Targeting pro-tumoral stromal exosomes by disrupting the syntenin-CD138/syndecan pathway as a novel therapy in Multiple Myeloma: Targeting pro-tumoral stromal exosomes by disrupting the syntenin-CD138/syndecan pathway as a novel therapy in Multiple Myeloma

Chenggong Tu

Targeting pro-tumoral stromal exosomes by disrupting the syntenin-CD138/syndecan pathway as a novel therapy in Multiple Myeloma: Targeting pro-tumoral stromal exosomes by disrupting the syntenin-CD138/syndecan pathway as a novel therapy in Multiple Myeloma

Onderzoeksoutput: Poster

Samenvatting

Exosomal communication between bone marrow stromal cells (BMSCs) and Multiple Myeloma (MM) cells induces the progression and drug resistance of myeloma. Syntenin which couples to syndecan 1, has been identified as an exosome marker which can regulate the biogenesis of exosomes.This study aims to investigate whether syntenin inhibition by knockout or a small inhibitor, termed SyntOFF
affects exosomal output by BMSCs and counteracts BMSC-induced drug resistance in MM.

Originele taal-2	English
Status	Unpublished - 8 okt. 2024

Citeer dit

@conference{5e44f44bb2624cb28cb26e1a508c7908,

title = "Targeting pro-tumoral stromal exosomes by disrupting the syntenin-CD138/syndecan pathway as a novel therapy in Multiple Myeloma: Targeting pro-tumoral stromal exosomes by disrupting the syntenin-CD138/syndecan pathway as a novel therapy in Multiple Myeloma ",

abstract = "Exosomal communication between bone marrow stromal cells (BMSCs) and Multiple Myeloma (MM) cells induces the progression and drug resistance of myeloma. Syntenin which couples to syndecan 1, has been identified as an exosome marker which can regulate the biogenesis of exosomes.This study aims to investigate whether syntenin inhibition by knockout or a small inhibitor, termed SyntOFFaffects exosomal output by BMSCs and counteracts BMSC-induced drug resistance in MM.",

author = "Chenggong Tu",

year = "2024",

month = oct,

day = "8",

language = "English",

}

TY - CONF

T1 - Targeting pro-tumoral stromal exosomes by disrupting the syntenin-CD138/syndecan pathway as a novel therapy in Multiple Myeloma

T2 - Targeting pro-tumoral stromal exosomes by disrupting the syntenin-CD138/syndecan pathway as a novel therapy in Multiple Myeloma

AU - Tu, Chenggong

PY - 2024/10/8

Y1 - 2024/10/8

N2 - Exosomal communication between bone marrow stromal cells (BMSCs) and Multiple Myeloma (MM) cells induces the progression and drug resistance of myeloma. Syntenin which couples to syndecan 1, has been identified as an exosome marker which can regulate the biogenesis of exosomes.This study aims to investigate whether syntenin inhibition by knockout or a small inhibitor, termed SyntOFFaffects exosomal output by BMSCs and counteracts BMSC-induced drug resistance in MM.

AB - Exosomal communication between bone marrow stromal cells (BMSCs) and Multiple Myeloma (MM) cells induces the progression and drug resistance of myeloma. Syntenin which couples to syndecan 1, has been identified as an exosome marker which can regulate the biogenesis of exosomes.This study aims to investigate whether syntenin inhibition by knockout or a small inhibitor, termed SyntOFFaffects exosomal output by BMSCs and counteracts BMSC-induced drug resistance in MM.

M3 - Poster

ER -