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Related Experiment Video

Updated: Jun 13, 2025

Isolation and Characterization of Tumor-initiating Cells from Sarcoma Patient-derived Xenografts

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Cellular origin and clonal evolution of human dedifferentiated liposarcoma.

Nadège Gruel^1,2, Chloé Quignot¹, Laëtitia Lesage³

¹INSERM U830, Diversity and Plasticity of Childhood Tumors Lab, PSL Research University, Institut Curie Research Center, Paris, France.

Nature Communications

|September 12, 2024

Summary

Dedifferentiated liposarcoma (DDLPS) originates from tumor adipocyte stem cells (ASC). These ASCs possess ancestral genomic alterations, driving both well-differentiated and dedifferentiated tumor components, while a TGF-β-rich microenvironment suppresses adipogenesis.

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Tumorsphere Derivation and Treatment from Primary Tumor Cells Isolated from Mouse Rhabdomyosarcomas

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Published on: September 13, 2019

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Dedifferentiated liposarcoma (DDLPS) is a high-grade soft tissue sarcoma characterized by coexisting undifferentiated and well-differentiated adipocytic tumor cells.
Both tumor components share MDM2 amplification, but their cellular origin is not well understood.

Purpose of the Study:

To investigate the cellular heterogeneity and origin of DDLPS.
To characterize the tumor microenvironment's role in DDLPS progression.

Main Methods:

Single-cell RNA sequencing
DNA sequencing
In situ multiplex immunofluorescence
Functional assays on paired tumor components

Main Results:

Identified a population of tumor adipocyte stem cells (ASCs) resembling white adipose tissue stromal progenitors.
ASCs harbor ancestral genomic alterations, indicating they are the progenitors of both well-differentiated and dedifferentiated DDLPS components.
Dedifferentiated tumor cells retain ASC pluripotency, with adipogenic potential inhibited by a TGF-β-high immunosuppressive tumor microenvironment.

Conclusions:

DDLPS arises from tumor adipocyte stem cells through clonal evolution.
The tumor microenvironment plays a critical role in regulating DDLPS cell behavior and progression.