Evidence map›Paper›PMID 42115585›Full record

ArticleSignal transduction and targeted therapy2026

SSTN

Oisun Jung, DeannaLee M Beauvais, Gavril L Ibaan, Colin C Wooldrik, Evan Flietner, Suyong Choi, Jing Zhang, Alan C Rapraeger

Abstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Oisun Jung *Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA. ojung@unmc.edu.
DeannaLee M Beauvais *Department of Human Oncology and School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.
Gavril L IbaanEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA.
Colin C WooldrikEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA.
Evan FlietnerMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI, USA.
Suyong ChoiEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE, USA. schoi@unmc.edu.
Jing ZhangMcArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI, USA.
Alan C RapraegerDepartment of Human Oncology and School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA.

Funding

Phosphoinositide Signaling in the Cytosol and NucleusR35GM134955 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI Richard A. Anderson · 2020 to 2026
$5.0M
Syndecan-1 (CD138) and its synstatins: targeting invasion, survival and angiogenesis in myelomaR01CA212413 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI RAPRAEGER, ALAN C · 2017 to 2021
$1.8M
Unexpected roles of phosphoinositides in the nucleusR35GM150504 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Suyong Choi · 2023 to 2026
$1.5M
NIGMS NIH HHS R35 GM150504U.S. Department of Defense (United States Department of Defense) CA230255U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) CA036727U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA212413U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R35GM134955
6 · The paper itself

Abstract

Despite therapeutic advances, multiple myeloma (MM) remains incurable, largely due to relapse and the emergence of drug resistance driven by clonal evolution and alterations in the bone marrow (BM) microenvironment that support tumor survival. This highlights the need for novel therapeutics targeting both tumor cells and the supportive BM niche, particularly for patients with relapsed/refractory MM. Syndecan-1 (Sdc1/CD138), a heparan sulfate proteoglycan, is abundantly expressed on both the surface of myeloma cells and within the MM microenvironment. It plays a critical role in MM pathogenesis by promoting cell survival, angiogenesis, and immune evasion. This study investigates a novel chimeric peptide, SSTN

Indexed as

Multiple MyelomaPeptidesSyndecan-1AnimalsApoptosisCell Line, TumorDisease ProgressionHumansMiceTumor MicroenvironmentPeptidesSDC1 protein, humanSyndecan-1

Identifiers

PMID42115585
PMCPMC13161272

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.