title: Distinct types of tumors exhibit differential grade of inflammation and angiogenesis in mice.
abstract: Inflammation, angiogenesis and cytokine production are common features of almost, if not all tumors. However, the extent of these processes induced by different types of tumors has not been evaluated. We investigated the growth pattern of the experimental metastatic tumors, B16F10 melanoma, CT26.WT colon and 4T1 mammary cells inoculated in the flank of syngeneic mice and determined the degree of inflammation, angiogenesis, and production level of pro-inflammatory and pro-angiogenic cytokines within the tumors. In addition, we have analyzed vascular changes in the interface between the tumors and the adjacent cutaneous tissue and levels of relevant pro-inflammatory and pro-angiogenic cytokines systemically. The weight of tumors 15 days post-inoculation of 10(6) cells was markedly different. Melanomas were 2 and 10-fold heavier than colon and mammary tumors, respectively. Locally, CT26.WT tumor cells induced more vessels in cutaneous tissue adjacent to the tumors but systemically, the plasma levels of VEGF were higher (approximately 2-fold) in 4T1 tumor-bearing mice compared with the other two tumors. Mammary tumors presented the most prominent inflammatory content as assessed by a range of markers (inflammatory enzymes and cytokines). The vascular index, as determined by the intra-tumor amount of hemoglobin and number of vessels in hot spot areas, was also higher (approximately 2-fold) in melanomas compared with the other two tumors. These findings showing that distinct tumor types determine differential grade of inflammation, angiogenesis and host interaction in mice may provide new insights to tailor differential therapeutic approach based on the status of tumor biomarkers.
authors.affiliation: Department of Physiology and Biophysics, Institute of Biological Sciences/Federal University of Minas Gerais, Av. Antônio Carlos 6627 - Pampulha, CEP 31.270-901, Belo Horizonte, Minas Gerais, Brazil.
authors.forename: C T R
authors.initials: CT
authors.lastname: Viana
authors.forename: P P
authors.initials: PP
authors.lastname: Campos
authors.forename: L A
authors.initials: LA
authors.lastname: Carvalho
authors.forename: J M
authors.initials: JM
authors.lastname: Cenedezi
authors.forename: L
authors.initials: L
authors.lastname: Lavall
authors.forename: M T P
authors.initials: MT
authors.lastname: Lopes
authors.forename: M A N D
authors.initials: MA
authors.lastname: Ferreira
authors.forename: S P
authors.initials: SP
authors.lastname: Andrade
mesh_terms: D000818:Animals; D015415:Biomarkers; D003110:Colonic Neoplasms / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics; D005260:Female; D006454:Hemoglobins / Q000032:analysis; D007249:Inflammation / Q000097:blood / Q000209:etiology*; D036341:Intercellular Signaling Peptides and Proteins / Q000096:biosynthesis / Q000235:genetics; D016246:Lymphocytes, Tumor-Infiltrating; D008297:Male; D008325:Mammary Neoplasms, Experimental / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D008546:Melanoma, Experimental / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D009363:Neoplasm Proteins / Q000096:biosynthesis / Q000235:genetics; D009389:Neovascularization, Pathologic / Q000209:etiology*; D017942:Nitric Acid / Q000378:metabolism; D012867:Skin / Q000098:blood supply; D047368:Tumor Burden; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D015415:Biomarkers; D016207:Cytokines; D006454:Hemoglobins; D036341:Intercellular Signaling Peptides and Proteins; D009363:Neoplasm Proteins; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse; D017942:Nitric Acid