In spontaneous intracerebral hematoma patients, prediction of the hematoma expansion risk and mortality risk using radiological and clinical markers and a newly developed scale

Objective: In patients with spontaneous intracerebral hematoma (ICH), early-stage hematoma expansion has been associated with poor prognosis in literature. This study aimed to develop predictive parameter(s) as well as a new scale to define hematoma expansion and short-term prognosis in patients with ICH. Methods: In 46 patients with ICH, Glasgow Coma Scale (GCS) scores, non-contrast CT (NCCT) markers (hematoma volume on admission and follow-up, hypodensity, intraventricular hemorrhage, blend and island sign, BAT score), and modified Rankin Scale scores were evaluated for predicting the hematoma expansion risk and mortality risk. Furthermore, a newly developed scale called the ‘HEMRICH scale’ was constituted using the GCS score, hematoma volumes, and some NCCT markers. Results: Roc-Curve and Logistic Regression test results revealed that GCS score, initial hematoma volume value, hypodensity, intraventricular haemorrhage, BAT score, and HEMRICH scale score could be the best markers in predicting hematoma expansion risk whereas GCS score, intraventricular haemorrhage, BAT score, hematoma expansion, and HEMRICH scale score could be the best markers in predicting mortality risk (p = 0.01). Moreover, Factor analysis and Reliability test results showed that HEMRICH scale score could predict both hematoma expansion and mortality risks validly (Kaiser-Meyer-Olkin test value = 0.729) and reliably (Cronbach’s alpha = 0.564). Conclusion: It was concluded that the GCS score, intraventricular haemorrhage, and BAT score could predict both hematoma expansion risk and mortality risk in the early stage in patients with ICH. Furthermore, it was suggested that the newly produced HEMRICH scale could be a valid and reliable scale for predicting both hematoma expansion and mortality risk

Villous Adenoma Coexisting with Non-Muscle Invasive Urothelial Carcinoma of the Bladder, Case Report

Occurrence of villous adenomas arising in the urinary tract is uncommon. They have been reported usually in the gastrointestinal tract. We reported a case of urinary bladder villous adenoma coexisting with urothelial carcinoma in a 72-year-old male. The patient underwent trans urethral resection because of diagnosis villous adenoma and non-muscle invasive urothelial carcinoma. Over the past twenty-nine months of follow up, the patient is alive and developed no metastasis. Patients with isolated villous adenomas in the urinary bladder have an excellent prognosis and surgical resection is curative. However, it is uncertain whether an untreated lesion might eventually develop into an adenocarcinoma. Therefore, close follow up is recommended because of the possibility that this condition might be premalignant

Primary Leiomyosarcoma of the Kidney: Four Cases

Renal sarcomas are rare tumors. They constitute only 1-2% of malignant renal tumors in adulthood. Leiomyosarcoma is the most common histological type of renal sarcoma (50-60%). Renal leiomyosarcomas are aggressive tumors arising from the renal capsule, renal vein, pelvic musculature or the renal parenchyma. Diagnosis is usually post operative and requires a thorough sampling of the tumor to rule out an epithelial component. We report 4 new cases of primary renal leiomyosarcomas. Typical morphologic pattern shows alternating fascicles of spindle cells with blunt-ended, non-tapering nuclei and eosinophilic cytoplasm. Nuclear pleomprphisim atypia, mitotic figures and necrosis are seen in different ratios. Immunohistochemically the tumor cells of leiomyosarcoma are positive for SMA, desmin, calponin and h-caldesmon and negative for CK, S-100, HMB-45 and CD117. These tumors are classified using the French Federation of Cancer Centers System. To make a diagnosis of a primary renal sarcoma the following criteria should be met: 1) The patient must not have a sarcoma elsewhere to rule out metastasis. 2) Gross must be compatible with origin in the kidney rather than involvement due to retroperitoneal sarcoma. 3) Sarcomatoid renal cell carcinoma must be excluded. They usually have poor prognosis. But small size (<5 cm), low histological grade, absence of lymph node metastases and radical operations are all associated with better prognosis. Despite radical nephrectomy the tumors can run an aggressive clinical course and early local and distant recurrences are common

Evaluation of the neuroendocrine tumors of urinary bladder in seven cases

In this study we reviewed 7 neuroendocrine tumors of bladder among 690 bladder carcinomas with their clinicopathologic characteristics diagnosed in Antalya region, in two medical centers. In each case, the following clinical data were recorded: age, sex, presenting symptoms, location of the tumor, clinical staging, treatment, follow-up and outcome. This study indicates that neuroendocrine carcinoma of the urinary bladder is as aggressive as its pulmonary counterpart and the overall prognosis of this tumor is very poor. [Cukurova Med J 2016; 41(3.000): 586-590

Effects of Monensin and Rapamycin Combination Therapy on Tumor Growth and Apoptosis in a Xenograft Mouse Model of Neuroblastoma

Neuroblastoma is the most common pediatric solid tumor originating from the neural crest. New treatment options are needed to improve treatment outcomes and the survival of patients with neuroblastoma. Monensin is an ionophore antibiotic with antiparasitic, antibacterial, and anticancer properties isolated from Streptomyces cinnamonensis. The aim of this study was to investigate the therapeutic effects of single and combined monensin and rapamycin treatments on mTOR (mammalian target of rapamycin) signaling pathway-mediated apoptosis and tumor growth in an SH-SY5Y neuroblastoma cell xenograft model. Control, monensin, rapamycin, and monensin + rapamycin groups were formed in the xenograft neuroblastoma model obtained from CD1 nude mice, and tumor volumes and animal weights were recorded throughout the treatment. In xenograft neuroblastoma tumor tissues, apoptosis was determined by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling) and cleaved-caspase 3 immunohistochemistry, and PI3K (phosphoinositide-3-kinase)/AKT/mTOR expression was determined by the immunohistochemistry and immunofluorescence methods. The combination of monensin and rapamycin was to reduce the growth of xenograft neuroblastoma tumor tissues, trigger apoptosis, and suppress the expression of PI3K/AKT/mTOR. A significant increase in apoptotic cell rate was demonstrated in the combination group, supported by cleaved-caspase 3 immunohistochemistry results. In addition, it was reported that the combination treatment regime triggered apoptosis by reducing the expression of phosphorylated PI3K/AKT/mTOR. Our preclinical results may be a precursor to develop new therapeutic approaches to treat neuroblastoma

C-MYC and BCL2 translocation frequency in diffuse large B-cell lymphomas: A study of 97 patients

Purpose: Diffuse large B-cell lymphoma (DLBCL) is an aggressive non-Hodgkin lymphoma with marked biologic heterogeneity. MYC and BCL2 rearrangements have been reported in a proportion of DLBCLs, where they may be associated with an adverse clinical outcome. The aim of this study was to determine the frequency of MYC and BCL2 translocations in DLBCL and assess the prognostic impact in DLBCL patients. Materials and Methods:   In the present study, we evaluated the expression patterns of CD 10, BCL6, and MUM 1 by immunohistochemistry in 121 cases with DLBCL in tissue microarray (TMA): 62 cases in germinal center B-cells (GCBs); and 59 cases in activated B-cells (ABCs) of which 60 were females and 61 were males. MYC and BCL2 rearrangements were investigated by interphase fluorescence in situ hybridization on TMAs in 97 DLBCLs. Result: MYC rearrangements were observed in 11 of 97 cases. There was no association with other clinical features, including age, sex, and nodal/extranodal disease. MYC rearrangement was associated with significantly worse overall survival (P < 0.01). BCL2 rearrangements were observed in 14 of 97 cases. There was no association with other clinical features including age and sex. BCL2 rearrangement had a worse outcome (P < 0.01). MYC and BCL2 rearrangements were observed in 3 of 97 cases with the age of  53 (female), 53, 63 years old, respectively, died in 24, 18, and 35 months after the diagnosis. Two cases had primary nodal and one case primary extranodal presentations. All these patients had stage IV disease. Conclusion: We concluded that C-MYC and BCL2 may contribute to aggressive transformation, and more mechanism-based therapy should be explored. Targeted therapies involving these rearrangements and its associated pathways may change the fate of DLBCLs. Analysis of MYC gene rearrangement along with BCL2 is critical in the identification of high-risk patients with poor prognosis

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TÜBİTAK TBAG01.06.200