[Clinicopathological features of non-neoplastic colorectal polyps].

Objective: To characterize clinicopathological characteristics of the non-neoplastic colorectal polyps for accurate diagnosis. Methods: 1 190 cases were collected from the Second Affiliated Hospital of Harbin Medical University from January 2012 to December 2016 and their clinicopathological characteristics were reviewed. Results: There were 746 males and 444 females patients with male/female ratio of 1.7∶1.0. The average age was 52 and 85.4% (1 016/1 190) of cases were over 40 years old. A total of 1 289 polyps were found in the study cohort including 1 238 inflammatory polyps (96.0%), 47 harmartomatous polyps (3.7%) and 4 other types of polypoid lesions (0.3%). Among 1 249 inflammatory polyps, 1 212 were inflammatory pseudopolyps (97.9%), 15 post-inflammatory polyps (1.2%), 8 inflammatory myoglandular polyps (0.6%), and 3 prolapse-type inflammatory polyps (colitis cystica profunda). Among 47 hamartomatous polyps, there were 39 juvenile polyps (83.0%), 8 Peutz-Jegher polyps (17.0%). Four polypoid lesions of endometriosis. Among 1 289 polyps, 751 polyps were located in sigmoid and rectum (58.3%). 168 polyps were pedunculated (12.9%) and 1 132 polyps were sessile (87.1%). Conclusions: For non-neoplastic colorectal polyps, the average age of patients is 40 years. The polyps generally involve the sigmoid colon and rectum. The most common pathological type is inflammatory pseudopolyp and the most common pathological type of hamartomatous polyp is juvenile subtype.

Analysis of Ki-ras gene mutations associated with DNA diploid, aneuploid, and multiploid colorectal carcinomas using a crypt isolation technique.

BACKGROUND AND AIM: Current evidence suggests a possible relationship between DNA ploidy status and Ki-ras gene mutations in human cancers. However, the conventional method does not enable accurate determination of DNA ploidy status of a tumor cell. The present study attempts to clarify whether Ki-ras gene mutations are associated with DNA ploidy status in sporadic colorectal carcinomas using a crypt isolation technique coupled with DNA cytometric sorting. METHODS: Polymerase chain reaction and single-strand conformation polymorphism and direct sequencing were used to analyze Ki-ras gene mutations in 82 sporadic colorectal carcinomas: 21 diploid, 12 aneuploid, and 49 multiploid. In addition, microsatellite instability (MSI) was assessed using seven microsatellite markers to study the relationship to Ki-ras mutations. RESULTS: Ki-ras mutations were found in 12 of 21 diploid carcinomas and in 8 of 12 aneuploid carcinomas. In contrast, Ki-ras gene mutations were detected infrequently in the 34 multiploid carcinomas examined, 8 of which were seen in diploid populations and 10 in aneuploid populations. On the other hand, Ki-ras gene mutations were inversely correlated with MSI, which was found in diploid carcinomas only. CONCLUSIONS: The low frequency of Ki-ras gene mutations that we observed in multiclonal colorectal carcinomas suggests that development of multiclonal colorectal carcinoma may involve a mechanism different from that involved in the development of diploid or aneuploid colorectal carcinomas.

Frequent allelic imbalance at the ATM locus in DNA multiploid colorectal carcinomas.

DNA multiploidy may involve specific DNA ploidy states with respect to genetic alterations such as oncogenes, tumor suppressor gene mutation and microsatellite instability. To clarify the role of DNA multiploidy in colorectal cancer, we analysed allelic imbalance involving the ATM gene, localized to chromosome 11q22-23 and thought to be involved in genetic stability, in a series of multiploid colorectal carcinomas. In addition, p53 gene mutation (exons 5-8) and allelic imbalance at 11q24 loci distal to the ATM locus were also examined. The crypt isolation technique coupled with DNA cytometric sorting and polymerase chain reaction assay using 10 microsatellite markers tightly linked to the ATM gene were used to study ATM allelic imbalance in 55 colorectal carcinomas (15 diploid, 13 aneuploid, 27 multiploid). While allelic imbalance at the ATM locus was rarely observed in diploid and aneuploid carcinomas, multiploid carcinomas exhibited a high frequency of ATM allelic imbalance. In multiploid carcinoma samples, diploid subpopulations showed a smaller range of allelic imbalance at the loci tested compared to aneuploid subpopulations that demonstrated allelic imbalance over a relatively large region. Also, the frequency of AI at 11q24 showed a similar tendency to that at the ATM locus for each DNA ploidy state. An association between p53 gene mutation and ATM allelic imbalance in multiploid carcinoma was also observed. Our results suggest that ATM allelic imbalance and p53 gene mutations occur during the progression from diploid to aneuploid cell populations in multiploid colorectal carcinomas.

Erythrocyte creatine as a marker of excessive erythrocyte destruction due to hypersplenism in patients with liver cirrhosis.

OBJECTIVE: Erythrocyte creatine is a sensitive marker of erythrocyte age, and can be used to detect slight and continuous hemolysis. Excessive blood cell destruction caused by increased spleen function is important evidence of hypersplenism. This study evaluates the usefulness of erythrocyte creatine as a sensitive marker of excessive erythrocyte destruction due to hypersplenism in patients with liver cirrhosis. DESIGN AND METHOD: Erythrocyte creatine was determined by an enzymatic method in 50 patients with postnecrotic liver cirrhosis and 50 healthy controls. The spleen size was measured by ultrasonography and expressed as a spleen index. RESULTS: The patients with splenomegaly showed significantly higher erythrocyte creatine than those without splenomegaly (p < 0.005) and healthy controls (p < 0.001), but there was no significant difference in erythrocyte creatine between healthy controls and those without splenomegaly. Fourteen (93%) of the 15 patients with abnormally high erythrocyte creatine (> 1.8 micromol/g hemoglobin) had splenomegaly. There were no significant differences in reticulocyte count between healthy controls and the patients with and without splenomegaly. Erythrocyte creatine showed good correlations with spleen index (r = 0.67; p < 0.001) and reticulocytes (r = 0.63; p < 0.001). CONCLUSIONS: Erythrocyte creatine can be used for predicting erythropoietic status and estimating hypersplenism in patients with liver cirrhosis.

Sebaceous gland metaplasia in intraductal papilloma of the breast.

We report here the first case of sebaceous gland metaplasia arising within an intraductal papilloma of the breast of a 70-year-old female. Several lobules and nests composed of clear cells closely resembling sebaceous glands of the skin were discovered within an intraductal papilloma of the breast. Squamous metaplasia was also noted in certain areas of the tumor. Immunohistochemically, the cells of the lobules and nests stained positively for monoclonal antibodies anti-cytokeratin 14 and epithelial membrane antigen. This study confirms a novel type of metaplasia of the breast.

Esophageal squamous cell carcinoma characterized by extensive chondroid differentiation.

A rare case of carcinoma characterized by extensive chondroid elements at a site of primary esophageal and metastatic lesion is reported. The patient was a 67-year-old man complaining of dysphagia due to an ulcerative lesion at the lower middle esophagus. He underwent irradiation treatment prior to surgery. Histologically, the tumor consisted of both carcinomatous and chondroid elements and had invaded deeply into the esophageal wall. The carcinomatous cells had gradually become chondroid cells embedded within an extensive extracellular matrix. In addition, the metastatic lesion showed findings similar to those of the primary lesion. Immunohistochemistry revealed that both carcinomatous and chondroid elements were immunostained with cytokeratin and epithelial membrane antigen, suggesting an epithelial nature to the chondroid cells. Conversely, only chondroid cells were positively stained for S-100 protein. Furthermore, bone morphogenetic proteins (BMP) were positive for chondroid cells and their surrounding carcinomatous cells. Given the apparent transition between carcinomatous and chondroid cells based on microscopy and immunohistochemical findings in the present case, we concluded that the chondroid cells were derived from carcinomatous cells. In addition, our findings suggest that BMP produced by carcinomatous cells lead to chondroid differentiation of the carcinoma cells.