Ganhos e perdas genômicas em momentos sucessivos do carcinoma urotelial de bexiga humana

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Segundo tumor em pacientes com neoplasias de cabeça e pescoço

Pós-graduação em Pesquisa e Desenvolvimento (Biotecnologia Médica) - FMB

Genomic profile of a Li-Fraumeni-like syndrome patient with a 45,X/46,XX karyotype, presenting neither mutations in TP53 nor clinical stigmata of Turner syndrome

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Evaluation of prognostic factors and survival rates in malignant feline mammary gland neoplasms

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Análise integrada entre dados de expressão global de transcritos codificadores e de miRNAs em carcinomas de células escamosas de laringe

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Elastografia acoustic radiation force impulse (ARFI), doppler e ultrassonografia contrastada do baço canino

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Inibição da metástase via transição epitélio-mesenquimal por shRNA, metformina e Y27632 em neoplasia mamária

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Possible association between Carney complex and multiple endocrine neoplasia type 1 phenotypes

Complexo de Carney (CNC) e neoplasia endócrina múltipla tipo 1 (MEN1) são formas de neoplasias endócrinas múltiplas de herança autossômica dominante. O diagnóstico do CNC ocorre quando dois critérios maiores (lentiginose, doença nodular pigmentosa primária das adrenais, mixomas cardíacos e cutâneos, acromegalia, neoplasia testicular, carcinoma de tireóide) são observados e/ou um critério maior associado a um critério suplementar (familiar afetado, mutação do gene PRKAR1A) ocorre. Por outro lado, o diagnóstico de MEN1 dá-se pela detecção de dois ou mais tumores localizados na glândula hipofisária, paratireóide e/ou células pancreáticas. O presente caso descreve um homem de 55 anos, com diagnóstico de acromegalia, hiperparatireoidismo primário e carcinoma papilífero de tireóide, exibindo critérios diagnósticos para as duas condições descritas. Embora possa ter ocorrido apenas uma associação esporádica, ou a acromegalia per se tenha predisposto ao carcinoma papilífero, novos mecanismos moleculares podem estar envolvidos.

Chromosomal imbalances detected in primary bone tumors by comparative genomic hybridization and interphase fluorescence in situ hybridization

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Challenges of modeling depth-integrated marine primary productivity over multiple decades: A case study at BATS and HOT

The performance of 36 models (22 ocean color models and 14 biogeochemical ocean circulation models (BOGCMs)) that estimate depth-integrated marine net primary productivity (NPP) was assessed by comparing their output to in situ (14)C data at the Bermuda Atlantic Time series Study (BATS) and the Hawaii Ocean Time series (HOT) over nearly two decades. Specifically, skill was assessed based on the models' ability to estimate the observed mean, variability, and trends of NPP. At both sites, more than 90% of the models underestimated mean NPP, with the average bias of the BOGCMs being nearly twice that of the ocean color models. However, the difference in overall skill between the best BOGCM and the best ocean color model at each site was not significant. Between 1989 and 2007, in situ NPP at BATS and HOT increased by an average of nearly 2% per year and was positively correlated to the North Pacific Gyre Oscillation index. The majority of ocean color models produced in situ NPP trends that were closer to the observed trends when chlorophyll-alpha was derived from high-performance liquid chromatography (HPLC), rather than fluorometric or SeaWiFS data. However, this was a function of time such that average trend magnitude was more accurately estimated over longer time periods. Among BOGCMs, only two individual models successfully produced an increasing NPP trend (one model at each site). We caution against the use of models to assess multiannual changes in NPP over short time periods. Ocean color model estimates of NPP trends could improve if more high quality HPLC chlorophyll-alpha time series were available.

Frequency of multiple endocrine neoplasia type 1 in a group of patients with pituitary adenoma: genetic study and familial screening

The purpose of this study it was to evaluate the frequency of Multiple Endocrine Neoplasia type 1 (MEN1) in patients with pituitary adenoma and to perform genetic analysis and familial screening of those individuals afflicted with MEN1. 144 patients with pituitary adenoma at Botucatu Medical School, UNESP-Univ Estadual Paulista, were assessed retrospectively for MEN1 during the years of 2005-2011. The patients were evaluated for the presence of primary hyperparathyroidism (PHP) and enteropancreatic tumors. Genetic analysis was performed for the individuals with clinically diagnosed MEN1. Thirteen patients met the diagnostic criteria for MEN1, but three individuals belong to the same family and they were considered as a single MEN1 event, revealing 7.7 % frequency of MEN1 in this patient group. Genetic analysis showed MEN1 mutations in four index cases: IVS4+1 G>A, IVS3-6 C>T, c.1547insC and a new D180A mutation. One patient did not agree to participate in the genetic study and another one was referred for follow up in other hospital. Only polymorphisms were found in the other individuals, one of which was novel. We identified a high frequency of MEN1 in pituitary adenoma patients. Since PHP is one of the most common MEN1 tumor and patients are mostly asymptomatic, we suggest that all pituitary adenoma patients have their calcium profile analyzed. © 2013 Springer Science+Business Media New York.

Evaluation of melatonin treatment in primary culture of canine mammary tumors

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

CDX2, a highly sensitive and specific marker of adenocarcinomas of intestinal origin - An immunohistochemical survey of 476 primary and metastatic carcinomas

CDX2 is a recently cloned homeobox gene that encodes an intestine-specific transcription factor, expressed in the nuclei of epithelial cells throughout the intestine, from duodenum to rectum. While expression of CDX2 protein in primary and metastatic colorectal carcinomas has been previously documented, neither the sensitivity nor the specificity of CDX2 expression, as determined by immunohistochemistry, for colorectal adenocarcinoma has been determined. We performed an immunohistochemical survey of 476 tumors with a monoclonal antibody, CDX2-88, including 89 tumors from the colon and duodenum and 95 tumors from other gastrointestinal sites, including the esophagus, stomach, pancreatobiliary system, gastrointestinal carcinoids, and liver. CDX2 was expressed uniformly (that is, in 76-100% of tumor cells) in all but one of the evaluated colorectal and duodenal tumors. High-level expression of CDX2 was also found, however, in mucinous ovarian carcinomas and adenocarcinomas primary to the urinary bladder of which 64% and 100% were positive, respectively. Gastric, gastroesophageal, and pancreatic adenocarcinomas and cholangiocarcinomas all showed similar, heterogeneous patterns of CDX2 expression. Most tumors in each group showed CDX2 expression by a minority of cells, whereas a substantial minority of cases in each group was completely negative and a smaller minority was uniformly positive. Gastrointestinal carcinoids gave similarly varied results, but the majority (58%) was negative. Hepatocellular carcinomas showed no expression of CDX2. Only very rare examples of carcinomas of the genitourinary and gynecologic tracts, breast, lung, and head and neck showed significant levels of CDX2 expression. In this study of primary and metastatic epithelial tumors, uniform CDX2 expression is demonstrated to be an exquisitely sensitive and highly, but incompletely, specific marker of intestinal adenocarcinomas. Compared with villin, a previously described marker of GI adenocarcinomas, CDX2 demonstrated superior sensitivity and comparable specificity. CDX2 expression can be seen, however, in selected non-GI adenocarcinomas such as mucinous ovarian carcinomas and adenocarcinomas of the urinary bladder.

DNA damage in multiple organs after exposure to chlorhexidine in Wistar rats

Since chlorhexidine is effective against microorganisms, it is widely recommended in dentistry. However, studies have provided evidence that chlorhexidine is toxic for a variety of cell types. In order to identify potential genotoxins in different cell types, the purpose of this study was to investigate whether chlorhexidine digluconate is able to cause, in terms of DNA damage, alterations in leukocytes, liver, kidney and urinary bladder by the single cell gel (comet) assay. Ten male Wistar rats were divided into two groups: a negative control and the experimental group treated with 3 ml of 0.12% chlorhexidine digluconate by gavage once a day for 8 days. Statistically significant increases of DNA damage was observed in leukocytes and kidney cells of the chlorhexidine digluconate treated group as depicted by the mean tail moment. Taken together, the data indicate that leukocytes and kidney cells are potential targets for primary DNA damage following oral exposure to chlorhexidine digluconate as detected by single cell gel (comet) assay. (c) 2006 Elsevier GmbH. All rights reserved.

Independent clonal origin of multiple uterine leiomyomas that was determined by X chromosome inactivation and microsatellite analysis

Objective: In an attempt to clarify the clonality and genetic relationships that are involved in the tumorigenesis of uterine leiomyomas, we used a total of 43 multiple leiomyomas from 14 patients and analyzed the allelic status with 15 microsatellite markers and X chromosome inactivation analysis.Study design: We have used a set of 15 microsatellite polymorphism markers mapped on 3q, 7p, 11, and 15q by automated analysis. The X chromosome inactivation was evaluated by the methylation status of the X-linked androgen receptor gene.Results: Loss of heterozygosity analysis showed a different pattern in 7 of the 8 cases with allelic loss for at least 1 of 15 microsatellite markers that were analyzed. A similar loss of heterozygosity findings at 7p22-15 was detected in 3 samples from the same patient. X chromosome inactivation analysis demonstrated the same inactivated allele in all tumors of the 9 of 12 informative patients;. different inactivation patterns were observed in 3 cases.Conclusion: Our data support the concept that uterine leiomyomas are derived from a single cell but are generated independently in the uterus. Loss of heterozygosity findings at 7p22-15 are consistent with previous data that suggested the relevance of chromosomal aberrations at 7p that were involved in individual uterine leiomyomas. (C) 2005 Mosby, Inc. All rights reserved.