title: Histopathological and genetic differences between polypoid and non-polypoid submucosal colorectal carcinoma.
abstract: OBJECTIVE
  To investigate the histopathological and genetic differences between polypoid growth (PG) and non-polypoid growth (NPG) submucosal invasive colorectal carcinoma (CRC).
  
  
  METHODS
  A total of 96 cases of submucosal CRC were divided into two groups according to their growth type; 60 cases of PG and 36 cases of NPG. The size, histological degree of dysplasia, depth of submucosal invasion and lymph node metastasis were compared between the two groups. Furthermore, expression of p53 was detected by immunohistochemical staining, and K-ras gene mutation was examined by polymerase chain reaction based single-strand conformation polymorphism (SSCP).
  
  
  RESULTS
  The average size of the lesions in the NPG group was significantly smaller than those in the PG group (7.5 mm vs 13.8 mm, P<0.001). The histological degree of dysplasia tended to be more severe in NPG group, while the incidence of submucosal massive invasion and the lymph node metastasis were both significantly higher in the NPG type than in the PG group (64.3% vs 43.3%, P=0.004; 43% vs 7%, P=0.008, respectively). In addition, K-ras gene mutations were detected in 67% of lesions in the PG group, but none in the NPG group, while no difference in p53 immunohistochemical expression was found between the two groups.
  
  
  CONCLUSIONS
  Compared with PG submucosal CRC, NPG type demonstrates more frequent submucosal massive invasion, more lymph node metastasis and a higher degree dysplasia. Genetically, NPG type shows much less frequent K-ras mutation.
authors.affiliation: Department of Gastroenterology, Fujita Health University, 1-98 Dengakugakubo Katsukage-Cho, Toyoake, Aichi 470-1192, Japan. ihirata@fujita-hu.ac.jp
authors.forename: Ichiro
authors.initials: I
authors.lastname: Hirata
authors.forename: Fang-Yu
authors.initials: FY
authors.lastname: Wang
authors.forename: Mitsuyuki
authors.initials: M
authors.lastname: Murano
authors.forename: Takuya
authors.initials: T
authors.lastname: Inoue
authors.forename: Ken
authors.initials: K
authors.lastname: Toshina
authors.forename: Takashi
authors.initials: T
authors.lastname: Nishikawa
authors.forename: Kentaro
authors.initials: K
authors.lastname: Maemura
mesh_terms: D000230:Adenocarcinoma / Q000175:diagnosis / Q000235:genetics / Q000473:pathology; D000236:Adenoma / Q000175:diagnosis / Q000235:genetics / Q000473:pathology; D002277:Carcinoma / Q000175:diagnosis / Q000235:genetics* / Q000473:pathology*; D049109:Cell Proliferation; D015179:Colorectal Neoplasms / Q000175:diagnosis / Q000235:genetics* / Q000473:pathology*; D003937:Diagnosis, Differential; D018450:Disease Progression; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008207:Lymphatic Metastasis / Q000235:genetics / Q000473:pathology; D009154:Mutation / Q000235:genetics; D018807:Polymorphism, Single-Stranded Conformational; D016283:Proto-Oncogene Proteins p21(ras) / Q000235:genetics / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism
chemical_list: D016159:Tumor Suppressor Protein p53; D016283:Proto-Oncogene Proteins p21(ras)