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1.
The Role of CK7, S100A1, and CD82 (KAI1) Expression in the Differential Diagnosis of Chromophobe Renal Cell Carcinoma and Renal Oncocytoma.
Sari, ZB, Açikalin, MF, Arik, D, Özen, A, Can, C, Çolak, E
Applied immunohistochemistry & molecular morphology : AIMM. 2021;(7):534-540
Abstract
Renal oncocytoma is a benign renal tumor originated from intercalated cells of collecting ducts like chromophobe renal cell carcinoma (RCC). The differential diagnosis of these 2 tumors is important because while they are histologically and cytologically similar, they show different biological behavior. For the differential diagnosis, several immunohistochemical markers have been investigated. But, differential diagnostic challenges remain and the identification of additional markers is needed. Cytokeratin 7 (CK7) is one of ductal-type keratins, which is expressed in tumors of breast, pancreas, lung, thyroid, ovary, endometrium, urinary bladder, and the kidney. S100A1 is the first defined member of the calcium-binding S100 protein family and it organizes several cellular functions including cell cycle progression and cell differentiation.CD82 is a tetraspanin membrane protein, which functions as a metastasis supressor. In this study, we immunohistochemically investigated the expressions of CK7, S100A1, and CD82 in 30 chromophobe RCC (23 classic and 7 eosinophilic variant) and 19 oncocytomas. When these markers were evaluated separately and together, their expressions in chromophobe RCC and renal oncocytoma show statistically significant difference (P<0.001). Similar statistically significant results were also seen between eosinophilic chromophobe RCC and oncocytoma (P<0.001). For both classic and eosinophilic-variant chromophobe RCCs, CK7+/S100A1-/CD82+ profile being the most common. In oncocytomas, the most frequently observed profile was CK7-/S100A1+/CD82-. Our results showed that the application of a panel consisting of CK7, S100A1, and CD82 may provide accurate categorization of the tumors in difficult cases.
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2.
S100A1 promotes cell proliferation and migration and is associated with lymph node metastasis in ovarian cancer.
Tian, T, Li, X, Hua, Z, Ma, J, Liu, Z, Chen, H, Cui, Z
Discovery medicine. 2017;(127):235-245
Abstract
S100A1 is a calcium-binding protein belonging to the family of S100 proteins, and is highly expressed in ovarian cancer. However, its role in ovarian cancer has not yet been fully elucidated. In this study, we examined S100A1 expression in ovarian cancer tissues and normal tissue controls and analyzed the correlation between S100A1 expression and clinicopathological parameters. We found that S100A1 expression was significantly upregulated in ovarian cancer tissues compared with fallopian and normal ovarian epithelium tissues and was significantly associated with lymph node metastasis and International Federation of Gynecology and Obstetrics (FIGO) stages and tumor grades. We then investigated the biological functions of S100A1 in ovarian cancer by cell proliferation, fluorescence-activated cell sorting (FACS), and migration and invasion assays. The results indicated that S100A1 enhanced the ovarian cancer cell proliferation and migration. Together, our findings demonstrated that S100A1 plays an important role in the malignancy of ovarian cancer, and serves as a useful marker for the detection of ovarian malignancy.
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Effects of adalimumab, etanercept and ustekinumab on the expression of psoriasin (S100A7) in psoriatic skin.
D'Amico, F, Trovato, C, Skarmoutsou, E, Rossi, GA, Granata, M, Longo, V, Gangemi, P, Pettinato, M, Mazzarino, MC
Journal of dermatological science. 2015;(1):38-44
Abstract
BACKGROUND Psoriasis is a chronic inflammatory skin disease. It is characterized by immune cell activation and altered epidermal differentiation. S100A7 (psoriasin) is overexpressed in psoriasis, suggesting a determinant role of this protein in inflammation and keratinocyte differentiation. OBJECTIVE The purpose of this study was to investigate the expression of S100A7 in the skin from psoriatic patients undergoing biological therapy with adalimumab, etanercept or ustekinumab. METHODS S100A7 expression and distribution were analyzed by immunohistochemistry. RESULTS S100A7, overexpressed in epidermal keratinocytes of psoriatic lesions, was downregulated, under the biological therapy with adalimumab, etanercept or ustekinumab, only in patients achieving a PASI score<15. CONCLUSIONS Dysregulation of S100A7 may represent a non-negligible player in the maintenance of psoriasis and the relative epidermal changes. Blockage of S100A7 may represent an additional therapeutic approach in the treatment of psoriasis.
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4.
Acute sleep deprivation increases serum levels of neuron-specific enolase (NSE) and S100 calcium binding protein B (S-100B) in healthy young men.
Benedict, C, Cedernaes, J, Giedraitis, V, Nilsson, EK, Hogenkamp, PS, Vågesjö, E, Massena, S, Pettersson, U, Christoffersson, G, Phillipson, M, et al
Sleep. 2014;(1):195-8
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Abstract
STUDY OBJECTIVES To investigate whether total sleep deprivation (TSD) affects circulating concentrations of neuron-specific enolase (NSE) and S100 calcium binding protein B (S-100B) in humans. These factors are usually found in the cytoplasm of neurons and glia cells. Increasing concentrations of these factors in blood may be therefore indicative for either neuronal damage, impaired blood brain barrier function, or both. In addition, amyloid β (Aβ) peptides 1-42 and 1-40 were measured in plasma to calculate their ratio. A reduced plasma ratio of Aβ peptides 1-42 to 1-40 is considered an indirect measure of increased deposition of Aβ 1-42 peptide in the brain. DESIGN Subjects participated in two conditions (including either 8-h of nocturnal sleep [22:30-06:30] or TSD). Fasting blood samples were drawn before and after sleep interventions (19:30 and 07:30, respectively). SETTING Sleep laboratory. PARTICIPANTS 15 healthy young men. RESULTS TSD increased morning serum levels of NSE (P = 0.002) and S-100B (P = 0.02) by approximately 20%, compared with values obtained after a night of sleep. In contrast, the ratio of Aβ peptides 1-42 to 1-40 did not differ between the sleep interventions. CONCLUSIONS Future studies in which both serum and cerebrospinal fluid are sampled after sleep loss should elucidate whether the increase in serum neuron-specific enolase and S100 calcium binding protein B is primarily caused by neuronal damage, impaired blood brain barrier function, or is just a consequence of increased gene expression in non-neuronal cells, such as leukocytes.
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Expression of S100A4 in renal epithelial neoplasms.
Wang, LJ, Matoso, A, Sciandra, KT, Yakirevich, E, Sabo, E, Zhang, Y, Meitner, PA, Tavares, R, Noble, L, Pareek, G, et al
Applied immunohistochemistry & molecular morphology : AIMM. 2012;(1):71-6
Abstract
Expression of S100A4 has been associated with progression and poor clinical outcome in a variety of malignancies including those of the breast, pancreas, bladder, and thyroid. To date, the expression of S100A4 protein in renal epithelial neoplasms is poorly understood. In this study, we evaluated the expression of S100A4 protein and mRNA in the nontumoral kidney and renal epithelial neoplasms of different types and correlated its expression with patient outcome. The study population included 155 clear cell renal cell carcinomas (cRCC), 22 papillary renal cell carcinomas (pRCC), 13 chromophobe renal cell carcinomas and 13 oncocytomas. In nontumoral kidney, nuclear and cytoplasmic S100A4 staining was detected in the glomerular epithelium and endothelium, distal tubules and collecting ducts, and loops of Henle. A different expression pattern was noted in the various neoplasms. S100A4 expression was significantly increased in the stromal cells in cRCC (83%) and pRCC (73%) compared with paired nontumoral kidney tissue (P<0.001). There was no increased stromal cell expression of S100A4 in oncocytomas and chromophobe carcinomas. Positive epithelial staining was more common in pRCC (58%) than cRCC (11%) (P=0.01). The level of mRNA detected by reverse transcription-polymerase chain reaction was significantly higher in the tumor as opposed to normal tissue in cRCC but not in the other neoplasms (P=0.03). Multivariate analysis revealed that epithelial S100A4 protein expression is an independent poor prognostic factor along with grade and stage only in cRCC (P<0.01). Although S100A4 protein was expressed in a minority of cRCC, its expression was associated with shorter overall patient survival.
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Differentiating ischemic from hemorrhagic stroke using plasma biomarkers: the S100B/RAGE pathway.
Montaner, J, Mendioroz, M, Delgado, P, García-Berrocoso, T, Giralt, D, Merino, C, Ribó, M, Rosell, A, Penalba, A, Fernández-Cadenas, I, et al
Journal of proteomics. 2012;(15):4758-65
Abstract
Although neuroimaging is useful in differentiating ischemic (IS) from hemorrhagic (ICH) stroke in the Emergency Department, a wide-available rapid biochemical test would add advantages in the pre-hospital triage and management of stroke patients. Our aim was to examine the predictive value of a panel of blood-borne biomarkers to differentiate IS from ICH. Admission blood samples obtained within 24h from stroke symptoms onset were tested by ELISA for CRP, D-dimer, sRAGE, MMP9, S100B, BNP, NT-3, caspase-3, chimerin-II, secretagogin, cerebellin and NPY. The complete protocol was achieved in 915 patients (776 IS, 139 ICH). Among blood samples obtained <6 h from symptoms onset (n=337), S100B levels were increased in ICH (107.58 vs 58.70 pg/mL; p<0.001) whereas sRAGE levels were decreased (0.77 vs 1.02 ng/mL; p=0.009) as compared to IS. In this subset of patients S100B (OR 3.97 95% CI 1.82-8.68; p=0.001) and sRAGE (OR 0.22 95% CI 0.10-0.52; p<0.001) were independently associated with ICH. A regression tree was created by CART method showing good classification ability (AUC=0.762). Similar results were found for samples obtained within 3 h. In conclusion, a combination of biomarkers including those of the S100B/RAGE pathway seems promising to achieve a rapid biochemical diagnosis of IS versus ICH in the first hours from symptoms onset. This article is part of a Special Issue entitled: Translational Proteomics.
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Microemboli from cardiopulmonary bypass are associated with a serum marker of brain injury.
Groom, RC, Quinn, RD, Lennon, P, Welch, J, Kramer, RS, Ross, CS, Beaulieu, PA, Brown, JR, Malenka, DJ, O'Connor, GT, et al
The journal of extra-corporeal technology. 2010;(1):40-4
Abstract
An increasing number of reports surrounding neurologic injury in the setting of cardiac surgery has focused on utilizing biomarkers as intermediate outcomes. Previous research has associated cerebral microemboli and neurobehavioral deficits with biomarkers. A leading source of cerebral microemboli is the cardiopulmonary bypass (CPB) circuit. This present study seeks to identify a relationship between microemboli leaving the CPB circuit and a biomarker of neurologic injury. We enrolled 71 patients undergoing coronary artery bypass grafting at a single institution from October 14, 2004 through December 5, 2007. Microemboli were monitored using Power-M-Mode Doppler in the inflow and outflow of the CPB circuit. Blood was sampled before and within 48 hours after surgery. Neurologic injury was measured using S100beta (microg/L). Significant differences in post-operative S100beta relative to microemboli leaving the circuit were tested with analysis of variance and Kruskal-Wallis. Most patients had increased serum levels of S100beta (mean .25 microg/L, median .15 microg/L) following surgery. Terciles of microemboli measured in the outflow (indexed to the duration of time spent on CPB) were associated with elevated levels of S100beta (p = .03). Microemboli leaving the CPB circuit were associated with increases in postoperative S100beta levels. Efforts aimed at reducing microembolic load leaving the CPB circuit should be adopted to reduce brain injury.
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CSF protein biomarkers for proximal axonal damage improve prognostic accuracy in the acute phase of Guillain-Barré syndrome.
Petzold, A, Brettschneider, J, Jin, K, Keir, G, Murray, NM, Hirsch, NP, Itoyama, Y, Reilly, MM, Takeda, A, Tumani, H
Muscle & nerve. 2009;(1):42-9
Abstract
Early predictors of prognosis in Guillain-Barré syndrome (GBS) are needed to identify patients who are likely to make a poor recovery and to guide therapeutic decision-making in the acute phase. Here we investigate whether axonal protein biomarkers released into the cerebrospinal fluid (CSF) following proximal axonal damage improve the early prognostic accuracy in GBS. A prospective multicenter study including 132 patients (38 GBS, 38 neurological controls, 42 headaches, 14 chronic inflammatory demyelinating neuropathy). CSF levels of axonal [neurofilament (NfH) and tau] and glial (S100B and glial fibrillary acidic protein) protein biomarkers were measured on admission. Nerve conduction studies were performed at the time of lumbar puncture and patients were classified according to neurophysiological criteria. Outcome was assessed on the Hughes functional score (F-score). Poor outcome was defined as the inability to walk independently (F-score > or = 3). High NfH levels (>0.73 ng/ml) predicted poor outcome (P = 0.01) with an odds ratio of 7.3 and correlated with the outcome F-score (R = 0.51, P < 0.01), as did hTau levels (R = 0.47, P < 0.01). Patients with poor outcome had significantly higher CSF NfH (median 1.78 ng/ml) when compared to those with good outcome (0.03 ng/ml) or all of the control groups (neurological controls 0.18 ng/ml, headaches 0.06 ng/ml, chronic inflammatory demyelinating neuropathy 0.05 ng/ml). Except for age (P < 0.05) and need for ventilatory support (P < 0.05), none of the other features reliably predicted outcome. Improved prognostic accuracy in the acute phase of GBS seems possible using CSF NfH levels.
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Oxidative-antioxidative systems and their relation with serum S100 B levels in patients with schizophrenia: effects of short term antipsychotic treatment.
Sarandol, A, Kirli, S, Akkaya, C, Altin, A, Demirci, M, Sarandol, E
Progress in neuro-psychopharmacology & biological psychiatry. 2007;(6):1164-9
Abstract
Oxidative stress may be a contributing factor in the etiopathophysiology of schizophrenia, which may be exacerbated by the treatment with antipsychotics with pro-oxidant properties. Increased levels of S100 B are associated with neurodegenerative disorders, including schizophrenia. The aim of the present study was to investigate the role of oxidative cell damage in the pathogenesis of schizophrenia. Forty patients who fully met the fourth Diagnostic and Statistical Manual of Mental Disorders criteria for schizophrenia and 35 healthy control subjects were included in the study. Serum S100 B level was determined to investigate brain damage. Plasma malondialdehyde (MDA) levels and susceptibility of red blood cell (RBC) to oxidation were determined to investigate the oxidative status and plasma vitamin E, vitamin C, serum total carotenoid levels and total antioxidant capacity and RBC superoxide dismutase (SOD) and whole blood glutathione peroxidase activities were measured to investigate the antioxidative defence before and after 6 weeks of antipsychotic treatment. Plasma MDA and serum S100 B levels and RBC-SOD activity were significantly higher in the schizophrenia group than those of the control group. Treatment did not modify any of the oxidative-antioxidative system parameters or serum S100 B levels. S100 B level was significantly higher in patients with negative symptoms than the patients with positive symptoms and the control subjects. S100 B levels were significantly reduced after 6 weeks of treatment in patients with negative symptoms. The results of the present study might support the oxidative cell injury hypothesis of the schizophrenia. Furthermore, the underlying mechanisms of the subgroups of schizophrenia might be different as suggested by the increased S100 B levels and its decrement after treatment in patients with negative symptoms.
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The effect of alpha-Tocopherol supplementation on training-induced elevation of S100B protein in sera of basketball players.
Schulpis, KH, Moukas, M, Parthimos, T, Tsakiris, T, Parthimos, N, Tsakiris, S
Clinical biochemistry. 2007;(12):900-6
Abstract
OBJECTIVE To investigate the effect of alpha-Tocopherol (alpha-T) supplementation on S100B elevated serum levels in basketball players' training. DESIGN Blood was obtained from 10 basketball players pre-exercise (group A), post-exercise (group B) and after 30 days on alpha-T (200 mg/24 h orally) supplementation pre- (group C) and post-training (group D). Blood samples were taken for the evaluation of total antioxidant status (TAS), alpha-T and catecholamines in plasma and S100B and muscle enzyme levels in serum. METHODS TAS, muscle enzymes: creatine kinase (CK), lactate dehydrogenase (LDH), and S100B protein levels were measured with commercial kits, whereas alpha-T and catecholamine levels with HPLC methods. RESULTS TAS was found higher in the groups with alpha-T addition (groups C and D) than in the other ones. On the contrary, CK, LDH and S100B were remarkably lower (116.8+9.5 U/L, 427+22 U/L, 0.18+0.04 microg/L, respectively) in group D than those in group B (286+12 U/L, 688+26 U/L, 0.28+0.06 microg/L, p<0.001, respectively). S100B levels were negatively correlated with TAS (r=-0.64, p<0.001) and positively with CK levels (r=0.58, p<0.001). CONCLUSIONS alpha-T supplementation may reduce S100B increased release from muscle and nerves induced by training. S100B serum evaluation may be a useful biomarker for the effect of training on the participation of the neuromuscular system.