[Tumor and angiogenesis]. / Tumor y angiogénesis.

Angiogenesis is a fundamental event in the process of tumour growth. Tumours recruit precursor cells originated in the bone marrow or stimulate local cells to form new blood vessels. Angiogenesis is not necessary initially for malignant transformation. Tumours acquire later the angiogenic phenotype after a variable period of time for each tumour. The molecular mechanism that promotes angiogenesis requires growth factors activation and loss of function of angiogenic inhibitors, although the full process has been poorly understood. Tumour vessel quantitation has been proposed as a prognostic factor predictive of metastatic dissemination. The microvessel density index usually can be assorted by tumour vessel counts at 200x magnification with the light microscopy. Thus, new therapies that have been reported to inhibit tumour angiogenesis are currently under investigation in clinical trials.

[Meningiomas: new prognostic factors]. / Meningiomas. nuevos factores pronósticos.

Meningiomas are still defined as benignant tumours although 25% of those tumours will have local recurrance in the follow-up period. The WHO (2000) classification divides meningiomas in three goups: Grade 1 for conventional meningioma. Grade 2 for atypical meningioma and Grade 3 for Anaplastic meningioma. Specific histological variants of meningiomas have been included in grade 2 tumours. Clear cell, rabdoid and papillary meningiomas. We obtained 250 meningiomas from our files and we analyzed 30 inmunohistochemical markers. Several markers can be actually used as prognostic indicators in meningiomas and may allow a more individualized management of patients.

Mixoma odontogénico / Odontogenic myxoma

Introducción: El mixoma odontogénico es un tumorpoco frecuente de la mandíbula, benigno pero localmenteinvasivo. Se caracteriza por mostrar escasas células de morfologíafusiforme o estrellada con abundante estromamixoide. Aunque la histogénesis es controvertida se creeque se origina a partir de la papila dental en desarrollo.Caso clínico: Se presenta el caso de un mixoma odontogénicoafectando el maxilar inferior derecho de un pacientevarón de 27 años de edad. Histológicamente el tumor estabacompuesto fundamentalmente por células de tamaño ymorfología uniformes inmersas en una matriz mixoide. Lastécnicas de inmunohistoquímica utilizadas muestran positividaduniforme con vimentina y parcheada con actina muscularespecífica. Las células son negativas para desmina,proteína S-100 y citoqueratinas. El índice proliferativo(medido con Ki-67) es muy bajo (inferior al 1%)

Introduction: Odontogenic myxoma is an uncommontumor of the jaws, benign but locally invasive. It consists ofscarce cells with a spindle or star shape embedded in amyxoid stroma. This tumor is considered to originate fromdental papilla of the developing teeth though there is somecontroversy about its histogenesis. Case presentation: Anodontogenic myxoma from the right lower jaw in a 27-yearold male patient is reported. Microscopically the tumor iscomposed mainly of relatively uniform cells lying in amyxofibroid background. Immunostaining of tumor cellsshows uniform positivity with vimentin and patchy stainingwith muscle specific actin. Cells are negative for keratin,desmin and S-100 protein. The proliferative index (measuredby Ki-67) is very low (lesser than 1%)

A computer-assisted morphometric quantitative analysis of iron overload in liver biopsies. A comparison with histological and biochemical methods.

The aim of this study was to evaluate a new method of image analysis used to quantify the iron load in routinely processed liver biopsies. Sixty-four liver biopsies from the same number of patients were studied. Both biochemical determination of iron concentration and histopathological semiquantification and quantification were performed. The latter was performed on Perls-stained liver sections by a semiautomatic system of image analysis that yields the percentage of stained liver tissue. In 43 samples with an hepatic iron content higher than 2000microg/mg of dry tissue, this morphometric index was compared to the liver iron load measured biochemically, showing a significant correlation (Spearman's test) between both variables (rho = 0.686, p<0.001). Moreover, there is a better correlation when the semiquantitative Deugnier's histological index is compared with the biochemical method (rho = 0.425, p<0.004). Thus, we conclude that image analysis may be a valid method to assess hepatic iron storage in patients with liver diseases and that it may be more accurate than semiquantitative grading systems, such as the one described by Deugnier, since the morphometric method shows a closer correlation with the hepatic iron concentration determined biochemically.

[Molecular pathology of brain tumors]. / Aplicaciones de la patología molecular en el estudio de los tumores cerebrales.

Somatic genetic alterations can be used to differentiate primary from secundary glioblastomas. The molecular pathways involved in tumerogenesis have been described and we now have a better knowledge of tumor biology. Central Nervous System Tumors classification will probably include genetic changes in an early future with potential implications for therapy and patients prognostic.

[Gastrointestinal stromal tumor]. / Tumores del estroma gastrointestinal. gist.

Gastrointestinal stromal tumour is the most common mesenchymal tumour of the human gastrointestinal tract. The c-kit receptor tyrosine Kinase is expressed by practically all GIST. Interstitial cells of Cajal are the pacemaker of the peristaltic movement of the G.I. tract and these tumors are considered to originate from this cells. A great majority of them occurs in the stomach (60-70%) and small intestine (25% to 35%). Some GIST are primary in the omentun, mesentery of retroperitoneum. Although the prediction of malignancy in this tumour group is notorious by difficult, tumors that have mitotic activity count, exceeding 5 per 50 HPF of those larger than 5 cm have a high frequency of intra-abdominal recurrence and liver metastasis. Functional analysis of the different c-kit mutations and their impact on the response to tyrosine Kinase inhibitor are under intense investigation.

Angioleiomioma intravascular / Intravascular angioleiomyoma

Los angioleiomiomas son neoplasias benignas que se originan a partir de las fibras musculareslisas de las paredes de los vasos de la dermis y tejido celular subcutáneo.Se presenta el caso de un varón de 68 años de edad con una tumoración subcutánea nodolorosa situada en el dorso de la mano. Histológicamente se trata de un nódulo bien delimitadoconstituido por fibras de músculo liso formando fascículos entrelazados que se continúan conla pared de múltiples canales vasculares revestidos por un endotelio plano. La lesión está localizadaen su totalidad en el interior de un vaso de tipo venoso.Los angioleiomiomas son tumores que se describen habitualmente en continuidad con lapared de los pequeños vasos sanguíneos de la dermis. El interés del caso descrito se deriva de su localización atípica intravascular

Angioleiomyomas are benign neoplasms arising from vessel wall smooth muscle.A 68-year old-male patient with a subcutaneous painless tumor on the dorsal aspect of thehand is reported. Histologically it consists of a well circumscribed nodule composed of intermingledfascicles of smooth muscle cells connected to the walls of multiple vascular channels linedby flat endothelia. The lesion is completely developed inside a vein.Angioleiomyomas are tumors that often appear in continuity with small vascular vessels of thedermis. The interest of this case is related to its atypical intravascular localization

3p21, 5q21, 9p21 and 17p13.1 allelic deletions are potential markers of individuals with a high risk of developing adenocarcinoma in Barrett's epithelium without dysplasia.

BACKGROUND/AIMS: A common genetic abnormality detected in Barrett's adenocarcinoma is LOH (loss of heterozygosity) at the sites of known or putative tumor suppressor genes. Thus, some deletions have also been determined in peritumoral Barrett's epithelium. These findings suggest that a tissue field of somatic genetic alterations precede the histopathological phenotypic changes of carcinoma. We investigated 32 cases of Barrett's esophagus with no evidence of dysplasia for LOH at 5q21 (APC), 3p21, 9p21 (p16) and 17p13.1 (p53) chromosomal regions. METHODOLOGY: Two groups were randomly selected and compared: 16 cases of Barrett's epithelium adjacent to adenocarcinoma and 16 cases of Barrett's epithelium with no evidence of malignant transformation in a 5-10 years follow-up period. In three adenocarcinomas cases several previous endoscopic biopsies of Barrett's esophagus were available. RESULTS: We determined frequent allelic losses in adenocarcinomas at p53 (54%), p16 (50%), 3p21 (40%) and 5q21 (33%). Identical LOH was present in most cases in the Barrett's epithelium adjacent to adenocarcinoma. LOH at these loci was unusual in Barrett's epithelium with no evidence of malignant transformation. However, in cases where sequential endoscopic biopsies were performed in advance to the adenocarcinoma diagnosis LOH was already present in the Barrett's epithelium. CONCLUSIONS: We suggest that LOH at these loci may be present before the onset of the malignant growth and LOH studies may supplement the histopathological evaluation of Barrett's epithelium. LOH at 3p21, 5q21, 9p21 and 17p13 chromosomal regions in cells of Barrett's epithelium without dysplasia may have a role as a potential marker for individuals with a high risk of developing adenocarcinoma.

[Predictive molecular marker of distant metastasis in colorectal cancer]. / Marcadores moleculares de riesgo de metástasis en el cáncer colorrectal.

Tumor development and progression is driven by the accumulation of somatic genetic alterations. Two major pathways have been suggested in colon tumorigenesis. The first one, the APC/B-catenin pathway consists of chromosomal imbalance (Instability) and therefore accumulation of different oncogenes and tumor supressor genes mutations associated with morphological changes. The second one is characterized by "DNA mismatch repair genes" damage with subsequent accumulation of somatic genetic predictive markers of distant metastasis using tissue microarrays in T2N0 colon cancer. In our series, we detected overexpression of survivin, CDK1, MIB1 and topoisomerase IIa in metastatic tumors.