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1.
J Transl Med ; 17(1): 307, 2019 Sep 09.
Artigo em Inglês | MEDLINE | ID: mdl-31500625

RESUMO

BACKGROUND: Conventional clinical biomarkers cannot accurately differentiate indolent from aggressive prostate cancer (PCa). We investigated the usefulness of a biomarker panel measured exclusively in biofluids for assessment of PCa aggressiveness. METHODS: We collected biofluid samples (plasma/serum/semen/post-prostatic massage urine) from 98 patients that had undergone radical prostatectomy. Clinical biochemistry was performed and several cytokines/chemokines including soluble(s) TWEAK, sFn14, sCD163, sCXCL5 and sCCL7 were quantified by ELISA in selected biofluids. Also, the expression of KLK2, KLK3, Fn14, CD163, CXCR2 and CCR3 was quantified by real-time PCR in semen cell sediment. Univariate, logistic regression, and receiver operating characteristic (ROC) analyses were used to assess the predictive ability of the selected biomarker panel in conjunction with clinical and metabolic variables for the evaluation of PCa aggressiveness. RESULTS: Total serum levels of prostate-specific antigen (PSA), semen levels of sTWEAK, fasting glycemia and mRNA levels of Fn14, KLK2, CXCR2 and CCR3 in semen cell sediment constituted a panel of markers that was significantly different between patients with less aggressive tumors [International Society of Urological Pathology (ISUP) grade I and II] and those with more aggressive tumors (ISUP grade III, IV and V). ROC curve analysis showed that this panel could be used to correctly classify tumor aggressiveness in 90.9% of patients. Area under the curve (AUC) analysis revealed that this combination was more accurate [AUC = 0.913 95% confidence interval (CI) 0.782-1] than a classical non-invasive selected clinical panel comprising age, tumor clinical stage (T-classification) and total serum PSA (AUC = 0.721 95% CI 0.613-0.830). CONCLUSIONS: TWEAK/Fn14 axis in combination with a selected non-invasive biomarker panel, including conventional clinical biochemistry, can improve the predictive power of serum PSA levels and could be used to classify PCa aggressiveness.

2.
Gastroenterol. hepatol. (Ed. impr.) ; 34(6): 406-410, jun. - jul. 2011.
Artigo em Espanhol | IBECS | ID: ibc-92948

RESUMO

IntroducciónLa fibromatosis es una proliferación fibroblástica benigna con crecimiento infiltrativo local. Se clasifica en una forma superficial y en una forma profunda, también denominada tumor desmoide (TD). Esta última puede presentarse en forma esporádica o asociada a la poliposis adenomatosa familiar y síndrome de Gardner. La presentación pancreática es excepcional y sólo existen 8 casos descritos en la literatura médica.Observación clínicaMujer de 29 años con antecedentes de PCF y 2 lesiones pancreáticas. En la pieza quirúrgica se observaron 2 lesiones mal delimitadas en el páncreas con infiltración de órganos vecinos. Histológicamente, correspondían a una proliferación de estirpe mesenquimatosa de patrón fusocelular sin atipias citológicas, que se diagnosticaron de TD.DiscusiónLa etiología de la fibromatosis es desconocida. En pacientes con PCF la localización más habitual de los TD es intraabdominal siendo inusual la presentación pancreática. Esto plantea el diagnóstico diferencial con otras neoplasias del páncreas(AU)


IntroductionFibromatosis consists of a benign fibroblastic proliferation with local infiltrative growth. Two types are recognized: a superficial and a deep form, also known as desmoid tumor. The latter may occur sporadically or in association with familial adenomatous polyposis and Gardner's syndrome. Pancreatic presentation is exceptional and only eight cases have been described in the literature.Case reportWe report the case of a 29-year-old woman with a history of familial colonic polyposis and two pancreatic lesions. In the surgical specimen, two poorly defined pancreatic lesions were observed with infiltration of neighboring organs. Histologically, the lesions corresponded to mesenchymal proliferation with a fusocellular pattern without cytological atypica, which were diagnosed as desmoid tumors.DiscussionThe etiology of fibromatosis is unknown. In patients with familial colonic polyposis, the most common localization of desmoid tumor is intra-abdominal. Pancreatic presentation is unusual, requiring differential diagnosis with other pancreatic neoplasms(AU)


Assuntos
Humanos , Feminino , Adulto , Polipose Adenomatosa do Colo/complicações , Fibromatose Agressiva/patologia , Neoplasias Abdominais/patologia , Neoplasias Pancreáticas/diagnóstico , Diagnóstico Diferencial
3.
Gastroenterol Hepatol ; 34(6): 406-10, 2011.
Artigo em Espanhol | MEDLINE | ID: mdl-21571398

RESUMO

INTRODUCTION: Fibromatosis consists of a benign fibroblastic proliferation with local infiltrative growth. Two types are recognized: a superficial and a deep form, also known as desmoid tumor. The latter may occur sporadically or in association with familial adenomatous polyposis and Gardner's syndrome. Pancreatic presentation is exceptional and only eight cases have been described in the literature. CASE REPORT: We report the case of a 29-year-old woman with a history of familial colonic polyposis and two pancreatic lesions. In the surgical specimen, two poorly defined pancreatic lesions were observed with infiltration of neighboring organs. Histologically, the lesions corresponded to mesenchymal proliferation with a fusocellular pattern without cytological atypica, which were diagnosed as desmoid tumors. DISCUSSION: The etiology of fibromatosis is unknown. In patients with familial colonic polyposis, the most common localization of desmoid tumor is intra-abdominal. Pancreatic presentation is unusual, requiring differential diagnosis with other pancreatic neoplasms.


Assuntos
Neoplasias Abdominais/complicações , Neoplasias Abdominais/diagnóstico , Polipose Adenomatosa do Colo/complicações , Fibromatose Agressiva/complicações , Fibromatose Agressiva/diagnóstico , Neoplasias Pancreáticas/diagnóstico , Adulto , Diagnóstico Diferencial , Feminino , Humanos
4.
Am J Dermatopathol ; 33(5): 516-20, 2011 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-21285861

RESUMO

The association of multiorgan histiocytosis after acute lymphoblastic leukemias is very rare as most cases are localized forms of Langerhans cell histiocytosis (LCH). We report on an 18-year-old man diagnosed with B-cell acute lymphoblastic leukemia (B-ALL) with p16 deletion (9p21). He was treated with induction chemotherapy using the Spanish PETHEMA group protocol and achieved complete remission. Three months after the diagnosis of B-ALL, he developed a severe multiorgan histiocytosis that is clinically suggestive of LCH but lacked typical immunohistochemical features of LCH and indeterminate cell histiocytosis: CD1a was strongly positive, CD68 and S-100 protein were moderately positive, and langerin was negative. The drugs of the first-line treatment recommended for LCH had been part of the chemotherapy of B-ALL that the patient had received. Therefore, we prescribed the second-line treatment for LCH (cytarabine and 2'-chlorodeoxyadenosine), and he achieved partial remission. The patient died during the aplasia induced by the third cycle of chemotherapy from pneumonia. We could not demonstrate the transdifferentiation of tumoral lymphocytes into histiocytes, using p16 deletion (9p21) as a marker, because these cells did not share the mutation. Neither could we study immunoglobulin-H rearrangement as we had exhausted all the tissue samples. In the medical literature, there are a few reported cases of T-cell acute lymphoblastic leukemia followed by disseminated LCH and just 1 case of B-ALL followed by localized LCH affecting the bones. Therefore, our patient may be the first published case of B-ALL followed by histiocytosis, which had 2 singularities: it was multiorgan and the immunohistochemistry was not typical of LCH.


Assuntos
Histiocitose/complicações , Histiocitose/patologia , Leucemia-Linfoma Linfoblástico de Células Precursoras B/complicações , Adolescente , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Evolução Fatal , Histiocitose/tratamento farmacológico , Humanos , Imuno-Histoquímica , Masculino , Leucemia-Linfoma Linfoblástico de Células Precursoras B/tratamento farmacológico
5.
Med. clín (Ed. impr.) ; 114(11): 411-413, mar. 2000.
Artigo em Espanhol | IBECS | ID: ibc-6333

RESUMO

Fundamento: Se pretende determinar la proporción de enfermedad de Hodgkin (EH) que expresa el virus de Epstein-Barr (VEB) en nuestro medio. Pacientes y métodos: Se ha realizado un estudio retrospectivo sobre 49 casos de EH usando la técnica inmunohistoquímica LMP-1 y la técnica de hibridación in situ para EBER-1. Resultados: Un 40,8 por ciento (20/49) de los casos expresaba VEB (EBER-1 y/o LMP-1 positivos). Este porcentaje fue significativamente mayor en EH diagnosticadas a pacientes mayores de 55 años y no hubo diferencias por sexo, aunque fue mayor, pero no de forma significativa, en el subtipo histológico de EH de celularidad mixta. Conclusiones: El VEB se asocia a un 40,8 por ciento de las EH en las comarcas de Tarragona (AU)


Assuntos
Pessoa de Meia-Idade , Criança , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Masculino , Feminino , Humanos , Herpesvirus Humano 4 , Espanha , Estudos Retrospectivos , Doença de Hodgkin
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