Knowledge (XXG)

Host response to cancer therapy

Source πŸ“

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Surgical resection of a tumor is one of the primary treatment modalities for cancer and can be curative especially for patients with early disease. However, there is evidence that tumor resection generates a permissive environment for tumor growth, in part, via host-mediated processes. As part of the
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and antibiotics, represent a major systemic therapeutic modality for many cancers. These agents induce death in rapidly dividing cells thus targeting tumor cells, but at the same time damaging healthy tissue. Consequently, non-malignant host cells activate wound healing and inflammatory mechanisms to
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Curigliano, G.; Petit, J. Y.; Bertolini, F.; Colleoni, M.; Peruzzotti, G.; de Braud, F.; Gandini, S.; Giraldo, A.; Martella, S. (2005). "Systemic Effects of Surgery: Quantitative Analysis of Circulating Basic Fibroblast Growth Factor (bFGF), Vascular Endothelial Growth Factor (VEGF) and Transforming
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Langenberg, Marlies H.G.; Nijkamp, Maarten W.; Roodhart, Jeanine M.L.; Snoeren, Nikol; Tang, Terence; Shaked, Yuval; Hillegersberg, Richard van; Witteveen, Petronella O.; Vermaat, Joost S.P.; Kranenburg, Onno; Kerbel, Robert S.; Medema, Rene H.; Borel Rinkes, Inne H.M.; Voest, Emile E. (27 October
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that ensues activates a range of compensatory mechanisms that sustain vascularization, leading to resistance to the anti-angiogenic drug. Many of these compensatory mechanisms involve host cells. For example, treating tumor-bearing mice with vascular-disrupting agents (that specifically target
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and enzymes accompanied by acute mobilization and tumor homing of bone-marrow derived cells. These therapy-induced effects have the potential to facilitate tumor growth and spread, counteracting the beneficial effects of therapy. Thus, the host response to cancer therapy creates a paradoxical
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Shojaei, Farbod; Wu, Xiumin; Zhong, Cuiling; Yu, Lanlan; Liang, Xiao-Huan; Yao, Jenny; Blanchard, Dominique; Bais, Carlos; Peale, Franklin V.; van Bruggen, Nicholas; Ho, Calvin; Ross, Jed; Tan, Martha; Carano, Richard A. D.; Meng, Y. Gloria; Ferrara, Napoleone (December 2007). "Bv8 regulates
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is a well-established treatment modality for several cancer types. However, relapses after radiotherapy are often more aggressive and associated with poor prognosis. Cumulative evidence shows that the host response to radiotherapy is a contributing factor to this effect. Tumors implanted in
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pre-irradiated tissue grow with slower kinetics, however, paradoxically exhibit enhanced invasive and metastatic properties, a phenomenon known as the β€œtumor bed effect”. This enhanced aggressiveness is attributed to radiation-induced modifications of the
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Shojaei, Farbod; Wu, Xiumin; Malik, Ajay K; Zhong, Cuiling; Baldwin, Megan E; Schanz, Stefanie; Fuh, Germaine; Gerber, Hans-Peter; Ferrara, Napoleone (29 July 2007). "Tumor refractoriness to anti-VEGF treatment is mediated by CD11b+Gr1+ myeloid cells".
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All cancer treatment modalities (e.g., chemotherapy, targeted drugs, radiation and surgery) trigger systemic and local effects in the treated subject (i.e., the host). These include a rapid elevation in the levels of circulating
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is defined as a physiological response of the non-malignant cells of the body (also known as host cells) to a specific cancer therapy. The response is therapy-specific, occurring independently of cancer type or stage.
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situation in which the desired therapeutic effect of treatment is reduced by its side effect on host cells. The balance between these two opposing activities determines the overall efficacy and outcome of treatment.
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Bono, Anna; Bianchi, Paolo; Locatelli, Andrea; Calleri, Angelica; Quarna, Jessica; Antoniott, Pierluigi; Rabascio, Cristina; Mancuso, Patrizia; Andreoni, Bruno; Bertolini, Francesco (27 October 2014).
173:) target the blood vessels required for tumor survival. The rationale behind this strategy is to starve the tumor of oxygen and nutrients, limiting its ability to grow. However, 223:. For example, lungs are more prone to metastatic seeding after a surgical incision in the abdominal region of mice. This effect is due to increased expression and activity of 251:. Experimental studies have shown that combining conventional cancer therapies with agents that selectively block therapy-induced factors improves treatment efficacies. 1623:"Depletion of Tumor-Associated Macrophages Enhances the Effect of Sorafenib in Metastatic Liver Cancer Models by Antimetastatic and Antiangiogenic Effects" 243:
Characterizing the host response to cancer therapy in patients has clinical implications especially in the field of personalized medicine (also known as
190:, and TIE2-expressing monocytes contribute to therapy resistance. In mouse tumor models, anti-angiogenic therapy causes an elevation in tumor-promoting 849:
Sofia Vala, I; Martins, L. R.; Imaizumi, N; Nunes, R. J.; Rino, J; Kuonen, F; Carvalho, L. M.; RΓΌegg, C; Grillo, I. M (2010). Gartel, Andrei L. (ed.).
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Voloshin, Tali; Voest, Emile E.; Shaked, Yuval (July 2013). "The host immunological response to cancer therapy: An emerging concept in tumor biology".
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that home to tumor margins where they facilitate revascularization. In addition, various types of pro-angiogenic bone marrow-derived cells such as
215:, extracellular matrix-modifying enzymes, and immune cells released during this process may also promote proliferation of residual tumor cells, 531:"Rapid Chemotherapy-Induced Acute Endothelial Progenitor Cell Mobilization: Implications for Antiangiogenic Drugs as Chemosensitizing Agents" 227:(LOX), an extracellular matrix remodeling enzyme produced at the hypoxic surgical site. In clinical settings, elevated levels of circulating 918:"Matrix Metalloproteinase-9 Is Required for Tumor Vasculogenesis but Not for Angiogenesis: Role of Bone Marrow-Derived Myelomonocytic Cells" 1917:
Rachman-Tzemah, C; Zaffryar-Eilot, S; Grossman, M; Ribero, D; Timaner, M; MΓ€ki, J. M.; Myllyharju, J; Bertolini, F; Hershkovitz, D (2017).
802:"Molecular Pathways: Emerging Pathways Mediating Growth, Invasion, and Metastasis of Tumors Progressing in an Irradiated Microenvironment" 1621:
Zhang, W.; Zhu, X.-D.; Sun, H.-C.; Xiong, Y.-Q.; Zhuang, P.-Y.; Xu, H.-X.; Kong, L.-Q.; Wang, L.; Wu, W.-Z.; Tang, Z.-Y. (22 June 2010).
1024:"Inhibition of the Kit Ligand/c-Kit Axis Attenuates Metastasis in a Mouse Model Mimicking Local Breast Cancer Relapse after Radiotherapy" 639:"Host Response to Short-term, Single-Agent Chemotherapy Induces Matrix Metalloproteinase-9 Expression and Accelerates Metastasis in Mice" 1022:
Kuonen, F.; Laurent, J.; Secondini, C.; Lorusso, G.; Stehle, J.-C.; Rausch, T.; Faes-van't Hull, E.; Bieler, G.; Alghisi, G.-C. (2012).
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Karagiannis, G. S.; Pastoriza, J. M.; Wang, Y; Harney, A. S.; Entenberg, D; Pignatelli, J; Sharma, V. P.; Xue, E. A.; Cheng, E (2017).
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Gingis-Velitski, S.; Loven, D.; Benayoun, L.; Munster, M.; Bril, R.; Voloshin, T.; Alishekevitz, D.; Bertolini, F.; Shaked, Y. (2011).
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Okubo, Makiko; Kioi, Mitomu; Nakashima, Hideyuki; Sugiura, Kei; Mitsudo, Kenji; Aoki, Ichiro; Taniguchi, Hideki; Tohnai, Iwai (2016).
1811:"Multiple circulating proangiogenic factors induced by sunitinib malate are tumor-independent and correlate with antitumor efficacy" 1071:
Timaner, M; Bril, R; Kaidar-Person, O; Rachman-Tzemah, C; Alishekevitz, D; Kotsofruk, R; Miller, V; Nevelsky, A; Daniel, S (2015).
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repair chemotherapy-induced damage. These repair mechanisms have the potential to exacerbate tumor promoting processes such as
1512:"G-CSF-initiated myeloid cell mobilization and angiogenesis mediate tumor refractoriness to anti-VEGF therapy in mouse models" 274:
Shaked, Yuval (26 April 2016). "Balancing efficacy of and host immune responses to cancer therapy: the yin and yang effects".
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Shaked, Y. (22 September 2006). "Therapy-Induced Acute Recruitment of Circulating Endothelial Progenitor Cells to Tumors".
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Shaked, Y; Henke, E; Roodhart, J. M.L.; Mancuso, P; Langenberg, M. H.G.; Colleoni, M; Daenen, L. G.; Man, S; Xu, P (2008).
2062:"Liver surgery induces an immediate mobilization of progenitor cells in liver cancer patients: A potential role for G-CSF" 580:"Stress-inducible gene Atf3 in the noncancer host cells contributes to chemotherapy-exacerbated breast cancer metastasis" 1128:
Chiang, Chi-Shiun; Fu, Sheng Yung; Wang, Shu-Chi; Yu, Ching-Fang; Chen, Fang-Hsin; Lin, Chi-Min; Hong, Ji-Hong (2012).
967:"Inhibition of vasculogenesis, but not angiogenesis, prevents the recurrence of glioblastoma after irradiation in mice" 228: 207:
wound healing process, surgical tissue trauma is rapidly followed by a cascade of inflammatory processes. Many of the
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that home to the tumor site where they promote angiogenesis. In addition, a variety of immune cell types, such as
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Seifert, L; Werba, G; Tiwari, S; Giao Ly, N. N; Nguy, S; Alothman, S; Alqunaibit, D; Avanzi, A; Daley, D (2016).
1189:"M2-polarized macrophages contribute to neovasculogenesis, leading to relapse of oral cancer following radiation" 1760:
PΓ ez-Ribes, M; Allen, E; Hudock, J; Takeda, T; Okuyama, H; ViΓ±als, F; Inoue, M; Bergers, G; Hanahan, D (2009).
131: 1360:"Tumor and Host-Mediated Pathways of Resistance and Disease Progression in Response to Antiangiogenic Therapy" 1968:"Angiogenic cells, macroparticles and RNA transcripts in laparoscopic vs open surgery for colorectal cancer" 743:
Arnold, K. M; Flynn, N. J; Raben, A; Romak, L; Yu, Y; Dicker, A. P; Mourtada, F; Sims-Mourtada, J (2018).
170: 151: 138:, are recruited to the tumor site in a chemotherapy-dependent manner, an effect that enhances metastasis. 402:
Katz, Ofrat Beyar; Shaked, Yuval (March 2015). "Host effects contributing to cancer therapy resistance".
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and tumor progression have been reported in response to major surgery in comparison to minimal surgery.
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Growth Factor Beta (TGF-Ξ²) in Patients with Breast Cancer Who Underwent Limited or Extended Surgery".
1254:"Radiation Therapy Induces Macrophages to Suppress T-Cell Responses Against Pancreatic Tumors in Mice" 320:
Daenen, L G M; Houthuijzen, J M; Cirkel, G A; Roodhart, J M L; Shaked, Y; Voest, E E (25 March 2013).
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Ebos, J.M.L.; Lee, C. R.; Cruz-Munoz, W; Bjarnason, G. A.; Christensen, J. G.; Kerbel, R. S. (2009).
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Shojaei, F.; Wu, X.; Qu, X.; Kowanetz, M.; Yu, L.; Tan, M.; Meng, Y. G.; Ferrara, N. (3 April 2009).
1424: 1200: 862: 745:"The Impact of Radiation on the Tumor Microenvironment: Effect of Dose and Fractionation Schedules" 248: 32: 2041: 1713:"Accelerated Metastasis after Short-Term Treatment with a Potent Inhibitor of Tumor Angiogenesis" 1603: 1492: 1448: 299: 244: 126:. In mouse tumor models, different chemotherapy types induce a rapid mobilization of circulating 851:"Low Doses of Ionizing Radiation Promote Tumor Growth and Metastasis by Enhancing Angiogenesis" 2083: 2033: 2025: 1989: 1948: 1899: 1858: 1840: 1791: 1742: 1693: 1685: 1644: 1595: 1551: 1484: 1440: 1397: 1379: 1340: 1322: 1283: 1234: 1216: 1169: 1151: 1110: 1092: 1053: 1045: 1004: 986: 947: 898: 880: 831: 823: 782: 764: 725: 707: 668: 660: 619: 601: 560: 511: 493: 454: 419: 384: 343: 291: 146: 688:"Neoadjuvant chemotherapy induces breast cancer metastasis through a TMEM-mediated mechanism" 2073: 2017: 1979: 1938: 1930: 1889: 1848: 1830: 1781: 1773: 1732: 1724: 1675: 1664:"Tie2-Expressing Monocytes and Tumor Angiogenesis: Regulation by Hypoxia and Angiopoietin-2" 1634: 1587: 1541: 1531: 1476: 1432: 1387: 1371: 1330: 1314: 1273: 1265: 1224: 1208: 1159: 1141: 1100: 1084: 1035: 994: 978: 937: 929: 888: 870: 813: 772: 756: 715: 699: 650: 609: 591: 550: 542: 501: 485: 446: 411: 374: 333: 283: 322:"Treatment-induced host-mediated mechanisms reducing the efficacy of antitumor therapies" 1919:"Blocking Surgically Induced Lysyl Oxidase Activity Reduces the Risk of Lung Metastases" 1826: 1583: 1527: 1428: 1204: 866: 1943: 1918: 1853: 1810: 1809:
Ebos, J. M. L.; Lee, C. R.; Christensen, J. G.; Mutsaers, A. J.; Kerbel, R. S. (2007).
1786: 1761: 1737: 1712: 1546: 1511: 1392: 1359: 1335: 1302: 1278: 1253: 1229: 1188: 1164: 1129: 1105: 1072: 999: 966: 942: 917: 893: 850: 777: 744: 720: 687: 614: 579: 555: 530: 506: 473: 114: 2100: 1894: 1877: 224: 208: 195: 174: 93: 2045: 1452: 303: 1878:"Surgery, wound healing, and metastasis: Recent insights and clinical implications" 1607: 1496: 232: 216: 155: 119: 110: 1680: 1663: 1639: 1622: 1375: 1040: 1023: 818: 801: 655: 638: 379: 362: 1934: 1269: 965:
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875: 703: 1303:"Antiangiogenic therapy: impact on invasion, disease progression and metastasis" 450: 415: 231:, bone marrow-derived cells as well as circulating factors with known roles in 2021: 1777: 1728: 1318: 933: 546: 489: 287: 220: 159: 135: 123: 2029: 1844: 1689: 1383: 1326: 1220: 1155: 1096: 1088: 1049: 990: 884: 827: 768: 760: 711: 664: 605: 497: 474:"Chemotherapy-induced metastasis: mechanisms and translational opportunities" 1835: 1536: 1436: 1146: 1073:"Dequalinium blocks macrophage-induced metastasis following local radiation" 596: 89: 41: 2087: 2037: 1993: 1984: 1967: 1952: 1903: 1862: 1795: 1746: 1697: 1648: 1599: 1555: 1488: 1444: 1401: 1344: 1287: 1238: 1173: 1114: 1057: 1008: 951: 902: 835: 786: 729: 672: 623: 564: 515: 458: 423: 388: 347: 295: 21: 2078: 2061: 363:"Prodding the Beast: Assessing the Impact of Treatment-Induced Metastasis" 212: 191: 85: 1591: 338: 321: 178:
tumor-associated vessels) triggers an acute mobilization of circulating
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that in turn augment the invasive and metastatic potential of tumors.
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Chang, Y. S; Jalgaonkar, S. P.; Middleton, J. D.; Hai, T (2017).
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Host response to different treatment modalities for cancer
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and recruitment of pro-metastatic bone marrow cells and
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Index


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cytokines
chemokines
growth factors
Chemotherapies
antimetabolites
angiogenesis
metastasis
endothelial progenitor cells
myeloid progenitors
macrophages
Radiotherapy
tumor microenvironment
angiogenesis
macrophages
angiogenesis inhibitors
tumor hypoxia
endothelial progenitor cells
myeloid-derived suppressor cells
tumor-associated macrophages
cytokines
growth factors
growth factors
cytokines
angiogenesis

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