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EGFR ligand amphiregulin in Myeloma?
Could radiation therapy stimulate EGFR ligand amphiregulin in Myeloma? And then could this stimulate distant MM growth in MM patients?
Full disclosure- I am a long-term MM survivor, not any type of medical professional. The studies linked below seem to say that “radiotherapy induces the expression of the EGFR ligand amphiregulin in tumour cells”, which could stimulate MM elsewhere in the MM patient, but I am a layman. Those studies are difficult for me to understand.
I will say that this basic explanation makes sense to me, in my case anyway. Local radiation in a single plasmacytoma in early 1994 led to a diagnosis of frank multiple myeloma less than a year later.
My relapse in less than a year has caused me to wonder if there was myeloma in other parts of my body, so that I did not have a single plasmacytoma. The articles linked below cause me to wonder if local radiation caused these myeloma cells to grow.
Are you an MM survivor? What do you think? Email me at David.PeopleBeatingCancer@gmail.com with your thoughts.
Thank you,
David Emerson
- MM Survivor
- MM Cancer Coach
- Director PeopleBeatingCancer
Radiation-induced amphiregulin drives tumour metastasis
“The anti-tumour effect of radiotherapy beyond the treatment field—the abscopal effect—has garnered much interest1. However, the potentially deleterious effect of radiation in promoting metastasis is less well studied.
Here we show that radiotherapy induces the expression of the EGFR ligand amphiregulin in tumour cells, which reprogrammes EGFR-expressing myeloid cells toward an immunosuppressive phenotype and reduces phagocytosis.
This stimulates distant metastasis growth in human patients and in pre-clinical mouse tumour models.
The inhibition of these tumour-promoting factors induced by radiotherapy may represent a novel therapeutic strategy to improve patient outcomes.”
Multiple myeloma-derived exosomes are enriched of amphiregulin (AREG) and activate the epidermal growth factor pathway in the bone microenvironment leading to osteoclastogenesis
“Background: Multiple myeloma (MM) is a clonal plasma cell malignancy associated with osteolytic bone disease. Recently, the role of MM-derived exosomes in the osteoclastogenesis has been demonstrated although the underlying mechanism is still unknown.
Since exosomes-derived epidermal growth factor receptor ligands (EGFR) are involved in tumor-associated osteolysis, we hypothesize that the EGFR ligand amphiregulin (AREG) can be delivered by MM-derived exosomes and participate in MM-induced osteoclastogenesis…
Results: We found that AREG was specifically enriched in exosomes from MM samples and that exosomes-derived AREG led to the activation of EGFR in pre-OC, as showed by the increase of mRNA expression of its downstream SNAIL in both RAW264.7 and CD14+ cells.
The presence of neutralizing anti-AREG monoclonal antibody (mAb) reverted this effect. Consequently, we showed that the effect of MM-derived exosomes on osteoclast differentiation was inhibited by the pre-treatment of exosomes with anti-AREG mAb. In addition, we demonstrated the ability of MM-derived AREG-enriched exosomes to be internalized into human mesenchymal stromal cells (MSCs) blocking osteoblast (OB) differentiation, increasing MM cell adhesion and the release of the pro-osteoclastogenic cytokine interleukin-8 (IL8). Accordingly, anti-AREG mAb inhibited the release of IL8 by MSCs suggesting that both direct and indirect effects are responsible for AREG-enriched exosomes involvement on MM-induced osteoclastogenesis.
Conclusions: In conclusion, our data indicate that AREG is packed into MM-derived exosomes and implicated in OC differentiation through an indirect mechanism mediated by OBs.”
EGFR ligand amphiregulin in Myeloma EGFR ligand amphiregulin in Myeloma