Virulence mechanisms of the pathogenic fungus Aspergillus fumigatus are multifactorial and depend on the immune state of the host, but little is known about the fungal mechanism that develops during the process of lung invasion. In this study, microarray technology was combined with a histopathology evaluation of infected lungs so that the invasion strategy followed by the fungus could be described. To achieve this, an intranasal mice infection was performed to extract daily fungal samples from the infected lungs over four days post-infection. The pathological study revealed a heavy fungal progression throughout the lung, reaching the blood vessels on the third day after exposure and causing tissue necrosis. One percent of the fungal genome followed a differential expression pattern during this process. Strikingly, most of the genes of the intertwined fumagillin/pseurotin biosynthetic gene cluster were upregulated as were genes encoding lytic enzymes such as lipases, proteases (DppIV, DppV, Asp f 1 or Asp f 5) and chitinase (chiB1) as well as three genes related with pyomelanin biosynthesis process. Furthermore, we demonstrate that fumagillin is produced in an in vitro pneumocyte cell line infection model and that loss of fumagillin synthesis reduces epithelial cell damage. These results suggest that fumagillin contributes to tissue damage during invasive aspergillosis. Therefore, it is probable that A. fumigatus progresses through the lungs via the production of the mycotoxin fumagillin combined with the secretion of lytic enzymes that allow fungal growth, angioinvasion and the disruption of the lung parenchymal structure.

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BSCCL is an aggressive variant of the squamous cell carcinoma and has a high expression of p53 and Ki-67 with a low expression of Ecadherin. These results could be related to the aggressiveness of the disease and its poor prognosis.

Oral leukoplakia (OL) is the most common and emblematic oral potentially malignant disorder (OPMD), and it was defined by the WHO Collaborating Centre as "a predominantly white plaque of questionable risk having excluded (other) known diseases or disorders that carry no increased risk for cancer". [1][2][3] In 1985, Hansen et al. 4 described a new clinical entity called "proliferative verrucous leukoplakia" (PVL), which was characterised by the development of multiple and proliferative oral leukoplakias,

Objective Granular cell tumour (GCT) is a benign neoplasm that originates from Schwann cells. Within the oral cavity, it usually appears as a lingual nodule and especially amongst female adults. Histologically, GCT shows a proliferation of polygonal cells with eosinophilic granular cytoplasm, which can be associated with a pseudoepitheliomatous hyperplasia (PEH). In this study, we analyse the main clinicopathological data of intraoral GCT and we compare our results with previous studies. Material and Methods We have studied a series of 56 cases of oral GCT in Spain and Brazil, and we have conducted a systematic review in PubMed, Web of Knowledge and Scopus databases, using the keywords: “granular cell tumour” and oral. Results In our series, GCT appeared as an asymptomatic benign tumour that is more frequent in women and in the tongue. PEH was observed in 32% of the lesions. In the review, we collected 282 cases of oral GCT with a similar clinical profile; seven patients had multiple lesions, and 33% of the cases presented PEH. No cases of malignant oral GCT have been described to date. GCT is an uncommon oral benign neoplasm, mainly unique and asymptomatic, derived from Schwann cells. Conclusions Although the etiopathogenesis of this oral tumour is unknown, its characteristics suggest that it could have a reactive nature. Conducting a complete clinicopathological study in all intraoral GCT is fundamental in order to dismiss other entities, including oral carcinoma.