Poorly differentiated colorectal adenocarcinoma accounts for 5-10% of all cases of colorectal cancer, and its poor prognosis is known, but there are many unclear points regarding its biological features. Because the histology of colorectal cancer is roughly classified into two patterns (severe and mild interstitial infiltration), in this study, we focused on this point and investigated clinicopathological findings and microsatellite instability (MSI) in the two interstitial infiltration patterns of poorly differentiated colorectal adenocarcinoma. We encountered 502 patients with colorectal cancer, and 30 patients (6%) who were diagnosed with the dominant histologic type of poorly differentiated colorectal adenocarcinoma were selected as subjects. The lesion was not resectable in three patients, and thus, the clinicopathology was unknown in these patients. In the 27 patients who underwent resection of poorly differentiated colorectal adenocarcinoma, the cancers were histologically classified based on the interstitial infiltration patterns into solid and non-solid types, and the clinicopathology and survival rates were investigated. DNA was extracted from the primary lesions, and normal tissue and MSI were investigated using five microsatellite markers. Histopathologically, 20 cancers were classified as the solid type and 7 as the nonsolid type. In the clinicopathological findings in the nonsolid and solid types, lymph node metastasis was observed in 100% and 60%; liver metastasis in 57% and 20%, and peritoneal dissemination in 29% and 5%, respectively, showing that the positive rates were higher in the nonsolid type. The 5-year survival rate was also poor in the nonsolid type. MSI was observed in 50% of the solid type and 20% of the nonsolid type, showing a high frequency in the solid type. Poorly differentiated colorectal adenocarcinoma was classified based on the infiltration pattern into the nonsolid and solid types. In the nonsolid type, the cancer was advanced in many cases, and the frequency of MSI was lower than that of the solid type. Therefore, there were differences in clinico-pathological features and biological malignancy between the nonsolid and solid types, suggesting different carcinogenesis mechanisms for the two types.