-Carcinomatous encephalitis is a rare entity, originally described by Madow and Alpers in 1951, which is characterized by tumoral spreading perivascular, without mass effect. Clinical manifestations such as hemiparesis, seizures, ataxia, speech difficulties, cerebrospinal fluid findings as well as computed tomography are nonspecific. This leads the physician to pursue more frequent diseases that could explain those manifestations -toxic, metabolic, and/or infectious encephalopathy. A magnetic resonance imaging (MRI) with gadolinium, the method of choice, presumes the diagnosis. Previous reports of this unusual form of metastatic disease have described patients with prior diagnosis of pulmonary adenocarcinoma. We present the case of carcinomatous encephalitis in a 76-years-old woman as the primary manifestation of occult pulmonary adenocarcinoma with its clinical, imaging, and anatomopathological findings.Key WoRdS: brain metastases, carcinomatous encephalitis, lung adenocarcinoma, miliary brain metastases.encefalite carcinomatosa como apresentação inicial de adenocarcinoma de pulmão oculto: relato de caso ReSUMo -A "encefalite" carcinomatosa é entidade rara, descrita originalmente por Madow e Alpers em 1951 e caracterizada pela disseminação tumoral perivascular, sem causar efeito de massa. As manifestações clínicas como hemiparesia, convulsões, ataxia, alterações de fala, os achados do líquido cefalorraquidiano e da tomografia computadorizada de crânio são inespecíficos, o que faz buscar outras causas mais freqüentes que justifiquem o quadro -encefalopatia tóxica, metabólica e/ou infecciosa. A ressonância magnética com gadolínio é o exame de eleição, frente à suspeita clínica. Todos os casos de

Background: Gliomas are aggressive and resilient tumors. Progression to advanced stages of malignancy, characterized by cell anaplasia, necrosis, and reduced response to conventional surgery or therapeutic adjuvant, are critical challenges in glioma therapy. Relapse of the disease poses a considerable challenge for management. Hence, new compounds are required to improve therapeutic response. As hydrolyzed rutin (HR), a compound modified via rutin deglycosylation, as well as some flavonoids demonstrated antiproliferative effect for glioblastoma, these are considered potential epigenetic drugs. Objective: The purpose of this study was to determine the antitumor activity and evaluate the potential for modifying tumor aggressivity of rutin hydrolysates for treating both primary and relapsed glioblastoma. Methods: The glioblastoma cell line, U251, was used for analyzing cell cycle inhibition and apoptosis and for establishing the GBM mouse model. Mice with GBM were treated with HR to verify antitumor activity. Histological analysis was used to evaluate HR interference in aggressive behavior and glioma grade. Immunohistochemistry, comet assay, and thiobarbituric acid reactive substance (TBARS) values were used to evaluate the mechanism of HR action. Results: HR is an antiproliferative and antitumoral compound that inhibits the cell cycle via a p53- independent pathway. HR reduces tumor growth and aggression, mainly by decreasing mitosis and necrosis rates without genotoxicity, which is suggestive of epigenetic modulation. Conclusion: HR possesses antitumor activity and decreases anaplasia in glioblastoma, inhibiting progression to malignant stages of the disease. HR can improve the effectiveness of response to conventional therapy, which has a crucial role in recurrent glioma.

selective condition, the effects of the mutation of interest can be analysed by measuring the proportion of each barcode in genomic DNA by real-time quantitative PCR or deep sequencing. Results and discussions We used this CRISPR-barcoding strategy to model different mechanisms of non-small-cell lung cancer resistance to EGFR inhibitors, and we established a multiplex system to evaluate the efficacy of combined drug therapies aimed at preventing or delaying the emergence of resistant cells. Through a similar approach, we assessed the effects of repairing oncogenic driver mutations in addicted cancer cells directly at the genome level. Finally, we used a highly complex set of CRISPR-barcodes to trace intratumor heterogeneity, as a convenient alternative strategy to lentiviral barcode libraries. Conclusion CRISPR-barcoding is a fast and highly flexible means to investigate the effects of different kinds of genomic modifications in a broad range of functional assays.