Editing Macrophage (section)

=== Cancer ===
Macrophages can contribute to tumor growth and progression by promoting tumor cell proliferation and invasion, fostering tumor angiogenesis and suppressing antitumor immune cells.<ref>{{cite journal | vauthors = Qian BZ, Pollard JW | title = Macrophage diversity enhances tumor progression and metastasis | journal = Cell | volume = 141 | issue = 1 | pages = 39–51 | date = April 2010 | pmid = 20371344 | pmc = 4994190 | doi = 10.1016/j.cell.2010.03.014 }}</ref><ref name="nature.com">{{cite journal | vauthors = Engblom C, Pfirschke C, Pittet MJ | title = The role of myeloid cells in cancer therapies | journal = Nature Reviews. Cancer | volume = 16 | issue = 7 | pages = 447–462 | date = July 2016 | pmid = 27339708 | doi = 10.1038/nrc.2016.54 | s2cid = 21924175 }}</ref> Inflammatory compounds, such as [[tumor necrosis factor]] (TNF)-alpha released by the macrophages activate the gene switch [[NF-κB|nuclear factor-kappa B]]. NF-κB then enters the nucleus of a tumor cell and turns on production of proteins that stop [[apoptosis]] and promote cell proliferation and inflammation.<ref>{{cite journal | vauthors = Stix G | title = A malignant flame. Understanding chronic inflammation, which contributes to heart disease, Alzheimer's and a variety of other ailments, may be a key to unlocking the mysteries of cancer | journal = Scientific American | volume = 297 | issue = 1 | pages = 60–67 | date = July 2007 | pmid = 17695843 | doi = 10.1038/scientificamerican0707-60 | bibcode = 2007SciAm.297a..60S }}</ref> Moreover, macrophages serve as a source for many pro-angiogenic factors including [[Vascular endothelial growth factor|vascular endothelial factor]] (VEGF), [[tumor necrosis factor-alpha]] (TNF-alpha), [[macrophage colony-stimulating factor]] (M-CSF/CSF1) and [[Interleukin 1|IL-1]] and [[Interleukin 6|IL-6]],<ref>{{cite journal | vauthors = Lin EY, Li JF, Gnatovskiy L, Deng Y, Zhu L, Grzesik DA, Qian H, Xue XN, Pollard JW | title = Macrophages regulate the angiogenic switch in a mouse model of breast cancer | journal = Cancer Research | volume = 66 | issue = 23 | pages = 11238–11246 | date = December 2006 | pmid = 17114237 | doi = 10.1158/0008-5472.can-06-1278 | s2cid = 12722658 | doi-access =  }}</ref> contributing further to the tumor growth. 

Macrophages have been shown to infiltrate a number of tumors. Their number correlates with poor prognosis in certain cancers, including cancers of breast, cervix, bladder, brain and prostate.<ref>Bingle L, Brown NJ, Lewis CE. The role of tumour-associated macrophages in tumour progression: implications for new anticancer therapies. J Pathol 2002; 196:254–65.</ref><ref>{{Cite journal| vauthors = de Groot AE |date=July 2018|title=In vitro human tumor-associated macrophage model implicates macrophage proliferation as a mechanism for maintaining tumor-associated macrophage populations|url=http://cancerres.aacrjournals.org/content/78/13_Supplement/4060.short|journal=Cancer Research|volume=78|issue=13 Supplement|pages=4060|doi=10.1158/1538-7445.AM2018-4060|s2cid=80769044 |doi-access=}}</ref> Some tumors can also produce factors, including M-CSF/CSF1, [[CCL2|MCP-1/CCL2]] and [[Angiotensin II]], that trigger the amplification and mobilization of macrophages in tumors.<ref>{{cite journal | vauthors = Lin EY, Nguyen AV, Russell RG, Pollard JW | title = Colony-stimulating factor 1 promotes progression of mammary tumors to malignancy | journal = The Journal of Experimental Medicine | volume = 193 | issue = 6 | pages = 727–740 | date = March 2001 | pmid = 11257139 | pmc = 2193412 | doi = 10.1084/jem.193.6.727 }}</ref><ref>{{cite journal | vauthors = Qian BZ, Li J, Zhang H, Kitamura T, Zhang J, Campion LR, Kaiser EA, Snyder LA, Pollard JW | title = CCL2 recruits inflammatory monocytes to facilitate breast-tumour metastasis | journal = Nature | volume = 475 | issue = 7355 | pages = 222–225 | date = June 2011 | pmid = 21654748 | pmc = 3208506 | doi = 10.1038/nature10138 }}</ref><ref>{{cite journal | vauthors = Cortez-Retamozo V, Etzrodt M, Newton A, Ryan R, Pucci F, Sio SW, Kuswanto W, Rauch PJ, Chudnovskiy A, Iwamoto Y, Kohler R, Marinelli B, Gorbatov R, Wojtkiewicz G, Panizzi P, Mino-Kenudson M, Forghani R, Figueiredo JL, Chen JW, Xavier R, Swirski FK, Nahrendorf M, Weissleder R, Pittet MJ | title = Angiotensin II drives the production of tumor-promoting macrophages | journal = Immunity | volume = 38 | issue = 2 | pages = 296–308 | date = February 2013 | pmid = 23333075 | pmc = 3582771 | doi = 10.1016/j.immuni.2012.10.015 }}</ref> Additionally, subcapsular sinus macrophages in tumor-draining lymph nodes can suppress cancer progression by containing the spread of tumor-derived materials.<ref>{{cite journal | vauthors = Pucci F, Garris C, Lai CP, Newton A, Pfirschke C, Engblom C, Alvarez D, Sprachman M, Evavold C, Magnuson A, von Andrian UH, Glatz K, Breakefield XO, Mempel TR, Weissleder R, Pittet MJ | title = SCS macrophages suppress melanoma by restricting tumor-derived vesicle-B cell interactions | journal = Science | volume = 352 | issue = 6282 | pages = 242–246 | date = April 2016 | pmid = 26989197 | pmc = 4960636 | doi = 10.1126/science.aaf1328 | bibcode = 2016Sci...352..242P }}</ref>