title: Clinicopathological analysis of factors related to colorectal tumor perforation: influence of angiogenesis.
abstract: Colorectal tumor perforation is a life-threatening complication of this disease. However, little is known about the anatomopathological factors or pathophysiologic mechanisms involved. Pathological and immunohistochemical analysis of factors related with tumoral neo-angiogenesis, which could influence tumor perforation are assessed in this study. A retrospective study of patients with perforated colon tumors (Group P) and T4a nonperforated (controls) was conducted between 2001 and 2010. Histological variables (differentiation, vascular invasion, and location) and immunohistochemical (CD31, Growth Endothelial Vascular Factor (VEGF) and p53) related with tumor angiogenesis were analyzed. Of 2189 patients, 100 (4.56%) met the inclusion criteria. Of these, 49 patients had nonperforated (2.23%) and 51 had perforated tumors (2.32%). The P group had lower number of right-sided tumors (7/51, 13.7%) compared with controls (13/49, 36.7%) (P = .01). The high-grade tumors (undifferentiated) represented only 3.9% of the perforated tumors; the remaining 96.1% were well differentiated (P = .01). No differences between groups in the frequency of TP53 mutation or VEGF and CD31 expression were found. In the P group, only 2 (3.9%) had vascular invasion (P = .01). Of the 12 tumors with vascular invasion, only 2 were perforated (16.6%). The median number of metastatic lymph-nodes in P Group was 0 versus 3 in controls (Z = -4.2; P < .01). Pathological analysis of variables that indirectly measure the presence of tumor angiogenesis (differentiation, vascular invasion, and the number of metastatic lymph nodes) shows a relationship between this and the perforation, location, and tumor differentiation. We could not directly validate our hypothesis, by immunohistochemistry of TP53, VEGF, and CD31, that perforated tumors exhibit less angiogenesis.
authors.affiliation: From the Department of General and Digestive Surgery (VMA, LDP, DRG, ABG, AAH); Department of Internal Medicine (AMR); Department of Pathology, Hospital Universitario de Canarias, La Laguna, Tenerife (HAA, ESR); and Department of Biology-Genetics. Universidad Autónoma de Madrid, Madrid, Spain (AMFP, JJGA).
authors.forename: Vicente
authors.initials: V
authors.lastname: Medina-Arana
authors.forename: Antonio
authors.initials: A
authors.lastname: Martínez-Riera
authors.forename: Luciano
authors.initials: L
authors.lastname: Delgado-Plasencia
authors.forename: Diana
authors.initials: D
authors.lastname: Rodríguez-González
authors.forename: Alberto
authors.initials: A
authors.lastname: Bravo-Gutiérrez
authors.forename: Hugo
authors.initials: H
authors.lastname: Álvarez-Argüelles
authors.forename: Antonio
authors.initials: A
authors.lastname: Alarcó-Hernández
authors.forename: Eduardo
authors.initials: E
authors.lastname: Salido-Ruiz
authors.forename: Antonia M
authors.initials: AM
authors.lastname: Fernández-Peralta
authors.forename: Juan J
authors.initials: JJ
authors.lastname: González-Aguilera
mesh_terms: D000368:Aged; D002454:Cell Differentiation; D015179:Colorectal Neoplasms / Q000150:complications* / Q000503:physiopathology; D005260:Female; D016158:Genes, p53; D006801:Humans; D007150:Immunohistochemistry; D007416:Intestinal Perforation / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000096:biosynthesis; D009389:Neovascularization, Pathologic / Q000150:complications* / Q000503:physiopathology; D012189:Retrospective Studies; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis
chemical_list: C527085:KLRK1 protein, human; D055655:NK Cell Lectin-Like Receptor Subfamily K; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A