Tumors of the salivary gland in Mexicans. A retrospective study of 360 cases

Objective: To establish distribution frequency and demographic characteristics of salivary gland tumours (SGT) in order to identify possible risk profiles. Design of study: The present report constitutes an eight year retrospective study (January 2000-August 2007). The archives of the Clinical and Experimental Pathology Laboratory (Graduate and Research Division, Dental School, National Autonomous University of Mexico) as well as archives of the Surgical Pathology Service (General Hospital, Mexico City) were subject to revision in order to select all cases where SGT tumour diagnoses were emitted. Age and gender of patients as well as SGT topography were obtained from medical records. Selected cases were classified according to location of the lesion, histological lineage and biological behaviour. Results: 360 cases of SGT were included, 227 (67%) cases were benign tumours, while 83 cases (23%) were malignant tumours. SGT were most frequent in women with ages ranging from their 3 rd to 5 th decades of life. 275 tumours were located in major salivary glands, 78.9% of them were identified in the parotid gland. The most frequent location of tumours arising from minor salivary glands (33 cases, 38%) was found in the palatine glands. Tumours of epithelial lineage were the predominant histological type. The most frequent benign tumours were pleomorphic adenomas (86.1%) and papillary cystadenoma lymphomatosum (7.3%). The most frequent malignant tumours were adenoid cystic carcinomas (25%) and mucoepidermoid carcinomas (23.6%) Conclusions: Salivary gland tumours in Mexican population appear principally in major salivary glands of women in their 3 rd to 5 th decade of life. © Medicina Oral S. L

Cambios morfológicos cerebrales en sujetos obesos :estudio posmortem

Ciencias Médica

Expression of Collagen VI, Anticollagenase, Laminin, MM9, Claudins 1 and 5, N and E Cadherins in Choroid Plexus Tumors

Background: CPTs are rare intraventricular papillary neoplasms derived from the choroid plexus epithelium. Anti-collagenase and extracellular matrix which have not been expressed in brain tumors. Objective: The purpose of this study was to investigate the expression levels of collagen type VI, anti-collagenase, laminin, MM9, claudins 1 and 5, N and E cadherins, and collagen VII, tejido, and collagen degradation enzyme complexes in choroid plexus tumors.Materials and methods: We studied the expression of adhesion molecules, extracellular matrix, and anticollagenase with an immunohistochemistry approach and electron microscopy analysis in 42 choroid plexus tumors. Results: 28(67%) were choroid plexus papillomas, 8 (19%) were atypical choroid plexus papillomas and 6 (14%) were choroid plexus carcinomas. The Ki67-li and MVD increased from CPC to ACPP, being the highest in malignant tumors as well as a strong immunoexpression of anti-collagenase and were inverse correlation with claudin 5, E, and N cadherin and collagen IV immunoexpressions which added further significant information to the prognosis and varied according to the histologic classification. By ultrastructure, the loss of basal membrane and cilia, disorganization, and proliferation of ECM were observed in CPC. Cerebral homeostasis largely results from the ability of both the Blood–Brain Barrier (BBB) at the brain microvascular endothelium and the Blood–Cerebrospinal Fluid Barrier (BCSFB) at the epithelium of the Choroid Plexuses (CPs), to control the composition of the CSF and cerebral extracellular fluid. Under expression of the tight junction proteins occludin, claudin-1 and claudin-5 are key molecular abnormalities responsible for the increased permeability of tumor endothelial tight junctions. Conclusion: The loss of basement membrane and ECM overexpression could be considered as a poor prognosis predictor in CPT. Anti-collagenase and MMP9 overexpression could be related to basal membrane and BBB plasticity in CPTs

Astrocytic Tumors in Mexico: An Overview of Characteristics and Prognosis in an Open Reference Center for Low-Income Population

Objective: The authors aimed to analyze the current epidemiology of high- and low-grade gliomas, follow-up strategies, and prognosis in a national reference center of a developing country. Materials and Methods: Medical records of patients diagnosed with intracranial gliomas from January 2012 to January 2016 were reviewed. Data were classified by age, symptoms, Karnofsky functional scale (KFS), tumor location, extent of resection (EOR), histopathology, hospital stay, Glasgow outcome scale (GOS), adjuvant treatments, overall survival (OS), and mortality. Results: Astrocytomas accounted for 28.2% of the intracranial tumors and 53.5% were male. Headache was the most common symptom, while sensory disturbance was the least frequent. The right cerebral hemisphere was involved in 56.5% of cases and frontal lobe in 31.3%. Gross total resection (GTR) was achieved in 18.1% cases, 35.3% subtotal resection, and 46.4% biopsy. Regarding the astrocytomas, 43.3% were low grade and 56.4% high grade. Low-grade tumors had the highest frequency in the fourth decade of life, while Grade III and IV in the fifth and seventh decades of life, respectively. In high-grade lesions, there was a slight male predominance (~1.4:1). The initial KFS was regularly 80 for low-grade gliomas and 60 for high-grade. By 1-month postdischarge, the score decreased by 10 points. About half of the patients (47.5%) received adjuvant therapy after surgery. From the Glasgow Outcome Scale (GOS), the majority had a form of disability and 30-month OS was above 88% for Grade I-II and 0% for Grade III and IV. Conclusions: Astrocytic tumors were the most frequently noted intra-axial tumors. Age, histological grade, and EOR are important prognostic factors. These results are similar to other reports; however, increased variability was noted when treatment-related factors were considered. Additional studies are necessary to identify the factors related to these treatment results. Highlights: • There are no data describing the basic epidemiology and prognosis of high-grade and low-grade gliomas in Mexico. • Intracranial astrocytomas account for 28.2% tumors in our institution. • Age, histological grade, and EOR are important prognostic factors. • Poor overall survival was achieved in our target population

Short-Spindled Cell Haemangioblastoma with CD34 Expression: New Histopathological Variant or Just a Stochastic Cytological Singularity?

Haemangioblastomas are neoplasms of uncertain histogenesis with cellular and reticular variants advocated in current lore. Herein we describe an intriguing cerebellar specimen with unusual traits including spindle cell morphology and CD34 positivity. A thirty-nine-year old man had an infratentorial tumour discovered incidentally and resected three times. In all the instances, histopathological diagnosis was haemangioblastoma; nonetheless, he had neither physical stigmata nor family history of von Hippel-Lindau disease. By histology, the lesion was composed of areas of conventional stromal cells admixed with territories populated by short-spindled cells packed in lobules, sometimes giving the appearance of gomitoli. Immunoperoxidase-coupled reactions confirmed the expression of inhibin A, neuron-specific enolase (NSE), PS100, and CD57 but also revealed focal immunolabeling for CD34, CD99, and FXIIIa. This case highlights the potential phenotypical diversity that can be found within these neoplasms. Rather than uncertain histogenesis, it may in fact reflect multiple lines of differentiation—histomimesis—prone to adopt unusual morpho- and immunophenotypes in a subset of haemangioblastomas

Aryl Hydrocarbon Receptor in Post-Mortem Hippocampus and in Serum from Young, Elder, and Alzheimer’s Patients

One of the characteristics of the cerebral aging process is the presence of chronic inflammation through glial cells, which is particularly significant in neurodegeneration. On the other hand, it has been demonstrated that the aryl hydrocarbon receptor (AHR) participates in the inflammatory response. Currently, evidence in animal models shows that the hallmarks of aging are associated with changes in the AHR levels. However, there is no information concerning the behavior and participation of AHR in the human aging brain or in Alzheimer’s disease (AD). We evaluated the expression of AHR in human hippocampal post-mortem tissue and its association with reactive astrocytes by immunohistochemistry. Besides this, we analyzed through ELISA the AHR levels in blood serum from young and elder participants, and from AD patients. The levels of AHR and glial fibrillar acid protein were higher in elder than in young post-mortem brain samples. AHR was localized mainly in the cytosol of astrocytes and displayed a pattern that resembles extracellular vesicles; this latter feature was more conspicuous in AD subjects. We found higher serum levels of AHR in AD patients than in the other participants. These results suggest that AHR participates in the aging process, and probably in the development of neurodegenerative diseases like AD

The Genomic Landscape of Corticotroph Tumors: From Silent Adenomas to ACTH-Secreting Carcinomas

Corticotroph cells give rise to aggressive and rare pituitary neoplasms comprising ACTH-producing adenomas resulting in Cushing disease (CD), clinically silent ACTH adenomas (SCA), Crooke cell adenomas (CCA) and ACTH-producing carcinomas (CA). The molecular pathogenesis of these tumors is still poorly understood. To better understand the genomic landscape of all the lesions of the corticotroph lineage, we sequenced the whole exome of three SCA, one CCA, four ACTH-secreting PA causing CD, one corticotrophinoma occurring in a CD patient who developed Nelson syndrome after adrenalectomy and one patient with an ACTH-producing CA. The ACTH-producing CA was the lesion with the highest number of single nucleotide variants (SNV) in genes such as USP8, TP53, AURKA, EGFR, HSD3B1 and CDKN1A. The USP8 variant was found only in the ACTH-CA and in the corticotrophinoma occurring in a patient with Nelson syndrome. In CCA, SNV in TP53, EGFR, HSD3B1 and CDKN1A SNV were present. HSD3B1 and CDKN1A SNVs were present in all three SCA, whereas in two of these tumors SNV in TP53, AURKA and EGFR were found. None of the analyzed tumors showed SNV in USP48, BRAF, BRG1 or CABLES1. The amplification of 17q12 was found in all tumors, except for the ACTH-producing carcinoma. The four clinically functioning ACTH adenomas and the ACTH-CA shared the amplification of 10q11.22 and showed more copy-number variation (CNV) gains and single-nucleotide variations than the nonfunctioning tumors