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Patients with ulcerative colitis (UC) are at risk of developing a colorectal cancer. The aim of this study was to examine our experience in the treatment of ulcerative Colitis Cancer (CC), the role of the ileal pouch-anal anastomosis (IPAA), and the clinical outcome of the operated patients. Data from 417 patients operated on for ulcerative colitis were reviewed. Fifty-two (12%) were found to have carcinoma of the colon (n = 43) or the rectum (n = 9). The indication to surgery, the histopathological type, the cancer stage, the type of surgery, the oncologic outcome, and the functional result of IPAA were examined. The majority of the patients had a mucinous or signet-ring carcinoma. An advanced stage (III or IV) was present in 28% of the patients. Early (stage I or II) CC was found in all except one patient submitted to surgery for high-grade dysplasia, low-grade dysplasia, or refractory colitis. Thirty-nine (75%) of the 52 patients underwent IPAA, 10 patients were treated with a total abdominal proctocolectomy with terminal ileostomy. IPAA was possible in 6/9 rectal CC. Cumulative survival rate 5 and 10 years after surgery was 61% and 53%, respectively. The survival rate was significantly lower for mucinous or signet-ring carcinomas than for other adenocarcinoma. No significant differences of the functional results and quality of life were observed between IPAA patients aged less than or more than 65 years. Failure of the pouch occurred in 5 of 39 (12.8%) patients for cancer of the pouch (2 pts) or for tumoral recurrence at the pelvic or peritoneal level. Early surgery must be considered every time dysplasia is discovered in patients affected by UC. The advanced tumoral stage and the mucous or signet-ring hystotype influence negatively the response to therapy and the survival after surgery. IPAA can be proposed in the majority of the patients with a functional result similar to that of UC patients not affected by CC. Failures of IPAA for peritoneal recurrence or metachronous cancer of the pouch can be observed when CC is advanced, moucinous, localized in the distal rectum, or is associated with primary sclerosing cholangitis., (© 2022. The Author(s).)

Most Crohn's disease-associated small bowel carcinomas (CrD-SBCs) are diagnosed in advanced stage and have poor prognosis. To improve diagnosis and therapy, a better knowledge of tumour precancerous lesions, histotypes and prognostic factors is needed. We investigated histologically and immunohistochemically 52 CrD-SBCs and 51 small bowel carcinomas unrelated to inflammatory disease, together with their tumour-associated mucosa, looking for Crohn-selective changes. Histologic patterns and phenotypic markers potentially predictive of CrD-SBC histogenesis and prognosis were analysed. Cytokeratin 7 or MUC5AC-positive metaplastic changes were found in about half of investigated CrD-SBCs, significantly more frequently than in CrD-unrelated SBCs. They correlated with metaplastic changes of their associated mucosa, while being absent in normal ileal mucosa. Histologic patterns suggestive for progression of some cytokeratin 7 and/or MUC5AC-positive metaplastic lesions into cancer of the same phenotype were also observed. Patient survival analyses showed that tumour cytokeratin 7 or MUC5AC expression and non-cohesive histotype were adverse prognostic factors at univariable analysis, while cytokeratin 7 and non-cohesive histotype were also found to predict worse survival in stage- and age-inclusive multivariable analyses. Besides conventional dysplasia, hyperplasia-like non-conventional lesions were observed in CrD-SBC-associated mucosa, with patterns suggestive for a histogenetic link with adjacent cancer. In conclusion the cytokeratin 7 and/or MUC5AC-positive metaplastic foci and the non-conventional growths may have a role in cancer histogenesis, while tumour cytokeratin 7 and non-cohesive histotype may also predict poor patient survival. Present findings are worth being considered in future prospective histogenetic and clinical studies., (© 2021. The Author(s).)

Hyperparathyrodism-jaw tumor (HPT-JT) syndrome is an autosomal dominant disorder. Loss of function of the cell division cycle protein 73 homolog (CDC73) gene is responsible for the syndrome. This gene encodes an ubiquitously expressed 531 amino acid protein, parafibromin, that acts as a tumor suppressor. Loss of heterozygosity (LOH) of the CDC73 locus in many HPT-JT associated parathyroid tumors from patients with germline mutation is in accordance with Knudson's "two-hit" model for hereditary cancer. A 41-year-old man with mandible ossifying fibroma suffered from severe hypercalcemia due to parathyroid carcinoma (PC). Genetic analysis was performed to evaluate germinal and somatic CDC73 gene mutation as well as real-time qRT-PCR to quantify CDC73 mRNA, miR-155 and miR-664 expression levels. Immunohistochemistry and Western blotting (WB) assay were carried out to evaluate parafibromin protein expression. A novel heterozygous nonsense mutation, c.191-192 delT, was identified in the CDC73 gene. No CDC73 LOH was found in PC tissue, nor any differences in expression levels for CDC73 gene, miR-155 and miR-664 between PC and parathyroid adenoma control tissues. On the contrary, both immunohistochemistry and WB assay showed an approximate 90% reduction of parafibromin protein expression in PC. In conclusion, this study describes a novel germinal mutation, c.191-192 delT, in the CDC73 gene. Despite normal CDC73 gene expression, we found a significant decrease in parafibromin. We hypothesize that a gene silencing mechanism, possibly induced by microRNA, could play a role in determining somatic post-transcriptional inactivation of the wild type CDC73 allele.

Non-familial small bowel carcinomas are relatively rare and have a poor prognosis. Two small bowel carcinoma subsets may arise in distinct immune-inflammatory diseases (celiac disease and Crohn's disease) and have been recently suggested to differ in prognosis, celiac disease-associated carcinoma cases showing a better outcome, possibly due to their higher DNA microsatellite instability and tumor-infiltrating T lymphocytes. In this study, we investigated the histological structure (glandular vs diffuse/poorly cohesive, mixed or solid), cell phenotype (intestinal vs gastric/pancreatobiliary duct type) and Wnt signaling activation (β-catenin and/or SOX-9 nuclear expression) in a series of 26 celiac disease-associated small bowel carcinoma, 25 Crohn's disease-associated small bowel carcinoma and 25 sporadic small bowel carcinoma cases, searching for new prognostic parameters. In addition, non-tumor mucosa of celiac and Crohn's disease patients was investigated for epithelial precursor changes (hyperplastic, metaplastic or dysplastic) to help clarify carcinoma histogenesis. When compared with non-glandular structure and non-intestinal phenotype, both glandular structure and intestinal phenotype were associated with a more favorable outcome at univariable or stage- and microsatellite instability/tumor-infiltrating lymphocyte-inclusive multivariable analysis. The prognostic power of histological structure was independent of the clinical groups while the non-intestinal phenotype, associated with poor outcome, was dominant among Crohn's disease-associated carcinoma. Both nuclear β-catenin and SOX-9 were preferably expressed among celiac disease-associated carcinomas; however, they were devoid, per se, of prognostic value. We obtained findings supporting an origin of celiac disease-associated carcinoma in SOX-9-positive immature hyperplastic crypts, partly through flat β-catenin-positive dysplasia, and of Crohn's disease-associated carcinoma in a metaplastic (gastric and/or pancreatobiliary-type) mucosa, often through dysplastic polypoid growths of metaplastic phenotype. In conclusion, despite their common origin in a chronically inflamed mucosa, celiac disease-associated and Crohn's disease-associated small bowel carcinomas differ substantially in histological structure, phenotype, microsatellite instability/tumor-infiltrating lymphocyte status, Wnt pathway activation, mucosal precursor lesions and prognosis.

The relationship between urothelial bladder cancer and high-risk human papillomaviruses (HR-HPV) is still a poorly understood entity, even if some studies have supposed a probably correlation. The aim of the present study was to assess the potential relationship between the presence of HR-HPV and non-muscle invasive urothelial bladder cancers (NMIBC). One hundred and thirty-seven subjects (78 patients affected by NMIBC and 59 controls) were recruited in this prospective study. HR-HPV DNA was evaluated both in urine and tumour tissues. Data from patients were compared with data from controls. The relationship between patients and controls, in terms of HR-HPV presence was performed. The relationship between all pathological data and HR-HPV presence in patient group was carried out. HR-HPV DNA in tissue was found in 27 of 78 (34.6%) tumour samples and in 6 of 59 (10.1%) specimens from TUR-P, with a statistically significant difference (p=0.0009; dF=1; χ2=10.98). HR-HPV DNA in urine was found in 36 of 78 (46.1%) samples obtained from patients, whereas in only 8 of 59 (13.5%) samples from controls (p<0.0001: dF=1; χ2=16.37). A statistical significant difference in terms of HR-HPV frequency between high-grade and low-grade urothelial bladder cancer, was found (p=0.032; RR=0.52-95% CI 0.27-0.93; OR=0.34-95% CI 0.13-0.90). In conclusion, this study highlights the correlation between urothelial bladder cancer and high-risk type HPV infection, suggesting the potential etiopathogenetic role of HR-HPV in urothelial bladder cancer development.

Background: Somatic alterations on chromosome (Chr) 18q21-23, such as loss of heterozygosity (LOH), have been indicated as a critical step in bladder carcinogenesis. The aim of this study was to evaluate the prognostic role of LOH on Chr 18q21-23 in patients affected by low-grade, nonmuscle-invasive bladder cancer (NMIBC)., Materials and Methods: A group of 108 consecutive subjects (65 affected by low-risk NMIBC and 43 controls) were selected for this prospective study. LOH on Chr 18 was assessed in the blood and urine samples. The primers used were D18S51, MBP LW, and MBP H. The data obtained were compared with follow-up information. Results were also analyzed by using artificial neural networks (ANN)., Results: Out of the 65 patients with NMIBC, 38 (58.4%) showed at least one alteration on Chr 18, while 27 (41.6%) showed no alteration. In the control group, only 2 out of 43 subjects showed LOH on Chr 18. At the end of follow-up, 29 patients were alive without recurrence, while 36 had at least one recurrence. A significant correlation between LOH on Chr 18 and status at follow-up was found (P = 0.022). Kaplan-Meier curves demonstrated a significant correlation between recurrence-free status and LOH on Chr 18 (P = 0.0003). At multivariate analysis, LOH on Chr 18 (P = 0.002) and the number of lesions (P = 0.03) were identified as independent predictors of recurrence-free probability. ANN analysis confirmed the results from multivariate analysis., Conclusions: This study highlights the role of LOH analysis on Chr 18 in improving recurrence prediction in patients affected by low-grade NMIBC., (Copyright (c) 2010 Elsevier Inc. All rights reserved.)

Adrenocortical carcinoma (ACC) is a rare aggressive tumor with a poor prognosis. The lack of a specific and effective medical treatment is due to the poor knowledge of the mechanisms underlying tumor growth. Research on potential drugs able to specifically interfere with tumor proliferation is essential to develop more efficacious therapies. We evaluated for the first time the in vivo effect of rosiglitazone (RGZ), an anti-diabetic drug with in vitro anti-tumor properties, on ACC proliferation in a xenograft model obtained by s.c. injection of human ACC H295R cells in athymic mice. When the tumor size reached 5 mm, animals were allocated to 5 mg/kg RGZ- or water-treated groups. Tumor volume was measured twice a week. A significant reduction of tumor growth in RGZ versus control (control) group was observed and was already maximal following 17 day treatment (1-T/C=75.4% (43.7-93.8%)). After 31 days of treatment, mice were killed and tumor analyzed. Tumor histological evaluation revealed characteristics of invasiveness, richness in small vessels and mitotic figures in control group, while RGZ group tumors presented non infiltrating borders, few vessels, and many apoptotic bodies. Tumor immunohistochemistry showed that Ki-67 was reduced in RGZ versus control group. Quantitative real-time RT-PCR demonstrated a significant reduction in the expression of angiogenic (VEGF), vascular (CD31), proliferation (BMI-1), and anti-apoptotic (Bcl-2) genes in RGZ versus control group tumors. The same inhibitory effects were confirmed in in vitro RGZ-treated H295R. Our findings support and expand the role of RGZ in controlling ACC proliferation and angiogenesis in vivo and in vitro.

Background: The incidence of nodal metastasis in early gastric cancer (EGC) ranges from 5.7 to 13% . Since most patients with EGC do not have lymph node metastasis, the validity of extended nodal dissection has been questioned., Patients and Methods: Clinicopathological data of 116 patients with EGC, all undergoing D2 lymphadenectomy, were analysed. Patients with or without lymph node metastases were compared in relation to age and gender distribution, tumour histopathology and 10-year prognosis., Results: The overall rate of nodal metastasis was 9.5%. The invasion of submucosa, Laurén's diffuse type, a diameter greater than 3 cm, and Pen-A and Pen-B growth patterns were significantly associated with an increased incidence of lymph node metastasis. On multivariate analysis, the diffuse type was an independent risk factor for lymph node involvement, regardless of tumour size and growth pattern (p=0.007). Ten-year survival analysis showed no significant correlation with lymph node metastasis (86.5% vs. 71.6%)., Conclusion: Submucosal carcinomas of intestinal type, under 2 cm in size, are eligible for minimally invasive surgery while, in diffuse-type carcinomas over 2 cm, standard surgery with D2 lymphadenectomy is recommended.

We have previously recorded 6 cases of serrated adenoma in the cardia. Here we report a case, which differed cytologically from the 6 preceding cases in as much as the adenomatous cells had clear, micro-vacuolated cytoplasm and secreted neutral mucins. Similar cellular features found in gastric carcinomas were classified by Mulligan as of pylorocardiac gland cell type. Six of the 7 cases (including the one reported here) showed areas of invasive carcinoma. Because of its location, histological and histochemical features, the reported neoplasia was called serrated adenoma malignum of the cardia (Mulligan type). Serrated adenomas of the cardia seem to have a particular proclivity to evolve into invasive carcinomas.

Many studies have indicated that the E-cadherin (E-CAD) expression loss is associated with the loss of cellular differentiation and increased cellular invasiveness and can be correlated with poor prognosis in urothelial carcinoma (UC) of the urinary bladder. The aim of this study was to define the role of E-CAD mRNA expression on recurrence, progression and survival in UC of the urinary bladder over a long follow-up period. From 30 patients with bladder UC, enrolled in our previous study, 27 were selected for this study. All patients were re-analyzed in terms of clinical and tumor characteristics, tumor pathological analysis and tumor E-CAD mRNA expression. The data were correlated to 12-year follow-up results. Significant correlations between stage (p=0.002), grade (p=0.008) and E-CAD mRNA expression were reported. E-CAD did not show any correlation in predicting recurrence or progression in bladder UC. The survival analysis demonstrated a significant relationship (p=0.019) between patients with expressed E-CAD mRNA levels and cancer-specific survival. Multivariate analysis demonstrated that expression of E-CAD mRNA levels is an independent prognostic factor in terms of cancer-specific survival in UC of the urinary bladder (p=0.002). Our study is the first to demonstrate that mRNA extraction and Northen blot analysis is to be considered a reliable method to evaluate E-CAD mRNA levels for predicting survival rate in patients affected by urothelial bladder cancers. We stress that a long follow-up period is needed to evaluate the role of molecular factors in predicting prognosis in patients affected by bladder UC.

The insulin-like growth factor 2 (IGF2) promotes cell growth by overactivating the IGF system in an autocrine loop in adrenocortical carcinomas (ACCs). The cytoskeleton protein filamin A (FLNA) acts as a repressor of IGF2 mitogenic signalling in ACC cells. The aims of this study were to test FLNA expression by immunohistochemistry in 119 ACCs and 26 adrenocortical adenomas (ACAs) and to evaluate its relationship with clinicopathological features and outcome in ACCs. We found that 71.4% of ACCs did not express FLNA, whereas FLNA absence was a rare event in ACAs (15.4%, p < 0.001 vs. ACCs). In addition, the expression of FLNA was associated with a less aggressive tumour behaviour in ACCs. Indeed, the subgroup of ACCs with high FLNA showed a lower ENSAT stage, Weiss score, and S-GRAS score compared to ACCs with low FLNA expression (p < 0.05). Moreover, patients with high FLNA had a longer overall survival than those with low FLNA (p < 0.05). In conclusion, our data suggest that FLNA may represent a "protective" factor in ACCs, and the integration of FLNA immunohistochemical expression in ACC tissues along with other clinical and molecular markers could be helpful to improve diagnostic accuracy and prognosis prediction in ACCs. [ABSTRACT FROM AUTHOR]

Purpose: We evaluated the role of loss of heterozygosity on the interferon-α locus to predict the response to bacillus Calmette-Guerin therapy in patients with nonmuscle invasive bladder cancer. Materials and Methods: A total of 117 consecutive patients were selected, including 77 with nonmuscle invasive bladder cancer and 40 controls. Loss of heterozygosity on the interferon-α locus (chromosome 9p21) was assessed in blood and urine samples before transurethral resection. All patients underwent transurethral resection and then 6 weekly bacillus Calmette-Guerin instillations. Those with nonmuscle invasive bladder cancer were assigned to groups 1 and 2 with and without loss of heterozygosity on the interferon-α locus, respectively. Results: Of the 77 patients with nonmuscle invasive bladder cancer 39 (50.6%) had loss of heterozygosity on the interferon-α locus (group 1) and 38 (49.4%) had no alteration (group 2). Only 1 of 40 controls showed loss of heterozygosity on the interferon-α locus. At the end of followup 13 patients in group 1 and 27 in group 2 were alive without recurrence. We noted a significant difference between loss of heterozygosity on interferon-α and followup status (dF 01, LR 11.252, p = 0.003). Kaplan-Meier analysis revealed a significant difference in recurrence probability (response to bacillus Calmette-Guerin) and loss of heterozygosity on interferon-α (p <0.0001). On multivariate analysis loss of heterozygosity (HR 4.09, 95% CI 2.59–6.28, p = 0.002), grade (grade 3 HR 3.31, 95% CI 1.38–3.35, p = 0.03) and the number of lesions (3 or greater HR 2.31, 95% CI 1.38–3.25, p = 0.03) were independent predictors of the bacillus Calmette-Guerin response. Conclusions: This study highlights the predictive value of loss of heterozygosity analysis on interferon-α in patients with nonmuscle invasive bladder cancer treated with bacillus Calmette-Guerin. [Copyright &y& Elsevier]

Purpose: We investigated the expression of the 2 spliced variants of the CXCR3 receptor (CXCR3-A and CXCR3-B) and their ligands (MIG, IP-10 and I-TAC) in patients with renal cell carcinoma according to conventional prognostic factors and the necrosis pattern. Materials and Methods: A total of 59 patients with renal cell carcinoma were selected for study. Histotype, stage, grade and tumor diameter were first analyzed. Subsequently tumor necrosis extension, stratified as low—less than 30%, intermediate—30% to 75% and high—greater than 75%, was determined while blinded to pathological data, and CXCR3-B, IP-10, MIG and I-TAC mRNA levels were assessed. The overall correlation between CXCR3-B expression with the specific ligands, and tumor histotype, stage, grade, volume, necrosis extension and ligand expression were assessed on univariate and multivariate analyses. CXCR3-B levels stratified according to necrosis pattern were analyzed with the unpaired t test. Results: CXCR3-B correlated with tumor necrosis and I-TAC (p = 0.0005 and 0.032, respectively). We did not note any correlation between CXCR3-B and histotype, stage, grade, diameter and expression of the other ligands IP-10 and MIG. Moreover, I-TAC did not correlate with tumor necrosis (p = 0.1102). In the multiple regression model a correlation between tumor necrosis and CXCR3-B expression was noted (p = 0.0005). Significant differences in CXCR3-B expression according to the necrosis pattern were observed between low and high, and between intermediate and high patterns (p = 0.0007 and 0.0183, respectively). Conclusions: Results demonstrate that CXCR3-B is an independent determinant factor for the extensive tumor necrosis pattern. These data emphasize the immunoangiostatic activity of the CXCR3/CXCR3 ligand biological axis for nonmetastatic human renal cell carcinoma. [Copyright &y& Elsevier]

Purpose: We defined the prognostic role of tumor necrosis and its extent in nonmetastatic clear cell renal cell carcinoma. Also, we further investigated its pathogenesis by correlating this tumor feature with other pathological characteristics and molecular markers related to the von Hippel Lindau-hypoxia inducible factor pathway and to tumor proliferation. Materials and Methods: A total of 213 patients with nonmetastatic clear cell renal cell carcinoma were evaluated. Mean followup was 66 months. The presence and extent of histological necrosis were correlated with clinicopathological factors, Ki-67 antigen expression calculated by the MIB-1 (Ki-67 antibody) index, pVHL, HIF-1α, the tumor infiltrating lymphocyte subset and cancer specific survival. Results: Histological necrosis was present in 63.8% of clear cell renal cell carcinoma cases. Necrosis was significantly associated with grade and the degree of tumor infiltrating lymphocytes, while its extent correlated significantly with grade, the degree of tumor infiltrating lymphocytes and stage. Tumor necrosis was a significant prognostic factor, which was confirmed even when limiting analysis to patients with intracapsular renal cell carcinoma. On multivariate analysis histological necrosis was not an independent predictor of cancer specific survival. The extent of tumor necrosis was not a significant prognostic factor. The presence and extent of histological necrosis was not associated with high Ki-67 expression and it did not correlate with pVHL expression or with nuclear and cytoplasmic HIF-1α expression. Conclusions: Based on our results we cannot support histological necrosis and its extent as prognostic factors for clear cell renal cell carcinoma. Efforts should be made to develop nomograms that use routinely available and objective predictor variables. The precise mechanism that causes tumor necrosis remains unknown but the host immune response might significantly contribute to its development. [Copyright &y& Elsevier]

Background and Aim: In 1999, a group of Western and Asian pathologists gathered in Vienna reached consensus regarding the classification of gastrointestinal epithelial neoplasia. In this study, that classification is applied to colorectal adenomas. Methods: Colorectal adenomas from 1552 patients were histologically classified according to the categories listed in Vienna: category 3, low-grade dysplasia; 4.1, high-grade dysplasia; 4.2, carcinoma in situ; 4.3, suspicious of intramucosal carcinoma; 5.1, intramucosal carcinoma; and 5.2, submucosal carcinoma. The criteria used to diagnose these lesions are described in detail. Adenomas with dysplasia (categories 3 and 4.1) or with carcinoma (categories 4.2, 4.3, 5.1 and 5.2) were analyzed separately. On basis of their configuration, adenomas were classified into tubular, tubulovillous, villous, serrated, microtubular and combined phenotypes (i.e. other than tubulovillous). Results: The highest percentage of adenomas with carcinoma was found amongst villous adenomas (29.6%), followed by combined adenomas (27.8%). Villous adenoma with carcinoma was the most frequent neoplasia at all ages; combined adenomas with carcinoma were more frequent among younger patients. In elderly patients (≥60 years of age) the highest percentage of adenomas with carcinoma was recorded in villous adenomas (28.1%), followed by serrated adenomas (19.2%). Villous adenomas and combined adenomas with carcinoma were more frequent in males. Conclusion: The Vienna classification of colorectal adenomas seems to be influenced by parameters inherent to the patient such as age and sex and by the histological phenotype of the adenoma. With the recent improvement in medical technology it is possible to laser-microdisect a defined group of neoplastic glands (such as with carcinoma in situ or with intramucosal carcinoma) for specific molecular analysis. This modern technology will permit in future the translation of histological structures into molecular terms. [ABSTRACT FROM AUTHOR]

Purpose: Several urinary markers have been recently introduced in clinical practice for improving the noninvasive diagnosis of transitional cell carcinoma. Although microsatellite analysis must be considered the best method in terms of results, its cost and method time are unacceptable for daily use. We validated a more rapid and inexpensive method of determination using rapid DNA extraction and automatic multiplex polymerase chain reaction amplification. Materials and Methods: A total of 120 patients who presented consecutively to a urological office, including 73 with transitional cell carcinoma and 43 who served as controls, were selected for study. Microsatellite analysis was performed in the blood/urine pair using 3 multiplex polymerase chain reactions per patient. Urine sediment inflammatory cells were assessed by urine dipstick test. Ten microsatellite loci were investigated. Numerical data collected during electrophoresis of the amplified segment in an ABI Prism® 310 Genetic Analyzer were used to calculate the cutoff for allelic imbalance. Method sensitivity, specificity, and positive and negative predictive values were calculated. Results: A total of 66 patients had microsatellite analysis alterations in urine sediment, of whom 59 had transitional cell carcinoma, while 7 had other urological diseases. Test sensitivity and specificity were 80.8% and 85.1%, respectively. Statistical analysis did not indicate any significant influence of inflammatory status on microsatellite analysis diagnostic performance. In the control group the allelic imbalance on chromosome 9 was significantly lower than on other chromosomes (p = 0.0143). This could confirm that chromosome 9 has a specific role in transitional cell carcinoma. The multiplex microsatellite analysis method was low cost and not time-consuming. Conclusions: Multiplex microsatellite analysis is a noninvasive, rapid, inexpensive and reproducible method for screening for and monitoring superficial transitional cell carcinoma. It should be considered an alternative method to urinary cytology and it should also be considered in the presence of urine sediment inflammatory cells. [Copyright &y& Elsevier]