Obesity promotes resistance to anti-VEGF therapy in breast cancer by up-regulating IL-6 and potentially FGF-2
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Targeting IL-6 and potentially FGF-2 overcomes resistance to anti-VEGF therapy in breast cancer.
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A less hypoxic tumor microenvironment makes tumors less aggressive.
“As a consequence, the TME becomes less hypoxic, rendering tumors less aggressive (14).”
Anti-VEGF treatment is ineffective in obese mice due to increased IL-6 and FGF-2 expression by adipocytes in the TME, while co-targeting these improves anti-VEGF therapy response.
“For example, anti‐VEGF treatment is ineffective in obese mice due to increased IL‐6 and FGF‐2 expression by the adipocytes in the TME, while co‐targeting these improve the anti‐VEGF therapy response [75].”
From Tumor microenvironment signaling and therapeutics in cancer progression (2023) · cites this paper as [75]
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References 92 · Cited by 222
- Authors
- Incio, J., Ligibel, J. A., McManus, D. T., Suboj, P., Jung, K., Kawaguchi, K., Pinter, M., Babykutty, S., Chin, S. M., Vardam, T. D., Huang, Y., Rahbari, N. N., Roberge, S., Wang, D., Gomes-Santos, I. L., Puchner, S. B., Schlett, C. L., Hoffmman, U., Ancukiewicz, M., Tolaney, S. M., Krop, I. E., Duda, D. G., Boucher, Y., Fukumura, D., & Jain, R. K.
- Affiliations
- Edwin L. Steele Laboratories, Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
- Harvard University (US)
- Corresponding author
- Fukumura, Dai
- Jain, Rakesh K.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2018-03-14
- Volume
- 10
- Issue
- 432
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC5936748
- OpenAlex
- W2792558334
- Cited by
- 222
- References
- 92
- Citations by year
- 2026: 21 · 2025: 20 · 2024: 18 · 2023: 27 · 2022: 34 · 2021: 36 · 2020: 39 · 2019: 17 · 2018: 10
- FWCI
- 9.07
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion)
- Funders
- U.S. Department of Defense (W81XWH-10-1-0016)
- National Cancer Institute (R01-CA126642, R35CA197743, P01-CA080124, R01-CA208205, P01-CA080124, R01-CA208205, R01-CA096915, S10-RR027070, Federal Share Proton Beam Program Income, R01-CA159258)
- FCT (POPH/FSE funding program)
- Erwin Schroedinger (J 3747-B28)
- Sao Paulo Research Foundation fellowship (FAPESP 2016/21320-1)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Oncology › Lymphatic System and Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- obesity, breast cancer, anti-VEGF therapy resistance, interleukin-6, fibroblast growth factor 2, tumor angiogenesis, tumor hypoxia, adipose tissue, tumor vasculature normalization, tumor immunosuppression, metformin, metastasis, myeloid cells
- MeSH terms
- Animals, Antineoplastic Agents, Breast Neoplasms, Enzyme-Linked Immunosorbent Assay, Female, Humans, Metformin, Obesity, Interleukin-6, Fibroblast Growth Factor 2, Vascular Endothelial Growth Factor A, Mice
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