Removal of lead and chromium from solution by organic peels: effect of particle size and bio-adsorbent.

A variety of organic wastes can be used in innovative methods to treat water pollution through the adsorption process. In this work, we evaluated the effect of particle size (500-2000, 250-500, and less than 250 µm) and bio-adsorbent (orange, potato, and passion fruit peels) on the removal of lead and chromium from solution. The size and type of peels affected the capacity to adsorb metal ions (p < 0.05). Passion fruit peel had the highest metal adsorption, followed by orange and potato, since the cation exchange capacity (217.70 ± 39.57 cmol (+) kg-1) and the specific surface area (141.10-1095.29 cm2 g-1) were higher in the passion fruit rind. The size of the adsorbent did not affect the organic matter, ash, exchange capacity, surface chemistry, or pH of the peels. However, these properties differed among the bio-adsorbents (p < 0.05). The Freundlich equation explained the adsorption of the metallic ions on the orange rind and of lead on the passion fruit. The linear model was the best fit for the adsorption isotherms of the metals on potato peel. The adsorption of chromium on the passion fruit had a maximum adsorption capacity of 3.3 mg g-1. These results indicate that plant waste materials, especially passion fruit peel, have the potential as feasible and low-cost adsorbents in pilot studies for the treatment of polluted water.

Epstein-Barr virus-associated large B-cell lymphoma transformation in marginal zone B-cell lymphoma: a series of four cases.

AIMS: To present four examples of clonally related Epstein-Barr virus (EBV)-associated large-cell transformation of marginal zone lymphoma (MZL) (of nodal, extranodal and splenic types), occurring 120, 11 and 5 months after the initial diagnosis in three instances, and concurrently in one case; and to discuss several interesting features of EBV infection. METHODS AND RESULTS: Somatic mutations were detected by use of a customised panel for next-generation sequencing and polymerase chain reaction studies of IgH in both low-grade and high-grade components of each case. In case 1, the initial biopsy of nodal MZL showed scattered EBV-positive cells, which might constitute an indication of EBV-induced progression. Case 2 showed heterogeneous EBV expression, a phenomenon attributable to loss of the EBV episomes during cell division, or to a secondary superinfection or reactivation of the virus. In case 3, p53 overexpression related to gene mutation and EBV-encoded small RNAs were identified in the same neoplastic component. In case 4, the mucosa-associated lymphoid tissue-type MZL and the high-grade component were identified concurrently in a patient previously treated with methotrexate for an autoimmune disorder. CONCLUSION: These data suggest that the presence of EBV should be added to the list of potential markers to be analysed for MZL prognosis.

The coexpression of fibroblast activation protein (FAP) and basal-type markers (CK 5/6 and CD44) predicts prognosis in high-grade invasive urothelial carcinoma of the bladder.

High-grade urothelial carcinoma (UC) of the bladder is a heterogeneous disease with dismal prognosis. Bladder tumors with basal phenotype are intrinsically aggressive, and morphological parameters that define disease staging remain main prognosticators. We intend to evaluate the role of cancer-associated fibroblasts (CAFs) in the prognosis of bladder cancer and its association with basal and luminal phenotypes. Clinical and pathological parameters, including the immunohistochemical expression of fibroblast activation protein (FAP) and markers of basal (CK5/6, CD44) and luminal (CK20, GATA3) phenotypes, have been investigated in a series of 121 patients with UC of the bladder treated by radical cystectomy with lymph node dissection, and their implication in long-term cancer-specific survival has been evaluated. A cytoplasmic immunostaining of FAP in CAFs implies worse disease-specific survival (hazard ratio [HR] = 1.68; P = .048). FAP expression is associated with tumor staging (P < .0001), with best discrimination at T2a/T2b level, and with negative expression of markers of luminal phenotype, such as CK20 (P < .0001) and GATA3 (P = .005). In the multivariate analysis, simultaneous expression of FAP, CK5/6, and CD44 is a strong prognosticator of disease-specific survival (HR = 2.3; P = .001), together with nodal invasion (HR = 3.47; P < .0001) and bladder infiltration up to deep muscle or beyond (HR = 2.47; P = .02). There is no association between positive FAP expression in primary tumor and nodal disease (P = .22). FAP expression in CAFs favors tumor invasion in high-grade invasive UC of the bladder with basal phenotype. This new immunohistochemical marker could be added to the routine immunohistochemical protocol to predict clinical behavior in these patients.

Clinicopathologic and pedigree differences in amsterdam I-positive hereditary nonpolyposis colorectal cancer families according to tumor microsatellite instability status.

PURPOSE: To establish the clinicopathologic and familial differences within Amsterdam I-positive families, showing either tumor microsatellite instability (MSI) or microsatellite stability (MSS) in order to confirm or deny the existence of hereditary nonpolyposis colorectal cancer (HNPCC) without defects in the mismatch repair system. PATIENTS AND METHODS: Sixty-four Amsterdam I-positive families were included in the study for which full, three-generation, family medical histories and colorectal paraffin-embedded tumors were obtained. Both personal and clinicopathologic information of patients were collected. In all cases, both the MSI status and the mismatch repair (MMR) protein expression were analyzed. MMR genetic testing was performed on the MSI families. RESULTS: Of the Amsterdam I-positive families, 59.4% were tumor MSI, and 40.6% were tumor MSS. When comparing both groups, the statistical differences were observed in the age of onset (MSI, 41 years; MSS, 53 years); in the colorectal tumor location, more frequently proximal in MSI cases; in fewer mucinous tumors in MSS; and loss of MMR protein expression in the MSI tumors. Regarding the individual and familial cancer history, we observed a predominance of individuals with multiple primary tumors in MSI pedigrees, as well as differences in the type of tumors developed within the family. CONCLUSION: Our findings support the suspicion of another hereditary colorectal syndrome different from HNPCC and characterized by MSS, the normal MMR immunohistochemical expression, the presence of only colorectal tumors, and the absence of individuals with multiple primary tumors. All these circumstances suggest the existence of a non-MMR gene being responsible for this new syndrome.

Angioma esplénico de células litorales. Descripción de un caso y revisión de la literatura / Littoral cell angioma of the spleen. A case report and review of the literature

Antecedentes: El angioma de células litorales es unatumoración vascular benigna del bazo con rasgos histopatológicoscaracterísticos, descrita por Falk y cols. en 1991 (1),que presumiblemente deriva de las células que revisten lossenos de la pulpa roja esplénica (células litorales). Métodos:Presentamos un angioma multifocal de células litoralesdiagnosticado en una mujer de 66 años con dolor discontinuoen hipocondrio derecho; los estudios de imagen (ecografíay TAC) mostraron múltiples lesiones esplénicasredondas e hipodensas de hasta 1,5 cm de diámetro. El diagnósticodiferencial clínico comprendía metástasis, linfoma,linfangiomas y procesos inflamatorios. Resultados: La piezade esplenectomía mostró afectación multifocal porangiomas de células litorales. Las células de revestimientoeran positivas para vimentina, CD31, factor de von Willebrandy CD68, y negativas para CD8. No se ha identificadotumoración alguna tras un control de 46 meses. Conclusiones:El angioma de células litorales es una proliferaciónvascular benigna que debe incluirse en el diagnóstico diferencialde los nódulos esplénicos hipodensos múltiples

Introduction: Littoral cell angioma is a benign splenicvascular neoplasm with characteristic histopathologic features,reported by Falk et al in 1991(1). It is thought to arisefrom the cells lining the red pulp sinuses (littoral cells).Patients and Methods: We report a case of multifocal littoralcell angioma in a 66-year-old woman with intermittentdiscomfort on her right hypochondrium. Imaging studies(ultrasound and CT scan) showed multiple hypodense,round lesions in the spleen, up to 1.5 cm in diameter.The differential diagnosis included metastatic disease,lymphoma, lymphangioma and inflammatory ailments.Results: Splenectomy specimen showed multiple littoralcell angiomas. Lining cells were positive for vimentin,CD31, von Willebrand factor and CD68; CD8 was negative.No neoplasm has been identified after a 46 monthsfollow-up. Conclusions: Littoral cell angioma is a benignvascular proliferation of the spleen that needs to be includedin the differential diagnosis of multiple hypodensesplenic nodules

Abnormal ezrin localization is associated with clinicopathological features in invasive breast carcinomas.

The membrane-cytoskeleton crosslinker ezrin is associated with malignant progression and metastasis in human neoplasias. To study the role of ezrin in breast cancer, we first assessed ezrin expression in a panel of breast cancer cell lines by western blot and confocal microscopy. Western blot revealed no differences in total ezrin levels among these breast cell lines. However, immunofluorescence staining revealed that Estrogen receptor (ER)-positive, noninvasive and nontumorigenic cell lines concentrated ezrin at the apical surface, whereas invasive cell lines localized ezrin in motile structures (membrane ruffles and filopodia) but also had more diffuse cytoplasmic staining. We next studied ezrin expression in 509 breast carcinomas using tissue microarrays. Immunohistochemical staining for ezrin, p53, Ki-67, phospho-Akt, HER2, and hormonal receptors was performed. Ezrin staining in normal breast epithelium localized at the apical, but not lateral, cell surface, whereas, in most breast tumor cases (331, 70.3%), it localized in the cytoplasm. Complete membranous staining occurred in 89 (18.9%) samples, and apical staining was seen in 51 (10.8%) cases. There were significant positive associations between cytoplasmic ezrin localization and adverse tumor characteristics such as high grade, high level of Ki-67 expression, hormonal-receptor negativity, and lymph-node metastases. Apical ezrin staining was associated with favorable clinicopathological features and node-negative tumors. Membranous ezrin staining was associated with high grade, strong HER2 and p-Akt expression. In conclusion, the switch of ezrin localization from the apical membrane to either the complete membrane or to the cytoplasm is correlated with dedifferentiation and adverse features in invasive breast tumors and cancer cell lines.

Posible implicación de las alteraciones moleculares de la vía de TNF en la tumorigénesis de la micosis fungoide. Descripción de un posible chip de diagnóstico molecular en micosis fungoide / Molecular alterations of the TNF pathway may be involved in the tumorigenesis of mycosis fungoides. Description of a possible molecular diagnostic chip in mycosis fungoides

Introducción. El diagnóstico de la micosis fungoide es difícil, sobre todo en las fases iniciales, debido a su similitud morfológica con las dermatosis inflamatorias y la baja proporción de células tumorales en el tejido. Pacientes, material y métodos. Se utilizaron muestras de 29 pacientes con micosis fungoide con lesiones de mancha, placa o tumor; de 24 pacientes con micosis fungoide en estadios Ia, Ib o IIa provenientes de un ensayo clínico; de 11 dermatosis inflamatorias y de piel sana no fotoexpuesta. Se analizaron empleando un chip de ADN-c construido en nuestro laboratorio. Resultados. Este estudio ha demostrado que, empleando estudios de micromatrices de ADN-c y normalización con muestras normales de la piel, es posible detectar una firma molecular que distingue este tipo de tumor de condiciones inflamatorias comunes de la piel. Se ha revelado una firma de 27 genes implicados en la tumorigénesis de micosis fungoide. Esta firma incluye la desregulación de señalización de factor de necrosis tumoral (TNF) además de un lazo autocrino de TNF que promueve señalización antiapoptótica. Además, fue posible identificar un modelo predictivo de sólo 6 genes que permite una distinción entre casos de micosis fungoide y casos de dermatosis inflamatorias con gran precisión. Este modelo predijo correctamente el diagnóstico del 97,3% de los casos en la serie original y en 97,0% de los casos en una serie de validación de 24 pacientes con micosis fungoide con estadios bajos. Conclusiones. Hemos encontrado un grupo de 27 genes posiblemente implicados en la tumorigénesis de la micosis fungoide.Hemos identificado un posible chip de diagnóstico de 6 genes (AU)

Composite Hodgkin lymphoma and mantle cell lymphoma: two clonally unrelated tumors.

Association of Hodgkin lymphoma and non-Hodgkin lymphoma is rare and, specifically, the combination of Hodgkin lymphoma and mantle cell lymphoma has not been previously described. Here we describe composite mantle cell lymphoma and Hodgkin lymphoma affecting the spleen in one case and the eyelid and cervical lymph nodes in a second. In both, nodules of classical Hodgkin lymphoma were intermixed with diffuse or nodular areas of typical mantle cell lymphoma. Immunohistochemical and molecular analyses confirmed cyclin D1 overexpression secondary to the translocation t(11;14) in the small mantle cell lymphoma component; with CD30, CD15, and EBV expression in the Hodgkin and Reed-Sternberg cells. Finally, clonal analysis of rearranged immunoglobulin genes performed on microdissected Hodgkin and Reed-Sternberg and mantle cell lymphoma cells provided definite evidence of separate clonal origins of the two tumors in the patients. These EBV-positive, clonally unrelated tumors seem to represent true composite neoplasms, in contrast to cases showing merely clonal progression.

Mycosis fungoides shows concurrent deregulation of multiple genes involved in the TNF signaling pathway: an expression profile study.

Mycosis fungoides (MF) is the most frequent type of cutaneous T-cell lymphoma, whose diagnosis and study is hampered by its morphologic similarity to inflammatory dermatoses (ID) and the low proportion of tumoral cells, which often account for only 5% to 10% of the total tissue cells. cDNA microarray studies using the CNIO OncoChip of 29 MF and 11 ID cases revealed a signature of 27 genes implicated in the tumorigenesis of MF, including tumor necrosis factor receptor (TNFR)-dependent apoptosis regulators, STAT4, CD40L, and other oncogenes and apoptosis inhibitors. Subsequently a 6-gene prediction model was constructed that is capable of distinguishing MF and ID cases with unprecedented accuracy. This model correctly predicted the class of 97% of cases in a blind test validation using 24 MF patients with low clinical stages. Unsupervised hierarchic clustering has revealed 2 major subclasses of MF, one of which tends to include more aggressive-type MF cases including tumoral MF forms. Furthermore, signatures associated with abnormal immunophenotype (11 genes) and tumor stage disease (5 genes) were identified.