Technology, Graduate School, Kyung Hee University, Seoul 02447, Korea.
Kyung Hee University · KRKyung Hee University East-West Neo Medical Center · KR

Funding

National Research Foundation of Korea 2015R1D1A1A09057839National Research Foundation of Korea 2017M3A9E4065331
6 · The paper itself

Abstract

Cancer cachexia is a multifactorial systemic inflammation disease caused by complex interactions between the tumor and host tissues via soluble factors. However, whether cancer cachexia affects the bone marrow, in particular the hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs), remains unclear. Here, we investigated the bone marrow and bone in a cancer cachexia animal model generated by transplanting Lewis lung carcinoma cells. The number of bone marrow mononuclear cells (BM-MNCs) started to significantly decrease in the cancer cachectic animal model prior to the discernable loss of muscle and fat. This decrease in BM-MNCs was associated with myeloid skewing in the circulation and the expansion of hematopoietic progenitors in the bone marrow. Bone loss occurred in the cancer cachexia animal model and accompanied the decrease in the bone marrow MSCs that play important roles in both supporting HSCs and maintaining bone homeostasis. Glucocorticoid signaling mediated the decrease in bone marrow MSCs in the cancer cachectic environment. The cancer cachexia environment also skewed the differentiation of the bone marrow MSCs toward adipogenic fate via JAK/STAT as well as glucocorticoid signaling. Our results suggest that the bone loss induced in cancer cachexia is associated with the depletion and the impaired differentiation capacity of the bone marrow MSCs.

Indexed as

bone marrowcancer cachexiaglucocorticoidJAKmesenchymal stem cellsSTAT3

Identifiers

PMID33801569
PMCPMC7958949
OpenAlexW3133510909

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.