Tumor-associated B-cells induce tumor heterogeneity and therapy resistance
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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.
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Tumor-associated B cells in melanoma are involved in drug resistance and retain a pro-tumorigenic property in part through insulin-like growth factor-I secretion.
“Moreover, tumor-associated B cells in melanoma are involved in drug resistance and retain a pro-tumorigenic property in part through insulin-like growth factor-I secretion.86”
From Autoimmune diseases and immune-checkpoint inhibitors for cancer therapy: Review of the literature and personalized risk-based prevention strategy (2020) · cites this paper as [86]
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- 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., Weihsengruber, F., Rappersberger, K., Koller, J., Lang, R., Hudgens, C., Chen, G., Tetzlaff, M., Wu, L., Frederick, D. T., Scolyer, R. A., Long, G. V., Damle, M., Ellingsworth, C., Grinman, L., Choi, H., Gavin, B. J., Dunagin, M., Raj, A., Scholler, N., Gross, L., Beqiri, M., Bennett, K., Watson, I., Schaider, H., Davies, M. A., Wargo, J., Czerniecki, B. J., Schuchter, L., Herlyn, D., Flaherty, K., Herlyn, M., & Wagner, S. N.
- Affiliations
- The Wistar Institute (US)
- University of Pennsylvania (US)
- Medical University of Vienna (AT)
- New Jersey Institute of Technology (US)
- Krankenanstalt Rudolfstiftung der Stadt Wien (AT)
- Paracelsus Medical University (AT)
- The University of Texas MD Anderson Cancer Center (US)
- Harvard University (US)
- The University of Sydney (AU)
- SRI International (US)
- Austrian Academy of Sciences (AT)
- McGill University (CA)
- Translational Research Institute (AU)
- Hospital of the University of Pennsylvania (US)
- Corresponding author
- Somasundaram, Rajasekharan
- Herlyn, Meenhard
- Wagner, Stephan N.
- ORCID
- Somasundaram, Rajasekharan
- Zhang, Gao
- Perego, Michela
- Xu, Xiaowei
- Hristova, Denitsa
- Zhang, Jie
- Tian, Tian
- Wei, Zhi
- Liu, Qin
- Garg, Kanika
- Griss, Johannes
- Karanikas, Georgios
- Jalili, Ahmad
- Rappersberger, Klemens
- Lang, Roland
- Hudgens, Courtney
- Tetzlaff, Michael
- Wu, Lawrence
- Frederick, Dennie Tompers
- Scolyer, Richard A.
- Long, Georgina V.
- Damle, Manashree
- Choi, Harry
- Dunagin, Margaret
- Raj, Arjun
- Scholler, Nathalie
- Beqiri, Marilda
- Bennett, Keiryn
- Watson, Ian
- Schaider, Helmut
- Davies, Michael A.
- Wargo, Jennifer
- Czerniecki, Brian J.
- Schuchter, Lynn
- Flaherty, Keith
- Herlyn, Meenhard
- Wagner, Stephan N.
- Venue
- Nature Communications
- Published
- 2017-09-19
- Volume
- 8
- Issue
- 1
- Pages
- 607-607
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5605714
- OpenAlex
- W2755929010
- Cited by
- 151
- References
- 61
- Citations by year
- 2026: 12 · 2025: 15 · 2024: 8 · 2023: 16 · 2022: 13 · 2021: 27 · 2020: 21 · 2019: 27 · 2018: 11 · 2017: 1
- FWCI
- 6.70
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- Cancer Institute NSW
- Vienna Science and Technology Fund (LS11-045)
- Universität Wien
- Medizinische Universität Wien
- Melanoma Institute Australia
- National Institutes of Health
- Medical Research Council
- National Health and Medical Research Council
- National Cancer Institute (R01CA047159, P01CA114046, P01CA025874, P50CA174523, P30CA010815)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- tumor-associated B cells, acquired drug resistance, melanoma, BRAF inhibitors, MEK inhibitors, insulin-like growth factor I, FGF2, FGFR3, tumor heterogeneity, tumor microenvironment, CD20, anti-CD20 monoclonal antibody, B-cell depletion, metastatic melanoma
- MeSH terms
- Antibodies, Monoclonal, Antineoplastic Agents, B-Lymphocytes, Cell Survival, Cisplatin, Humans, Insulin-Like Growth Factor I, Melanoma, Pilot Projects, Skin Neoplasms, Fibroblast Growth Factor 2, Lymphocytes, Tumor-Infiltrating, Paclitaxel, Drug Resistance, Neoplasm, Protein Kinase Inhibitors, Proto-Oncogene Proteins B-raf, Receptor, Fibroblast Growth Factor, Type 3, Tumor Microenvironment, Antibodies, Monoclonal, Humanized, In Vitro Techniques
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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