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To study the clinical and pathologic characteristics of small cell neuroendocrine carcinoma of urinary tract.All cases of urinary tract carcinoma encountered in the General Hospital of People Liberation Army during the period from 1999 to 2010 were retrospectively reviewed. The clinicopathologic data of small cell neuroendocrine carcinomas were further analyzed, with literature review.A total of 16 cases of small cell neuroendocrine carcinoma were identified, including 10 from urinary bladder, 2 from ureter, 3 from renal pelvis, and 1 multifocal tumor involving renal pelvis and ureter. There were altogether 8 males and 8 females. The median age of the patients was 63 years (range = 24 to 79 years). Gross hematuria (11 cases) represented the main presenting symptom. Four patients had flank pain and 4 had urinary irritation symptoms. Seven patients underwent radical cystectomy. Six other patients underwent radical nephroureterectomy, 1 partial cystectomy, 1 TURBT and the remaining case biopsy only. The size of the tumor ranged from 0.8 to 8.0 cm (median = 4.5 cm). Histologically, 15 cases represented mixed small cell neuroendocrine carcinoma (with 13 mixed with transitional cell carcinoma and 2 with adenocarcinoma). Immunohistochemical study showed positive staining for neuroendocrine markers. On presentation, 1 patient was in stage pT1, 7 in stage pT2, 6 in stage pT3, 2 in stage pT4. Six patients died of the disease after operation. The overall survival was 25 months and the 5-year survival rate was 32.4%.Small cell neuroendocrine carcinoma of urinary bladder is a highly malignant disease and associated with poor prognosis. The diagnosis relies on detailed histologic examination. Early diagnosis, when coupled with cystectomy or nephroureterectomy and adjuvant chemotherapy, represents the mainstay of management.

To study the clinicopathologic features and histologic differential diagnosis of small cell neuroendocrine carcinoma (SmCC) of kidney.The clinicopathologic features of 12 cases of SmCC of kidney encountered during the period from 1999 to 2010 were retrospectively reviewed.Six cases of primary and 6 cases of metastatic SmCC involving kidney were identified. Amongst the primary renal SmCC, 2 were located in renal parenchyma and 4 in renal pelvis. Chest X-ray showed negative findings. Five of them underwent radical nephrectomy. On gross examination, the tumor was located centrally around the renal pelvis in 4 cases and peripherally in renal parenchyma in 1 case. On the other hand, 4 of the 6 cases of metastatic SmCC were discovered during therapy for pulmonary SmCC. Two of these patients presented with abdominal pain and gross hematuria, with lung and renal tumor masses identified simultaneously. The diagnosis of all the 6 cases of metastatic SmCC was confirmed by fine needle aspiration biopsy. Microscopically, pure SmCC was demonstrated in the 2 cases of primary renal parenchymal SmCC and 6 cases of metastatic SmCC. The 4 primary renal pelvic SmCC coexisted with urothelial carcinoma component. On immunohistochemical study, all cases were positive for cytokeratin, synaptophysin and CD56. All metastatic cases and 4 primary cases were also positive for TTF-1. Of six patients with primary SmCC two died 4 and 9 months after operation, and two were alive with a follow-up of 25 and 138 months, respectively. Five of six cases with metastatic SmCC died 3 - 8 months after diagnosis. The other 3 cases were failed to follow-up.Both primary and metastatic SmCC can be found in the kidney. Although rare, primary SmCC is located either in renal parenchyma or in pelvis. The diagnosis of SmCC relies on morphologic examination and immunohistochemical study. TTF-1 immunostaining cannot reliably distinguish primary from metastatic SmCC in kidney. Correlation with clinicoradiologic findings and demonstration of coexisting urothelial carcinoma component (if any) is helpful in delineation of the tumor origin.

To explore prognostic factors and the expression of glypican-3, hepatocyte antigen (HEP), alpha-fetoprotein (AFP), CD34 and CD10 in hepatocellular carcinoma (HCC) and their prognostic value.Clinicopathologic data were analyzed in 375 cases of HCC, in which 80 cases with follow-up were examined by immunohistochemical staining to detect the expression of glypican-3, HEP, AFP, CD34 and CD10 proteins. The relationship between the proteins expression and clinicopathologic features was also evaluated.Tumor number (P = 0.000), tumor size (P = 0.025), tumor differentiation (P = 0.001) and vessel invasion (P = 0.000) were closely related to prognosis of HCC patients; the expression of glypican-3 (66/80,82.5%; P = 0.002), HEP (64/80,80.0%; P = 0.021), AFP (38/80,47.5%; P = 0.014) and CD10 (28/80,35.0%; P = 0.002) was significantly related to tumor differentiation; that of glypican-3 was significantly correlated with tumor number and presence of satellite nodules (P = 0.028) and that of AFP and CD10 was significantly correlated with portal vein thrombi (P = 0.000, P = 0.010). On Kaplan-Meier regression analysis, both low expression of HEP and high expression of AFP were closely related to poor prognosis.Tumor number, size, differentiation and vessel invasion were important factors affecting the prognosis of patients with HCC. HEP and AFP have prognostic significance in HCC.

To examine granulocyte colony stimulating factor (G-CSF) expression in human non-small cell lung cancer (NSCLC) as well as discuss its clinicopathological significance.Specimens were obtained from 114 cases (53 cases with granulocyte infiltration) diagnosed pathologically as NSCLC in General Hospital of PLA. Paraffin-embedded tissues from these 114 cases of NSCLC were examined for expression of G-CSF by immunohistochemical staining. Correlation between G-CSF expression and pathological features, clinical manifestation, prognosis of patients with NSCLC was analyzed statistically. All the patients were retrospectively followed-up.Fifty-five of the 114 NSCLC specimens expressed G-CSF, and among these 41 (41/54, 75.9%) were large cell carcinoma, nine (9/30, 30.0%) were adenocarcinoma and five (5/30, 16.7%) were squamous cell carcinoma. The expression was significantly correlated with infiltration of tumor mass by neutrophilic granulocytes, histological type, necrosis, differentiation, lymph node metastases, distant metastases, recurrence and survival period (P0.01). There was no significant correlation with primary tumor size (P0.05). Logistic multi-factor analysis revealed that necrosis, lymph nodes metastases and distant metastases RR (risk ratio) in G-CSF positive group was 5.57, 6.28 and 5.24 times higher than those of G-CSF negative group (P0.05). There were remarkable difference of 5-year survival rates (0 and 12.1% respectively) and survival period (42 and 62 months respectively) between positive and negative groups (P0.01).NSCLC with G-CSF excretion are mainly large cell lung cancer. The pathologic characteristics of these cases with G-CSF expression included poor differentiation, remarkable atypia, prominent necrosis and infiltration of tumor mass by neutrophils or emperipolesis. These tumors are usually more aggressive in biological behavior and have worse prognosis than those without G-CSF expression.

To clarify the various diagnostic connotations of pseudomyxoma peritonei (PMP) and to study their prognostic implications.Clinicopathologic features and follow-up data of 40 patients with PMP diagnosed in The General Hospital of PLA were retrospectively reviewed. The cases were histologically classified into 3 subcategories: disseminated peritoneal adenomucinosis (DPAM), peritoneal mucinous carcinomatosis (PMCA), and PMCA with intermediate or discordant features (PMCA-I/D). The survival rate was calculated using Kaplan-Meier method and the difference was statistically analyzed.Twelve of the 40 patients died on follow up. The duration of survival ranged from 2 to 348 months (medium = 37.5 months). In general, the 3-year, 5-year and 10-year survival rates were 79.0%, 69.4% and 53.0%, respectively. The mean age of the patients at the time of diagnosis was 50.3 years (age range = 22 to 76 years). The male-to-female ratio was 1:1. The age and sex of patients, frequency of operation and presence of ovarian involvement did not correlate with duration of survival. On the other hand, the presence of appendiceal tumor, parenchymal invasion of abdominal viscera, cellularity, architecture, nuclear atypia and mitotic activity of the peritoneal lesion significantly correlated with survival. There was also significant difference in survival between DPAM, PMCA-I/D and PMCA subcategories (P = 0.018). The difference in survival rate between PMCA-I/D and PMCA subgroups however was not statistically significant (P = 0.096). The outcome of DPAM was significantly better when compared with the combined group of PMCA-I/D and PMCA (P = 0.006).In general, the 10-year survival rate of PMP was low, despite the relatively benign-looking or low-grade pathologic appearance. Peritoneal lesions with higher cellularity, conspicuous nuclear atypia and higher mitotic activity are associated with a lower survival rate. The prognosis was even worse in the presence of appendiceal carcinoma or parenchymal invasion of abdominal viscera. It is thus advisable to subclassify PMP into DPAM, PMCA and PMCA-I/D, due to the difference in prognostic implication.

To analyze the relationship between oxidized low density lipoprotein (oxLDL), angiogenesis and stabilization of atherosclerotic plaques in human coronary arteries; and to investigate the role of oxLDL in creating vulnerable sites in atherosclerotic plaques.Samples of coronary arteries were obtained at autopsies of 42 patients with acute coronary syndrome. Eighty randomly selected blocks were studied by immunohistochemistry using antibodies against oxLDL and endothelial cells (factor VIII). Computer-aided planimeter was used for quantitative analysis.In unstable plaques, percentage of immunoreactive areas for oxLDL was significantly higher than that in stable plaques. Most of the oxLDL were located in shoulder region of these plaques, as compared to the fibrous cap and basal regions. The details of distribution of oxLDL were as follows: shoulder region (20.43 +/- 3.12 for unstable plaques and 17.65 +/- 4.22 for stable plaques), fibrous cap (4.77 +/- 2.03 for unstable plaque and 2.80 +/- 0.22 for stable plaques) and basal region (5.65 +/- 1.65 for unstable plaques and 3.22 +/- 1.02 for unstable plaques). OxLDL was also a main component in the lipid core. In the shoulder region, there was a significant positive correlation between neovascularization and oxLDL (r = 0.8247, P = 0.000).The amount of oxLDL is significantly higher in unstable atherosclerotic plaques, especially over the shoulder region. OxLDL in coronary atherosclerotic plaques is thus an important factor in determining stabilization of the plaques. OxLDL may induce influx of inflammatory cells which subsequently leads to decreased plaque stabilization.

To compare the angiogenesis in unstable and stable plaques and to investigate the potential role of neovessels in creating vulnerable sites for atherosclerotic plaques.Specimens of coronary arteries were obtained from 52 autopsy cases with acute coronary syndromes. Plaque morphology was studied by use of stained slides. 922 tissue blocks of late-stage lesions were classified into two groups: (1) unstable plaque (n = 153), the plaque was characterized by a large extracellular lipid core (more than 40% of the plaque area); (2) stable plaque (n = 769), lipid core less than 40% of the plaque area. Forty blocks were selected randomly from each group and serial sections were stained immunohistochemically with a polyclonal antibody against F VIII RAg. Computer-aided planimeter was used for quantitative analysis.In unstable plaques, the occurrence of neovessels was more frequent and the neovessel density (number/mm(2)) was significantly increased as compared to that of stable plaques (frequency: 80.4% vs 66.6%, P0.01; shoulder: 22.16 +/- 19.96 vs 10.04 +/- 11.52, base: 21.68 +/- 20.44 vs 9.68 +/- 11.52, fibrous cap: 3.80 +/- 5.32 vs 1.48 +/- 2.28, P0.05). Most neovessels were located in the shoulder region and at the base of plaques.These findings suggest that neovessels in coronary atherosclerotic plaques are closely associated with the decreased stabilization of the plaques.