The DOI matches its Crossref record; 134 of the 136 references it cites were found in a registry or an index.
Tumor-Associated Macrophages: From Mechanisms to Therapy
Open accessAbstract
The tumor microenvironment is a complex ecology of cells that evolves with and provides support to tumor cells during the transition to malignancy. Among the innate and adaptive immune cells recruited to the tumor site, macrophages are particularly abundant and are present at all stages of tumor progression. Clinical studies and experimental mouse models indicate that these macrophages generally play a protumoral role. In the primary tumor, macrophages can stimulate angiogenesis and enhance tumor cell invasion, motility, and intravasation. During monocytes and/or metastasis, macrophages prime the premetastatic site and promote tumor cell extravasation, survival, and persistent growth. Macrophages are also immunosuppressive, preventing tumor cell attack by natural killer and T cells during tumor progression and after recovery from chemo- or immunotherapy. Therapeutic success in targeting these protumoral roles in preclinical models and in early clinical trials suggests that macrophages are attractive targets as part of combination therapy in cancer treatment.
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“Accordingly, TAM-based therapeutic strategies are being developed that aim at TAM targeting, TAM re-education, and TAM depletion [88, 96, 101, 102].”
From Tumor microenvironment complexity and therapeutic implications at a glance (2020) · cites this paper as [88]
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“Many therapy strategies have attempted to alter the polarization of macrophages’ “re-programming” or prevent monocyte tumor infiltration (Noy and Pollard, 2014).”
From Sysrev: A FAIR Platform for Data Curation and Systematic Evidence Review (2021) · cites this paper as Noy and Pollard, 2014
In the citing paper
“In preclinical models, both of these innate immune cell types aid tumor growth and metastasis through their secretion of factors that suppress antitumor immune responses, especially those of CD8 + T cells and NK cells (166, 167).”
From Immune Checkpoint Inhibitors for the Treatment of Cancer: Clinical Impact and Mechanisms of Response and Resistance (2021) · cites this paper as [167]
In the citing paper
“The production of colony stimulating factor 1 (CSF-1; also known as macrophage colony stimulating factor) by BCCs, has been reported to stimulate the recruitment of macrophages to primary breast tumors, leading to the secretion by tumor-associated macrophages (TAMs) of epidermal growth factor, which binds to its cognate receptor on BCCs to stimulate invasion and metastasis [36–38].”
From The hypoxic tumor microenvironment: A driving force for breast cancer progression (2016) · cites this paper as [38]
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1 retracted
Forget, M. A., Voorhees, J. L., Cole, S. L., Dakhlallah, D. A., Patterson, I. L., Gross, A. C., Moldovan, L., Mo, X. M., Evans, R., Marsh, C. B., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0098623 · Cited by 79 · cited 2×
“Interestingly, CSF1 upregulates TIE2 on TAMs (Forget et al., 2014) indicating a link between CSF1, TIE2 macrophages, and the induction of the angiogenic switch.”
BackgroundRetractedHallmarks of Cancer: The Next Generation
Hanahan, D., & Weinberg, R. A. (2011) · Cell · doi:10.1016/j.cell.2011.02.013 · Cited by 66,590 · cited 1×
“…the ways in which the microenvironmental support to tumors is the acquisition of a vasculature that provides oxygenation, as well as the nutrition and waste disposal required for growth above a certain size in a process often referred to as the ‘‘angiogenic switch’’ (Hanahan and Weinberg, 2011).”
BackgroundCoussens, L. M., & Werb, Z. (2002) · Nature · doi:10.1038/nature01322 · Cited by 15,111 · cited 1×
“Furthermore, inflammatory conditions such as Crohn’s disease dramatically increase the risk of colorectal cancer (Balkwill et al., 2005; Balkwill and Mantovani, 2012; Coussens and Werb, 2002; Grivennikov et al., 2010).”
BackgroundImmunity, Inflammation, and Cancer
Grivennikov, S. I., Greten, F. R., & Karin, M. (2010) · Cell · doi:10.1016/j.cell.2010.01.025 · Cited by 10,755 · cited 4×
“Furthermore, inflammatory conditions such as Crohn’s disease dramatically increase the risk of colorectal cancer (Balkwill et al., 2005; Balkwill and Mantovani, 2012; Coussens and Werb, 2002; Grivennikov et al., 2010).”
BackgroundInfluentialMicroenvironmental regulation of tumor progression and metastasis
Quail, D. F., & Joyce, J. A. (2013) · Nature Medicine · doi:10.1038/nm.3394 · Cited by 7,994 · cited 3×
“…SPARC) that increases tumor cell-ECM interaction and thus migration (Sangaletti et al., 2008), Cathepsin proteases that remodel the matrix and release sequestered growth factors (Laoui et al., 2011; Quail and Joyce, 2013) and TGF-b that promotes EMT of the invading tumor cells (Bonde et al., 2012).”
BackgroundMolecular Mechanisms of Stress-Responsive Changes in Collagen and Elastin Networks in Skin
Aziz, J., Shezali, H., Radzi, Z., Yahya, N. A., Abu Kassim, N. H., Czernuszka, J., & Rahman, M. T. (2016) · Skin Pharmacology and Physiology · doi:10.1159/000447017 · Cited by 7,323
Myeloid-derived-suppressor cells as regulators of the immune system
Gabrilovich, D. I., & Nagaraj, S. (2009) · Nature Reviews Immunology · doi:10.1038/nri2506 · Cited by 6,753 · cited 1×
“TheseM-MDSCs have greater immunosuppressive potency than the granulocytic ones and are further defined as F4/80+ a marker also found on inflammatory monocytes (Gabrilovich and Nagaraj, 2009; Gabrilovich et al., 2012).”
BackgroundMacrophage plasticity and polarization: in vivo veritas
Sica, A., & Mantovani, A. (2012) · Journal of Clinical Investigation · doi:10.1172/jci59643 · Cited by 6,335 · cited 2×
“References to these polarizing agents can be found in (De Palma and Lewis, 2013; Sica and Mantovani, 2012). above strongly support targeting the destruction or redifferentiation of macrophages as an important part of combinatorial therapies in human cancer patients.”
BackgroundAlternative activation of macrophages
Gordon, S. (2003) · Nature Reviews Immunology · doi:10.1038/nri978 · Cited by 6,189 · cited 1×
“…the activated macrophages responding to IFN-g, TNF-a, and Toll-like receptor 4 (TLR4) activation capable of killing pathogens through mechanisms such as iNOS, and (2) alternatively activated macrophages responding to IL-4 and IL-13 involved in antiparasitic immunity and in asthma (Gordon, 2003).”
BackgroundMacrophage Diversity Enhances Tumor Progression and Metastasis
Qian, B., & Pollard, J. W. (2010) · Cell · doi:10.1016/j.cell.2010.03.014 · Cited by 5,338 · cited 11×
“Furthermore, in most large-scale transcriptome analysis, macrophages have a mixed phenotype expressing both M1 and M2 markers (Qian and Pollard, 2010).”
BackgroundInfluentialSelf-citation
Flagged first, then by citations
2 of the 136 references couldn’t be matched to a known paper.
Cited by
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Tumour-associated macrophages as treatment targets in oncology
Mantovani, A., Marchesi, F., Malesci, A., Laghi, L., & Allavena, P. (2017) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2016.217 · Cited by 4,157
Wound Healing: A Cellular Perspective
Rodrigues, M., Kosaric, N., Bonham, C. A., & Gurtner, G. C. (2018) · Physiological Reviews · doi:10.1152/physrev.00067.2017 · Cited by 3,211
Inflammation and tumor progression: signaling pathways and targeted intervention
Zhao, H., Wu, L., Yan, G., Chen, Y., Zhou, M., Wu, Y., & Li, Y. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-021-00658-5 · Cited by 3,058
Murray, P. J. (2017) · Annual Review of Physiology · doi:10.1146/annurev-physiol-022516-034339 · Cited by 2,981
Recommendations for myeloid-derived suppressor cell nomenclature and characterization standards
Bronte, V., Brandau, S., Chen, S.-H., Colombo, M. P., Frey, A. B., Greten, T. F., Mandruzzato, S., Murray, P. J., Ochoa, A., Ostrand-Rosenberg, S., et al. (2016) · Nature Communications · doi:10.1038/ncomms12150 · Cited by 2,751
Metadata
- Authors
- Noy, R., & Pollard, J. W.
- Affiliations
- Albert Einstein College of Medicine (US)
- Corresponding author
- Pollard, Jeffrey W.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 41
- Issue
- 1
- Pages
- 49-61
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC4137410
- OpenAlex
- W1971620413
- Cited by
- 4,089
- References
- 136
- Citations by year
- 2026: 258 · 2025: 326 · 2024: 359 · 2023: 393 · 2022: 485 · 2021: 479 · 2020: 424 · 2019: 379 · 2018: 297 · 2017: 285 · 2016: 215 · 2015: 157 · 2014: 27
- FWCI
- 22.25
- Type
- journal article
- Language
- en
- Update notices
- erratum (2014-11-20)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Wellcome Trust (101067, 101067/Z/13/Z)
- National Institutes of Health (UL1TR001073)
- National Cancer Institute (P01CA100324, R01CA172451)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- tumor-associated macrophages, tumor microenvironment, tumor angiogenesis, tumor invasion, metastasis, pre-metastatic niche, immunosuppression, natural killer cells, T cells, macrophage-targeted therapy, combination cancer therapy
- MeSH terms
- Animals, Cell Movement, Cell Survival, Cell Transformation, Neoplastic, Humans, Immunosuppression Therapy, Macrophages, Neoplasm Invasiveness, Neoplasm Metastasis, Neoplasms, Neovascularization, Pathologic, Cell Lineage, Cell Proliferation, Mice, Tumor Microenvironment
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