Meningioma rabdoide. Ejemplo poco frecuente de tumor meningotelial agresivo (meningioma grado III) / Rhabdoid meningioma: a rare example of aggressive meningioma (grade III meningioma)

Presentamos un ejemplo de meningioma rabdoide diagnosticado en una mujer de 54 años. El tumor, de localización parasagital, mostró numerosas células de aspecto rabdoide, con un amplio citoplasma en el que se identificaban típicas inclusiones acidófilas. Las técnicas de inmunohistoquímica, imprescindibles para establecer el diagnóstico diferencial con otras neoplasias de morfología igualmente rabdoide, confirmaron el carácter meningoteliomatoso de la lesión, que mostró positividad para vimentina, EMA y receptores de progesterona, siendo negativa para citoqueratinas, S-100, HMB-45, actina, desmina, PGFA, CD38, enolasa, sinaptofisina y neurofilamentos. Se comentan brevemente las principales características de esta lesión y su inclusión dentro de los meningiomas de mayor agresividad (meningiomas grado III)(AU)

A parasagittally located rhabdoid meningioma occurring in a 54 year-old woman showed numerous rhabdoid-like cells with abundant cytoplasm in which typical acidophil inclusions were found. Inmunohistochemistry was positive for vimentin, EMA and progesterone receptors and negative for cytokeratins, S-100, HMB-45, actin, desmin, PGFA, CD38, enolase, synaptophysin and neurofilaments; confirming the meningothelial character of the tumour and differentiating it from other rhabdoid-like neoplasms. The main characteristics of the lesion and its inclusion in the aggressive meningiomas group (grade III meningiomas) are discussed(AU)

Hibernoma inguinal. Ejemplo de tumor adiposo poco frecuente / Inguinal hibernoma, a rare tumour of the adipose tissue. A case report

Presentamos en nuestro trabajo un hibernoma localizado en la región inguinal, diagnosticado en un varón de 64 años. Elementos clave para el diagnóstico fueron la identificación del tejido graso pardo y la ausencia de lipoblastos, lo que nos permitió descartar la posibilidad de un liposarcoma. Los estudios inmunohistoquímicos y citogenéticos apoyaron nuestra sospecha diagnostica(AU)

A case of hibernoma located in the inguinal region in a 64 year old male is presented. The identification of brown adipose tissue and the absence of lipoblasts were the most important diagnostic features, essential in the differential diagnosis with liposarcoma. Immunohistochemistry and cytogenetics confirmed the diagnosis of a hibernoma(AU)

Subependimoma del septum pellucidum. Un caso poco frecuente de tumor cerebral causante de hidrocefalia / Subependymoma of septum pellucidum. An unusual case of a brain tumor causing hydrocephaly

Presentamos en nuestro trabajo un caso de subependimoma cerebral, observado en una mujer de 42 años, aquejada de un cuadro de hidrocefalia obstructiva. El tumor localizado en el septum pellucidum provocaba obstrucción del agujero de Monro. Tras su extirpación total, el estudio histológico de la pieza reveló una neoplasia de arquitectura nodular, con presencia de quistes y pequeños grupos celulares dentro de una trama fibrilar, halallazgos típicos del subependimoma(AU)

We present a case of a subependymoma in a 42-year-old woman presenting with obstructive hydrocephaly. The tumour was located in the septum pellucidum obstructing Monro's foramen. Following total surgical removal, the neoplasm was seen to have a nodular architecture with microcysts and clusters of cells in a fibrillary background, all features typical of subependymoma(AU)

Sarcoma sinovial: hallazgos morfológicos en un caso estudiado por punción aspiración con aguja fina / Synovial sarcoma: morphological findings in a case studied with fine needle aspiration

Introducción: El frecuente uso de la punción aspiración con aguja fina (PAAF) como técnica diagnóstica obliga a los patólogos a un conocimiento cada vez mas profundo del aspecto citológico de las lesiones, tanto de las mas frecuentes y elementales, como de aquellas que se observan rara vez en la diaria labor asistencial. Caso clínico: Varón, de 42 años de edad, con una tumoración, de 3,5 cm de diámetro máximo, de 10 meses de evolución, palpable en la región submandibular. Practicada PAAF, el examen microscópico de las extensiones citológicas, mostró una celularidad abundante, constituida por elementos fusiformes, de elevada relación núcleo/citoplasma. Los cortes histológicos obtenidos a partir del bloque celular, mostraron una proliferación de células fusiformes que fueron positivas para vimentina y citoqueratinas (positividad focal para AE1/AE3 / citoqueratinas 7 y 19), siendo negativas para actina, desmina, HMB-45, calretinina, proteína S-100 y CD31. Con una fuerte sospecha de sarcoma, se realizó la extirpación quirúrgica de la tumoración, en cuyo estudio histológico se emitió el diagnóstico definitivo fue de sarcoma sinovial bifásico, confirmado posteriormente mediante estudios citogénéticos. Conclusión: Podemos comprobar que a las tradicionales ventajas de PAAF (rapidez, inocuidad, bajo costo) podemos añadir, en ocasiones, la posibilidad de ampliar el estudio citológico al campo histológico e inmunohistoquímico, a través del manejo de bloques celulares

Introduction: The frequent use of fine needle aspiration (FNA) as a diagnostic technique, applicable to the study of tumours accessible both radiologically and by simple palpation requires that pathologists must have an increasingly profound knowledge of the cytological aspects of the lesions, both of the most frequent and elementary types and those that are only observed rarely in daily clinical practice. Case report: Male, aged 42, with a 3.5 cm mass, during the last 10 months, palpable, and located in submaxillar area. FNA showed abundant cellular material, mainly composed of fusiform elements, with high nuclear-cytoplasmic ration. Cellular block sections confirmed fusocelular elements that were positive for vimentin and focally positive for cytokeratin (CK) AE1/AE3, and CK7 and 19. They were negative for actin, desmin, HMB-45, calretinin, S-100, and CD31. A diagnosis of suggestive of sarcoma was made. Surgical excision of the tumour allowed a histopathological diagnosis of biphasic synovial sarcoma, which was confirmed by cytogenetic studies. Conclusion: The traditional advantages of FNA (speed, harmlessness, low cost) may sometimes be accompanied by the possibility of extending the cytological study to the fields of histology and immunocytochemistry through the handling of cell blocks (AU)

Expresión de E-cadherina, laminina y colágeno IV en la evolución de displasia a carcinoma epidermoide oral / E-cadherin, laminin and collagen IV expression in the evolution from dysplasia to oral squamous cell carcinoma

Objetivos: Estudiar la pérdida o reducción de la adhesión celular mediada por E-cadherina en leucoplasias, carcinomas epidermoides y metástasis ganglionares. Estudiar la pérdida de continuidad de la expresión de laminina y colágeno IV en la membrana basal epitelial en el desarrollo biológico de las leucoplasias y carcinomas orales.Material y metodo: Hemos estudiado 124 muestras de pacientes portadores de leucoplasias y carcinomas orales con diversos diagnósticos que abarcan desde epitelio normal (13 muestras), displasias leves (2), displasias moderadas (12), carcinomas in situ (13) carcinomas microinvasores (11) Carcinoma epidermoide oral (64 muestras) y metástasis ganglionar(9). Se construyeron 7 bloques de tissue microarrays con aguja de 2mm y se realizó un estudio mediante técnica inmunohistoquímica para E-cadherina (clona 36, T.D. ABD Company), Laminina (078P, Biogenex) y Colágeno IV (PHM12, Biogenex).Resultados: En Displasias Leves y Moderadas presentan pérdida de expresión de E-cadherina, Laminina, y ColágenoIV (20%). En Carcinomas in situ y Microinvasores, presentaron pérdida de expresión de E-cadherina (73%), y en Laminina y Colágeno IV (57%). En los carcinomas epidermoides, encontramos pérdida de expresión de E-cadherina (90%) y discontinuidad en la M. basal (70%). Todas las metástasis ganglionares presentaron pérdida de E-cadherina y discontinuidad en Laminina y Colágeno IV.Conclusiones: La pérdida de expresión de E-cadherina se incrementa al aumentar el grado de displasia de las lesiones. La perdida de continuidad en la expresión de laminina y Colágeno IV sigue una evolución paralela desde displasias a metástasis ganglionares. La disminución en la expresión de los tres marcadores ha sido significativa en la evolución de las lesiones orales

Objectives: Study the loss or reduction of the cellular adhesion mediated for E-cadherin in oral leukoplakias, oral squamouscell carcinomas and metastatic nodules. Study the loss of continuity of the laminin and collagen IV expression in the epithelial basal membrane from the biological development of the oral leukoplakias and oral carcinomas.Material and method: we have studied 124 samples of patient payees leukoplakias and oral carcinomas with diverse diagnosis that embrace from normal epithelium (13 samples), mild dysplasias (2), moderate dysplasias (12), “in situ” carcinomas (13), microinvasive carcinomas (11) oral squamous cell carcinomas (64 samples) and metastatic nodules (9). 7 blocks of tissue microarrays were built with needle of 2mm and was carried out a study by means of immunohistochemicaltechnique for E-cadherin (clone 36, Biogenex), Laminin (078P, Biogenex) and Collagen IV (PHM12, Biogenex).Results: In Mild and Moderate Dysplasias the results present loss of E-cadherin, Laminin, and Collagen IV (20%) expression. “in situ” and microinvasive carcinomas, the results presented loss of E-cadherin expression (73%), and loss in Laminin and Collagen IV expression (57%). In the squamous cell carcinomas , we find E-cadherin underexpression (90%) and discontinuity in the Basal Membrane. (70%). All the metastatic nodules presented loss of E-cadherin expressionand discontinuity in Laminin and Collagen IV expression.Conclusions: The loss of E-cadherin expression is increased when increasing the dysplasia grade of lesions. The loss of continuity in the laminin and Collagen IV expression follow a parallel evolution from dysplasias to metastatic nodules. The underexpression of the three markers has been significant in the evolution of the oral lesions

E-cadherin, laminin and collagen IV expression in the evolution from dysplasia to oral squamous cell carcinoma.

OBJECTIVES: Study the loss or reduction of the cellular adhesion mediated for E-cadherin in oral leukoplakias, oral squamous cell carcinomas and metastatic nodules. Study the loss of continuity of the laminin and collagen IV expression in the epithelial basal membrane from the biological development of the oral leukoplakias and oral carcinomas. MATERIAL AND METHOD: we have studied 124 samples of patient pays leukoplakias and oral carcinomas with diverse diagnosis that embrace from normal epithelium (13 samples), mild dysplasias (2), moderate dysplasias (12), in situ carcinomas (13), microinvasive carcinomas (11) oral squamous cell carcinomas (64 samples) and metastatic nodules (9). 7 blocks of tissue microarrays were built with needle of 2mm and was carried out a study by means of immunohistochemical technique for E-cadherin (clone 36, Biogenex), Laminin (078P, Biogenex) and Collagen IV (PHM12, Biogenex). RESULTS: In Mild and Moderate Dysplasias the results present loss of E-cadherin, Laminin, and Collagen IV (20%) expression. in situ and microinvasive carcinomas, the results presented loss of E-cadherin expression (73%), and loss in Laminin and Collagen IV expression (57%). In the squamous cell carcinomas , we find E-cadherin underexpression (90%) and discontinuity in the Basal Membrane. (70%). All the metastatic nodules presented loss of E-cadherin expression and discontinuity in Laminin and Collagen IV expression. CONCLUSIONS: The loss of E-cadherin expression is increased when increasing the dysplasia grade of lesions. The loss of continuity in the laminin and Collagen IV expression follow a parallel evolution from dysplasias to metastatic nodules. The underexpression of the three markers has been significant in the evolution of the oral lesions.

Expresión proteica de p53 y proliferación celular en leucoplasias orales / Proteic expressión of p53 and cellular proliferation in oral leukoplakias

Objetivos: Conocer la expresión proteica de las alteraciones genéticas que se producen en las etapas precoces de la cancerización del campo de cavidad oral en nuestro medio. Estudiar la proliferación celular mediante Ki-67 y la expresión de la proteína p53 para valorar si las alteraciones en la expresión proteica de estos marcadores suceden de forma secuencial a través de las distintas etapas en la cancerización del campo de la cavidad oral. Material y métodos: Se realizó un estudio mediante técnicas de inmunohistoquímica sobre 53 pacientes que presentaron lesiones de leucoplasia oral, atendidos por el Servicio de O.R.L del Hospital Universitario de Salamanca, desde 1.990 hasta 2000. Se incluyen en el estudio 11 muestras de epitelio normal, 15 displasias leves y moderadas, 15 carcinomas in situ, y 12 carcinomas microinvasores. Resultados: Encontramos la proliferación celular aumentada y sobreexpresión de p53 a medida que avanzamos en el grado de severidad histopatológica de las lesiones. Las alteraciones más precoces son el aumento significativo de la proliferación celular en displasias leves y moderadas y el aumento de expresión de p53. Conclusión: La leucoplasia oral es un estado precanceroso quec onstituye una lesión cancerizable debido a las alteraciones genéticas que intervienen en la evolución de la lesión. El estudio inmunohistoquímico y molecular de las lesiones es un medio rutinario que permite conocer la expresión proteica de las alteraciones genéticas, que puede ayudar en el diagnóstico precoz y tratamientode esta patología, teniendo especial relevancia el estudio de Ki-67 en etapas iniciales y p53 en lesiones más avanzadas

OBJECTIVES: We intend to know the protein expression of genetic alterations that take place in the early stages in the field cancerization of oral cavity in our means as well as to study the cellular proliferation by means of Ki-67 and the protein product expression of p53 to value if the alterations in the protein products expression of these markers happen in a sequential pathway through the different stages in the field cancerization of oral cavity. MATERIALS AND METHODS: A study was made by immunohistochemistry on 53 patients that presented lesions of oral leukoplaquia, assisted by the ENT service at University Hospitalof Salamanca, from 1.990 up to 2000. 11 samples of normal epithelium,15 mild to moderate dysplasias, 15 in situ carcinomas and 12 microinvasive carcinomas are included in the study. RESULTS: we find an increased cellular proliferation and p53 over-expression as we advance in the grade of severity histopathologic of these lesions. The most early alterations are a significant increase of cell proliferation in mild and moderate dysplasias and an increased p53 over-expression. CONCLUSIONS: Oral leukoplaquia is a precancerous stage that constitutes a canzerisable lesion due to the genetic alterations that mediate in the evolution of lesion. Routine Immunohistochemical and molecular study of these lesions allow us to know the protein expression of genetic alterations that can help in the early diagnosis and treatment of this pathology, having special relevance the study of Ki-67 in early stages and p53 inadvanced lesions

Proteic expression of p53 and cellular proliferation in oral leukoplakias.

OBJECTIVES: We intend to know the protein expression of genetic alterations that take place in the early stages in the field cancerization of oral cavity in our means as well as to study the cellular proliferation by means of Ki-67 and the protein product expression of p53 to value if the alterations in the protein products expression of these markers happen in a sequential pathway through the different stages in the field cancerization of oral cavity. MATERIALS AND METHODS: A study was made by immunohistochemistry on 53 patients that presented lesions of oral leukoplaquia, assisted by the ENT service at University Hospital of Salamanca, from 1.990 up to 2000. 11 samples of normal epithelium, 15 mild to moderate dysplasias, 15 in situ carcinomas and 12 microinvasive carcinomas are included in the study. RESULTS: we find an increased cellular proliferation and p53 over-expression as we advance in the grade of severity histopathologic of these lesions. The most early alterations are a significant increase of cell proliferation in mild and moderate dysplasias and an increased p53 over-expression. CONCLUSIONS: Oral leukoplaquia is a precancerous stage that constitutes a cancerisable lesion due to the genetic alterations that mediate in the evolution of lesion. Routine Immunohistochemical and molecular study of these lesions allow us to know the protein expression of genetic alterations that can help in the early diagnosis and treatment of this pathology, having special relevance the study of Ki-67 in early stages and p53 in advanced lesions.

[Peri-testicular fibromatosis (testicular fibrous pseudotumor)]. / Periorquitis fibromatosa (pseudotumor fibroso testicular).

OBJECTIVE: We report a case of fibromatous periorchitis, a rare entity that may have differential diagnosis problems with other lesions. METHODS: Our patient underwent a surgical procedure with resection of the tunica vaginalis testis after intraoperative histological evaluation. RESULTS: Findings observed in both intraoperative biopsy and specimen histopathological study were key for diagnosis. CONCLUSIONS: Although macroscopic appearance of the lesion can be of great value, fibromatous periorchitis diagnosis is based on the histologic features, being important to avoid erroneous therapeutic decisions.

Periorquitis fibromatosa (pseudotumor fibroso testicular) / Fifromatous periorchitis (testicular fibrous pseudotumour)

Objetivo: Presentamos un caso de periorquitis fibromatosa, rara entidad que puede plantear problemas de diagnóstico diferencial con otras lesiones. Métodos: Nuestro paciente fue intervenido quirúrgicamente, practicándose la resección de la vaginal testicular, tras estudio histológico intraoperatorio de la lesión. Resultados: Los hallazgos observados tanto en la biopsia intraoperatoria como en el estudio histopatológico de la pieza quirúrgica, fueron claves para el diagnóstico de la lesión. Conclusiones: El diagnóstico de la periorquitis fibromatosa se basa en el aspecto histológico de lesión, si bien su apariencia macroscópica parece ser de gran valor orientativo, lo que resulta muy importante a la hora de evitar conductas terapéuticas improcedentes (AU)