Plasma ghrelin O-acyltransferase (GOAT) enzyme levels: A novel non-invasive diagnosis tool for patients with significant prostate cancer.

Early detection of PCa faces severe limitations as PSA displays poor-specificity/sensitivity. As we recently demonstrated that plasma ghrelin O-acyltransferase (GOAT)-enzyme is significantly elevated in PCa-patients compared with healthy-controls, using a limited patients-cohort, we aimed to further explore the potential of GOAT to improve PCa diagnosis using an ample patients-cohort (n = 312) and defining subgroups (i.e. significant PCa/metastatic patients, etc.) that could benefit from this biomarker. Plasma GOAT-levels were evaluated by ELISA in patients with (n = 183) and without (n = 129) PCa. Gleason Score ≥ 7 was considered clinically significant PCa. GOAT-levels were higher in PCa patients vs control patients, and in those with significant PCa vs non-significant PCa. GOAT-levels association with the diagnoses of significant PCa was independent from traditional clinical variables (i.e. PSA/age/DRE). Remarkably, GOAT outperformed PSA in patients with PSA-levels ranging 3-20 ng/mL for the significant PCa diagnosis [GOAT-AUC = 0.612 (0.531-0.693) vs PSA-AUC = 0.494 (0.407-0.580)]. A panel of key variables including GOAT/age/DRE/testosterone also outperformed the same panel but with PSA [AUC = 0.720 (0.710-0.730) vs AUC = 0.705 (0.695-0.716), respectively]. Notably, GOAT-levels could also represent a novel predictive biomarker of aggressiveness, as its levels are positively associated with Gleason Score and the presence of metastasis at the time of diagnoses. Altogether, our data reveal that GOAT-levels can be used as a non-invasive biomarker for significant PCa diagnosis in patients at risk of PCa (with PSA: 3-20 ng/mL).

Dysregulation of RNA-Exosome machinery is directly linked to major cancer hallmarks in prostate cancer: Oncogenic role of PABPN1.

Novel biomarkers and therapeutic strategies for prostate-cancer (PCa) are required to overcome its lethal progression. The dysregulation/implication of the RNA-Exosome-complex (REC; cellular machinery controlling the 3'-5'processing/degradation of most RNAs) in different cancer-types, including PCa, is poorly known. Herein, different cellular/molecular/preclinical approaches with human PCa-samples (tissues and/or plasma of 7 independent cohorts), and in-vitro/in-vivo PCa-models were used to comprehensively characterize the REC-profile and explore its role in PCa. Moreover, isoginkgetin (REC-inhibitor) effects were evaluated on PCa-cells. We demonstrated a specific dysregulation of the REC-components in PCa-tissues, identifying the Poly(A)-Binding-Protein-Nuclear 1 (PABPN1) factor as a critical regulator of major cancer hallmarks. PABPN1 is consistently overexpressed in different human PCa-cohorts and associated with poor-progression, invasion and metastasis. PABPN1 silencing decreased relevant cancer hallmarks in multiple PCa-models (proliferation/migration/tumourspheres/colonies, etc.) through the modulation of key cancer-related lncRNAs (PCA3/FALEC/DLEU2) and mRNAs (CDK2/CDK6/CDKN1A). Plasma PABPN1 levels were altered in patients with metastatic and tumour-relapse. Finally, pharmacological inhibition of REC-activity drastically inhibited PCa-cell aggressiveness. Altogether, the REC is drastically dysregulated in PCa, wherein this novel molecular event/mechanism, especially PABPN1 alteration, may be potentially exploited as a novel prognostic and therapeutic tool for PCa.

Tumor suppressor role of RBM22 in prostate cancer acting as a dual-factor regulating alternative splicing and transcription of key oncogenic genes.

Prostate cancer (PCa) is one of the leading causes of cancer-related deaths among men. Consequently, the identification of novel molecular targets for treatment is urgently needed to improve patients' outcomes. Our group recently reported that some elements of the cellular machinery controlling alternative-splicing might be useful as potential novel therapeutic tools against advanced PCa. However, the presence and functional role of RBM22, a key spliceosome component, in PCa remains unknown. Therefore, RBM22 levels were firstly interrogated in 3 human cohorts and 2 preclinical mouse models (TRAMP/Pbsn-Myc). Results were validated in in silico using 2 additional cohorts. Then, functional effects in response to RBM22 overexpression (proliferation, migration, tumorspheres/colonies formation) were tested in PCa models in vitro (LNCaP, 22Rv1, and PC-3 cell-lines) and in vivo (xenograft). High throughput methods (ie, RNA-seq, nCounter PanCancer Pathways Panel) were performed in RBM22 overexpressing cells and xenograft tumors. We found that RBM22 levels were down-regulated (mRNA and protein) in PCa samples, and were inversely associated with key clinical aggressiveness features. Consistently, a gradual reduction of RBM22 from non-tumor to poorly differentiated PCa samples was observed in transgenic models (TRAMP/Pbsn-Myc). Notably, RBM22 overexpression decreased aggressiveness features in vitro, and in vivo. These actions were associated with the splicing dysregulation of numerous genes and to the downregulation of critical upstream regulators of cell-cycle (i.e., CDK1/CCND1/EPAS1). Altogether, our data demonstrate that RBM22 plays a critical pathophysiological role in PCa and invites to suggest that targeting negative regulators of RBM22 expression/activity could represent a novel therapeutic strategy to tackle this disease.

[Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia with tumorlet formation: A case report and review of the literature]. / Hiperplasia difusa idiopática de células neuroendocrinas pulmonares con formación de tumorlets: presentación de un caso clínico y revisión de la literatura.

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia is an infrequent lesion recently classified by the WHO as preinvasive. It can present with the formation of tumorlets (neuroendocrine cell groups up to 5 mm) which result in a typical histological and radiological image. We report a case of a 67-year-old women who presented with a chronic cough. The CT scan showed bilateral minute, multiple pulmonary nodules. A biopsy revealed a diffuse idiopathic pulmonary neuroendocrine cell hyperplasia with several tumorlets. After two years of follow-up, imaging studies showed no significant changes.

Dysregulation of the splicing machinery is directly associated to aggressiveness of prostate cancer.

BACKGROUND: Dysregulation of splicing variants (SVs) expression has recently emerged as a novel cancer hallmark. Although the generation of aberrant SVs (e.g. AR-v7/sst5TMD4/etc.) is associated to prostate-cancer (PCa) aggressiveness and/or castration-resistant PCa (CRPC) development, whether the molecular reason behind such phenomena might be linked to a dysregulation of the cellular machinery responsible for the splicing process [spliceosome-components (SCs) and splicing-factors (SFs)] has not been yet explored. METHODS: Expression levels of 43 key SCs and SFs were measured in two cohorts of PCa-samples: 1) Clinically-localized formalin-fixed paraffin-embedded PCa-samples (n = 84), and 2) highly-aggressive freshly-obtained PCa-samples (n = 42). FINDINGS: A profound dysregulation in the expression of multiple components of the splicing machinery (i.e. 7 SCs/19 SFs) were found in PCa compared to their non-tumor adjacent-regions. Notably, overexpression of SNRNP200, SRSF3 and SRRM1 (mRNA and/or protein) were associated with relevant clinical (e.g. Gleason score, T-Stage, metastasis, biochemical recurrence, etc.) and molecular (e.g. AR-v7 expression) parameters of aggressiveness in PCa-samples. Functional (cell-proliferation/migration) and mechanistic [gene-expression (qPCR) and protein-levels (western-blot)] assays were performed in normal prostate cells (PNT2) and PCa-cells (LNCaP/22Rv1/PC-3/DU145 cell-lines) in response to SNRNP200, SRSF3 and/or SRRM1 silencing (using specific siRNAs) revealed an overall decrease in proliferation/migration-rate in PCa-cells through the modulation of key oncogenic SVs expression levels (e.g. AR-v7/PKM2/XBP1s) and alteration of oncogenic signaling pathways (e.g. p-AKT/p-JNK). INTERPRETATION: These results demonstrate that the spliceosome is drastically altered in PCa wherein SNRNP200, SRSF3 and SRRM1 could represent attractive novel diagnostic/prognostic and therapeutic targets for PCa and CRPC.

Spliceosome component SF3B1 as novel prognostic biomarker and therapeutic target for prostate cancer.

Prostate cancer (PCa) is one of the most common cancers types among men. Development and progression of PCa is associated with aberrant expression of oncogenic splicing-variants (eg, AR-v7), suggesting that dysregulation of the splicing process might represent a potential actionable target for PCa. Expression levels (mRNA and protein) of SF3B1, one of the main components of the splicing machinery, were analyzed in different cohorts of PCa patients (clinically localized [n = 84], highly aggressive PCa [n = 42], and TCGA dataset [n = 497]). Functional and mechanistic assays were performed in response to pladienolide-B in nontumor and tumor-derived prostate cells. Our results revealed that SF3B1 was overexpressed in PCa tissues and its levels were associated with clinically relevant PCa-aggressive features (eg, metastasis/AR-v7 expression). Moreover, inhibition of SF3B1 activity by pladienolide-B reduced functional parameters of aggressiveness (proliferation/migration/tumorspheres-formation/apoptosis) in PCa cell lines, irrespective of AR-v7 expression, and reduced viability of primary PCa cells. Antitumor actions of pladienolide-B involved: (1) inhibition of PI3K/AKT and JNK signaling pathways, (2) modulation of tumor markers and splicing variants (AR-v7/In1-ghrelin), and (3) regulation of key components of mRNA homeostasis-associated machineries (spliceosome/SURF/EJC). Altogether, our results demonstrated that SF3B1 is overexpressed and associated with malignant features in PCa, and its inhibition reduces PCa aggressiveness, suggesting that SF3B1 could represent a novel prognostic biomarker and a therapeutic target in PCa.

Oncogenic Role of Secreted Engrailed Homeobox 2 (EN2) in Prostate Cancer.

Engrailed variant-2 (EN2) has been suggested as a potential diagnostic biomarker; however, its presence and functional role in prostate cancer (PCa) cells is still controversial or unknown. Here, we analyzed 1) the expression/secretion profile of EN2 in five independent samples cohorts from PCa patients and controls (prostate tissues and/or urine) to determine its utility as a PCa biomarker; and 2) the functional role of EN2 in normal (RWPE1) and tumor (LNCaP/22Rv1/PC3) prostate cells to explore its potential value as therapeutic target. EN2 was overexpressed in our two cohorts of PCa tissues compared to control and in tumor cell lines compared with normal-like prostate cells. This profile was corroborated in silico in three independent data sets [The Cancer Genome Atlas(TCGA)/Memorial Sloan Kettering Cancer Center (MSKCC)/Grasso]. Consistently, urine EN2 levels were elevated and enabled discrimination between PCa and control patients. EN2 treatment increased cell proliferation in LNCaP/22Rv1/PC3 cells, migration in RWPE1/PC3 cells, and PSA secretion in LNCaP cells. These effects were associated, at least in the androgen-sensitive LNCaP cells, with increased AKT and androgen-receptor phosphorylation levels and with modulation of key cancer-associated genes. Consistently, EN2 treatment also regulated androgen-receptor activity (full-length and splicing variants) in androgen-sensitive 22Rv1 cells. Altogether, this study demonstrates the potential utility of EN2 as a non-invasive diagnostic biomarker for PCa and provides novel and valuable information to further investigate its putative utility to develop new therapeutic tools in PCa.

Primary giant cell tumor of soft tissue in the finger.

Primary giant cell tumor of soft tissue (GCTST) arising in a finger is a rare event. We report a case of a 54-year-old man with a primary finger giant cell tumor that appeared histologically identical to giant cell tumor of bone. The patient presented with a cystic mass of the finger. The magnetic resonance imaging showed no relation between the nodule and bone, tendons or synovial tissues. The distinction of this entity from other more common primary finger tumors with giant cell morphology is emphasized.

Tumor de células de Sertoli-Leydig poco diferenciado de ovario con elementos heterólogos endodérmicos de tipo colónico / Poorly differentiated Sertoli-Leydig cell tumour of the ovary with heterologous endodermal colonic type tissue

Introducción. Los tumores de células de Sertoli-Leydig (TCSL) de ovario son neoplasias infrecuentes que suponen el 1% de todos los tumores de los cordones sexuales estromal, estando constituidas por células de Sertoli, células de Leydig y/o células fibroblásticas en proporciones diferentes y con varios niveles de diferenciación. En ocasiones estos tumores contienen elementos heterólogos del tipo epitelio mucinoso, cartílago, músculo estriado y/o carcinoide, que pueden remedar a otras neoplasias y provocan errores diagnósticos. Método. Se ha realizado una revisión de los datos clínicos, analíticos, las características histológicas y de la literatura médica. Se han seleccionado cortes representativos los cuales han sido teñidos con hematoxilina eosina y posteriormente se ha realizado estudio inmunohistoquímico con el método estreptavidina biotina peroxidasa para CD56, proteina S-100, citoqueratinas (AE1/AE 3), CEA, vimentina, inhibina, calretinina y CDX2. Resultado y conclusión. La neoplasia está constituida por una población preferentemente estromal con escasos grupos de túbulos y cordones correspondientes a células de Sertoli entremezcladas con células de Leydig, sueltas o en nidos, de aspecto característico al de los tumores de esta estirpe(AU)

Introduction. Sertoli-Leydig cell tumours (SLCT) of the ovary are rare, accounting for only 1% of all sex cord-stromal tumours and are formed by Sertoli and Leydig cells and/or fibroblasts in different proportions and various degrees of differentiation. Sometimes they may contain heterologous elements, such as mucinous epithelium, cartilage, skeletal muscle and/or carcinoid and therefore should be considered in the differential diagnosis of various types of tumours. Methods. The clinical, histological and immunohistochemical features of a case of Sertoli Leydig tumour of the ovary are presented and the literature is reviewed. Sections were stained with hematoxylin-eosin and immunohistochemistry using the streptavidin-biotin-peroxidase method for CD56, S-100 protein, cytokeratin (AE1/AE and 20), CEA, vimentin, inhibin, calretinin and CDX2 was performed. Results and conclusions. The tumour had a characteristic appearance, being composed mainly of stromal cells with few Sertoli cell tubules, admixed with Leydig cells. Immunohistochemistry confirmed the diagnosis(AU)

Tumor mülleriano mixto maligno del cérvix uterino. A propósito de un caso y revisión de la literatura / Malignant mixed müllerian tumour of the uterine cervix. Report of a case and review of the literature

Introducción: Los tumores müllerianos mixtosmalignos (TMMM) de cervix o tumores mesodérmicosmixtos malignos son neoplasias infrecuentes con pocomás de 50 casos descritos en la literatura y probablementeconstituyen <3% de todos los TMMM uterinos. Sonmuy agresivos y generalmente se asocian a mal pronóstico.Método: Hemos revisado las características histológicas,clínicas y la literatura médica. Secciones representativashan sido teñidas con hematoxilina-eosina. El estudioinmunohistoquímico se realizó con el método estreptavidina-biotina-peroxidasa para citoqueratina, antígeno carcinoembrionario,CD10, calretinina, vimentina, desminay mioglobina. Resultado: El tumor es bifásico compuestode una mezcla de componente epitelial y mesenquimalhomólogo y heterólogo. Las tinciones inmunohistoquímicasmostraron positividad para citoqueratina y antígenocarcinoembrionario y negatividad para CD10, calretininay vimentina en el componente epitelial. El componenteheterólogo mostró positividad para desmina y mioglobina.Conclusión: Aportamos un nuevo caso de tumormülleriano mixto maligno originado en cérvix uterino yrevisamos la literatura(AU)

Introduction: Malignant mixed müllerian tumors(MMMTs) or malignant mixed mesodermal tumours of thecervix are exceptionally rare, probably accounting for<3% of all uterine MMMTs; fewer than 50 cases havebeen reported to date. They tend to be highly aggressiveand generally have a poor prognosis. Methods:We presentthe clinical and histological features of a case of MMMTof the cervix and review the literature. Representative sectionswere stained with hematoxylin-eosin and immunohistochemistrywas performed using the streptavidin-biotinperoxidase method for cytokeratin, carcinoembryonicantigen, CD10, calretinin, vimentin, desmin and myoglobin.Results: the tumour was biphasic, composed of anadmixture of neoplastic epithelial and homologous andheterologous mesenchymal components. The epithelialcomponent was positive for cytokeratin and carcinoembryonicantigen and negative for CD10, calretinin andvimentin. The heterologous component was positive fordesmin and myoglobin. Conclusions: we report a case ofmalignant mixed müllerian tumour arising in the uterinecervix and review the literature(AU)

Carcinoide-adenocarcinoma mixto de apéndice cecal. Aspectos terminológicos a propósito de un caso / Mixed carcinoid-adenocarcinoma of the appendix. Terminology aspects and report of a case

Introducción: Los tumores carcinoides de células caliciformes representan menos del 5% de los tumores primarios del apéndice. Son tumores raros y distintivos compuestos de células mucinosas con apariencia de anillo de sello que infiltran circunferencialmente el apéndice y expresan marcadores neuroendocrinos. El término carcinoide-adenocarcinoma mixto ha sido propuesto para designar a carcinomas del apéndice que se originan por progresión de un carcinoide de células de caliciformes preexistente. Método: hemos revisado las características histológicas, clínicas y la literatura médica. Secciones representativas han sido teñidas con hematoxilina-eosina, ácido peryódico de Schiff y azul alcian. El estudio inmunohistoquímico se realizó con el método estreptavidina-biotina-peroxidasa para Citoqueratina 20, cromogranina A, sinaptofisina y antígeno carcinoembrionario. Resultado: El tumor mostró un patrón de crecimiento carcinomatoso en más del 50% de su volumen. El estudio inmunohistoquímico (citoqueratina 20, cromogranina A, sinaptofisina y antígeno carcinoembrionario), ácido peryódico de Schiff y azul alcian fueron difusamente positivos. Conclusión: La inmunohistoquímica es de ayuda para diferenciar estos tumores del adenocarcinoma mucinoso y carcinoides

Background: Goblet cell carcinoids tumours accounts for less than 5% of primary tumors of the appendix. They are rare and distinctive tumours, composed of clusters of mucinous cells with a signet ring cell appearance that infiltrate the appendix circumferentially and express neuroendocrine markers. The term mixed carcinoid-adenocarcinoma has been proposed to designate carcinomas of the appendix that arise by progression from a pre-existing goblet-cell carcinoid. Methods: We have reviewed the histological features, clinical features and the medical literature. Representative sections were stained with hematoxylin-eosin, periodic-acid-Schiff and alcian blue. Immunohistochemical stains were performed by using the streptavidin-biotin peroxidase method for cytokeratin 20, chromogranin A, synaptophysin and carcinoembryonic antigen. Results: The tumour showed carcinomatous growth pattern in greater than 50% of total volume. Immunohistochemical stains (cytokeratin 20, chromogranin A, synaptophysin and carcinoembryonic antigen), periodic-acid-Schiff and alcian blue were diffusely positive. Conclusions: Immunohistochemical stains were helpful to separate these tumors from mucinous adenocarcinoma, signet-ring cell carcinoma and carcinoid tumours

Hemangioma epitelioide en localización profunda y extrafacial. A propósito de dos casos y revisión de la literatura / Epithelioid hemangioma in deep and non facial location. Report of two cases and review of the literature

Resumen: El hemangioma epitelioide es una infrecuente proliferación vascular benigna e idiopática. Típicamente ocurre en la piel y tejido subcutáneo de cabeza y cuello, especialmente en área preauricular, aunque ha sido publicada en tronco y extremidades. Las principales características histológicas del hemangioma epitelioide son la proliferación de grandes células edoteliales lineando espacios vasculares e infiltrado de linfocitos y eosinófilos. El diagnóstico diferencial incluye granuloma piogeno, angiosarcoma y enfermedad de Kimura. Método: Se aportan dos nuevos casos de Hemangioma epitelioide. Revisamos las características histológicas, clínicas, la literatura médica y las diferentes teorías acerca de su histogénesis. Resultados: Se describen dos nuevos casos con origen en extremidades y con variable respuesta inflamatoria. Conclusión: La principal característica histológica del Hemangioma epitelioide es la apariencia endotelial y no la intensidad inflamatoria

Background: Epithelioid hemangioma is an uncommon benign and idiopathic vasculoproliferative condition. Typically occurs in the skin and subcutaneous tissues of the head and neck region, especially the preauricular area, though it has been reported on the trunk and extremities. The main histologic features of epithelioid hemangioma are proliferation of large endothelial cells lining vascular spaces, and lymphocytic and eosinophilic infiltrate. The differential diagnoses include pyogenic granuloma, angiosarcoma, and Kimura’s disease. Methods: Two new cases of Epithelioid hemangioma were report. We have reviewed the histological features, clinical features, the medical literature and the different theories about its histogénesis. Results: We report two new cases arising in extremities and with variable inflammatory response. Conclusions: The main histological characteristic of epithelioid hemangioma is the endothelial appearance and not the inflammatory intensity

Adenocarcinoma papilar seroso en colon sigmoide originado sobre endosalpingiosis quística. A propósito de un caso y revisión de la literatura / Serous papillary adenocarcinoma of the sigmoid colon arising in cystic endosalpingiosis. Report of a case and review of the literature

Resumen: La endosalpingiosis es definida histológicamente por la presencia de glándulas lineadas por epitelio de tipo tubárico y es frecuentemente observada en vísceras pélvicas y peritoneo abdominal. Aunque raramente adenocarcinomas serosos, similares a los que ocurren en ovario, se originan en retroperitoneo, éste es el segundo caso que ocurre en asociación con una endosalpingiosis. Método: Hemos revisado las características histológicas, clínicas y la literatura médica. Secciones representativas se tiñeron con hematoxilina-eosina y se realizaron tinciones inmunohistoquímicas usando el método de estreptavidina-biotina-peroxidasa para citoqueratina 20, citoqueratina 7, calretinina, CA125, CA19.9 y receptores de estrógenos. Resultados: histológicamente las áreas de adenocarcinoma papilar seroso estaban compuestas por células con atipia nuclear moderada organizadas en estructuras glandulares y papilas complejas. Se observaron áreas de transición entre el epitelio ciliado benigno y el adenocarcinoma seroso bien diferenciado. Inmunohistoquimicamente, las células tumorales fueron positivas para citoqueratina 7, CA125 y receptores de estrógenos, pero negativas para citoqueratina 20, calretinina y CA19.9. Conclusión: Presentamos un nuevo caso de adenocarcinoma papilar seroso en colon sigmoideo originado en el seno de una endosalpingiosis quística

Background: Endosalpingiosis is defined as the presence of histologically benign glands lined by tubal-type epithelium and is commonly encountered in the visceral pelvic and abdominal peritoneum. Although rarely serous adenocarcinomas, similar to those occurring within the ovary, arise in the retroperitoneum, this is the second reported occurrence in association with a endosalpingiosis. Methods: We have reviewed the histological features, clinical features and the medical literature. Representative sections were stained with hematoxylin-eosin and inmunohistochemical stains were performed by using the streptavidin-biotin peroxidase method for cytokeratin 20, cytokeratin 7, calretinin, CA125, CA19.9 and estrogen receptor. Results: histologically serous papillary adenocarcinoma areas was composed of a complex papillary and glandular arrangement of cuboidal cells with moderate nuclear atypia. Areas of transition could be seen between the benign ciliated lining and the well differentiated serous adenocarcinoma. Immunohistochemically, the tumour cells were positive for cytokeratin 7, CA125 and estrogen receptor, but were negative for cytokeratin 20, calretinin and CA19.9. Conclusions: we report a new case of a serous papillary adenocarcinoma arising in the sigmoid colon within cystic endosalpingiosis

Esclerosis múltiple unifocal de médula cervical. Pseudotumor desmielinizante / Unifocal cervical spine multiple sclerosis. Demyelinating pseudotumor

Antecedentes: La esclerosis múltiple es una enfermedaddesmielinizante con expresión clínica, radiológica eincluso patológica variables. Los casos que remedan un procesoneoplásico del S.N.C., y los unifocales, especialmentelos medulares, son bastante raros. Métodos: Se presenta uncaso de autopsia de E.M. unifocal de médula cervical, queclínica y radiológicamente se confundió con una neoplasia,llegándose al diagnóstico en el estudio microscópico delmaterial procedente de la autopsia. Resultados: Mediantetécnicas radiológicas adecuadas y/o el estudio del materialprocedente de biopsia en ciertos casos, es posible realizarun diagnóstico precoz del proceso. Conclusiones: Los autoresproponen la definición de Pseudotumor desmielinizante.Y creen necesario considerar la posibilidad de esta entidadclínicopatológica en el diagnóstico diferencial de los procesosexpansivos del S.N.C., y es preciso diagnosticarlamediante la utilización de técnicas no agresivas antes deinstaurar un posible tratamiento inadecuado

Background: Multiple sclerosis (MS) is a demyelinizatingdisease with variable clinic, radiologic and even pathologicfeatures. Those cases simulating a neoplastic disease, especiallythe unifocal forms of the spinal chord are very rare.Patients and methods: An autopsy case of unifocal MS ofcervical spinal cord is reported. After clinical and radiologicalexaminations a neoplastic condition was suspected. Diagnosiswas made after microscopic study of autopsy specimens.Results (pathologic diagnosis): After routine histological examinationof cervical spinal cord and by using special techniques(luxol fast blue), demyelinating plaques, lymphocyticand macrophagic perivascular and interstitial inflammatoryinfiltrate were found. Conclusions: The authors propose insuch cases the use of the term «demyelinating pseudotumor».The authors consider necessary to include this clinicopathologicentity in the differential diagnosis of other expansive processesof the CNS and diagnose it using non aggressive techniquesso avoiding an inadequate treatment

Hemangioendotelioma retiforme: descripción de dos casos y revisión de la literatura / Retiform hemangioendothelioma: A report od two cases and literature review

El hemangioendotelioma retiforme (HR) es una neoplasia vascular rara y con rasgos morfológicos distintivos que por su elevada tasa de recidivas locales y ocasionales metástasis fue descrita inicialmente como angiosarcoma de bajo grado de malignidad. En la literatura revisada hemos encontrado un total de 23 casos bien documentados. Describimos dos nuevos casos de HR y realizamos una revisión de la literatura. Una paciente de 82 años se presentó con una placa indurada, mal definida y de crecimiento lento, situada en el dorso de la mano derecha; la segunda paciente tenía 31 años y consultó por una lesión en la planta del pie. En el estudio histológico ambas lesiones presentaban las características propias del HR con una proliferación dermohipodérmica infiltrativa de canales vasculares elongados, arborescentes de paredes finas, tapizados por células endoteliales con morfología en tachuela y sin atipia ni figuras de mitosis. El diagnóstico diferencial se establece fundamentalmente con el tumor de Dabska, el hemangioma en tachuela y el angiosarcoma convencional. La aportación de nuevos casos de este infrecuente tumor vascular puede ayudar a definir con mayor precisión el espectro clínico y morfológico del HR (AU)