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Cited by 1,036

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Exosomes Released by Melanoma Cells Prepare Sentinel Lymph Nodes for Tumor Metastasis

Hood, Joshua L., San, Roman Susana, Wickline, Samuel A.·2011·Cancer Research

Abstract

Exosomes are naturally occurring biological nanovesicles utilized by tumors to communicate signals to local and remote cells and tissues. Melanoma exosomes can incite a proangiogenic signaling program capable of remodeling tissue matrices. In this study, we show exosome-mediated conditioning of lymph nodes and define microanatomic responses that license metastasis of melanoma cells. Homing of melanoma exosomes to sentinel lymph nodes imposes synchronized molecular signals that effect melanoma cell recruitment, extracellular matrix deposition, and vascular proliferation in the lymph nodes. Our findings highlight the pathophysiologic role and mechanisms of an exosome-mediated process of microanatomic niche preparation that facilitates lymphatic metastasis by cancer cells. Cancer Res; 71(11); 3792–801. ©2011 AACR.

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Metadata

Authors
Hood, J. L., San, R. S., & Wickline, S. A.
Venue
Cancer Research
Published
2011-05-31
Volume
71
Issue
11
Pages
3792-3801
ISSN
  • 0008-5472 (ISSN-L)
  • 1538-7445
OpenAlex
W2048883725
Cited by
1,036
References
3
FWCI
20.10
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Exosomes Released by Melanoma Cells Prepare Sentinel Lymph Nodes for Tumor Metastasis. https://app.cochat.ai/papers/10.1158/0008-5472.can-10-4455
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Hood, J. L., San, R. S., & Wickline, S. A. (2011). Exosomes Released by Melanoma Cells Prepare Sentinel Lymph Nodes for Tumor Metastasis. Cancer Research. https://doi.org/10.1158/0008-5472.can-10-4455

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.