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Tumor-associated B-cells induce tumor heterogeneity and therapy resistance.

Abstract：

:In melanoma, therapies with inhibitors to oncogenic BRAFV600E are highly effective but responses are often short-lived due to the emergence of drug-resistant tumor subpopulations. We describe here a mechanism of acquired drug resistance through the tumor microenvironment, which is mediated by human tumor-associated B cells. Human melanoma cells constitutively produce the growth factor FGF-2, which activates tumor-infiltrating B cells to produce the growth factor IGF-1. B-cell-derived IGF-1 is critical for resistance of melanomas to BRAF and MEK inhibitors due to emergence of heterogeneous subpopulations and activation of FGFR-3. Consistently, resistance of melanomas to BRAF and/or MEK inhibitors is associated with increased CD20 and IGF-1 transcript levels in tumors and IGF-1 expression in tumor-associated B cells. Furthermore, first clinical data from a pilot trial in therapy-resistant metastatic melanoma patients show anti-tumor activity through B-cell depletion by anti-CD20 antibody. Our findings establish a mechanism of acquired therapy resistance through tumor-associated B cells with important clinical implications.Resistance to BRAFV600E inhibitors often occurs in melanoma patients. Here, the authors describe a potential mechanism of acquired drug resistance mediated by tumor-associated B cells-derived IGF-1.

journal_name

Nat Commun

journal_title

Nature communications

authors

Somasundaram R,Zhang G,Fukunaga-Kalabis M,Perego M,Krepler C,Xu X,Wagner C,Hristova D,Zhang J,Tian T,Wei Z,Liu Q,Garg K,Griss J,Hards R,Maurer M,Hafner C,Mayerhöfer M,Karanikas G,Jalili A,Bauer-Pohl V,Weihsengru

doi

10.1038/s41467-017-00452-4

subject

Has Abstract

pub_date

2017-09-19 00:00:00

pages

607

issue

1

issn

2041-1723

pii

10.1038/s41467-017-00452-4

journal_volume

8

pub_type

杂志文章

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