System-based approaches as prognostic tools for glioblastoma.

BACKGROUND: The evasion of apoptosis is a hallmark of cancer. Understanding this process holistically and overcoming apoptosis resistance is a goal of many research teams in order to develop better treatment options for cancer patients. Efforts are also ongoing to personalize the treatment of patients. Strategies to confirm the therapeutic efficacy of current treatments or indeed to identify potential novel additional options would be extremely beneficial to both clinicians and patients. In the past few years, system medicine approaches have been developed that model the biochemical pathways of apoptosis. These systems tools incorporate and analyse the complex biological networks involved. For their successful integration into clinical practice, it is mandatory to integrate systems approaches with routine clinical and histopathological practice to deliver personalized care for patients. RESULTS: We review here the development of system medicine approaches that model apoptosis for the treatment of cancer with a specific emphasis on the aggressive brain cancer, glioblastoma. CONCLUSIONS: We discuss the current understanding in the field and present new approaches that highlight the potential of system medicine approaches to influence how glioblastoma is diagnosed and treated in the future.

Gliomatosis cerebri: evolución a glioblastoma multiforme / Gliomatosis cerebri: evolution to glioblastoma multiforme

Introducción. La gliomatosis cerebri es un trastorno neoplásico caracterizado por una infiltración difusa de células gliales con relativa conservación de las estructuras subyacentes. Las crisis comiciales, la cefalea y los trastornos del comportamiento suelen ser las manifestaciones iniciales.Caso clínico. Hombre de 38 años que presenta crisis parciales complejas y trastorno del comportamiento de 3 meses de evolución. En la resonancia magnética cerebral presenta lesiones hiperintesas en T2 sugerentes de gliomatosis cerebri, confirmándose con la biopsia cerebral. Varios meses después sufre un empeoramiento clínico rápido, evidenciándose el desarrollo de un glioblastoma multiforme sobre la lesión.Conclusiones. La gliomatosis cerebri, pese a su rareza, debe tenerse en cuenta en el diagnóstico diferencial de las lesiones infiltrativas difusas de la sustancia blanca. El empeoramiento clínico de rápida evolución y la aparición de lesiones focales que captan contraste nos deben hacer sospechar una trasformación a lesiones de mayor malignidad

Introduction. Gliomatosis cerebri is a neoplastic disorder characterized by diffuse infiltration of glial cells with relative conservation of the underlying structures. Seizures, headache and behavior disorders are generally the initial manifestations.Clínical case. A 38 year-old male who had complex partial seizures and behavior disorder of three months' evolution. The brain magnetic resonance imaging showed hyperintense lesions in T2 suggestive of gliomatosis cerebri, this being confirmed with the brain biopsy. Several months later, he suffered rapid clinical deterioration, observing the development of a glioblastoma multiforme over the lesion.Conclusions. In spite of its rareness, gliomatosis cerebri should be taken into account in the differential diagnoses of diffuse infiltrative lesions of the white matter. Rapid evolution clinical deterioration and the appearance of focal lesions that capture contrast should make us suspect a transformation to lesions of greater malignancy

Case-control study of use of nonsteroidal antiinflammatory drugs and glioblastoma multiforme.

Evidence from epidemiologic and experimental studies suggests that use of nonsteroidal antiinflammatory drugs (NSAIDs) reduces risk of colon and breast cancer. The association between use of aspirin and other NSAIDs and risk of adult glioblastoma multiforme (GBM) was evaluated among 236 incident GBM cases and 401 population-based controls frequency-matched on age, gender, and ethnicity from the San Francisco Bay Area Adult Glioma Study. Cases (or proxies) and controls were interviewed in person between May 1997 and August 2000. Cases with self-reported GBM reported less use of at least 600 pills of all types of NSAIDs combined during the 10-year prediagnostic period than did controls (odds ratio (OR) = 0.53, 95% confidence interval (CI): 0.3, 0.8). Findings were consistent for aspirin (OR = 0.51, 95% CI: 0.3, 0.8), ibuprofen (OR = 0.41, 95% CI: 0.2, 0.8), and naproxen/other NSAIDs (OR = 0.34, 95% CI: 0.1, 0.8). GBM cases also reported less use of acetaminophen than did controls (OR = 0.51, 95% CI: 0.3, 1.0). Eliminating participants who initiated NSAID use within 2 years of diagnosis yielded similar results. These findings show an inverse association between NSAID use and GBM. Further studies are warranted to determine whether NSAIDs might be effective in the inhibition of GBM development or progression.

Synchronous occurrence of glioblastoma multiforme and esophageal adenocarcinoma.

Synchronous malignancies are rare occurrences for which there may be a genetic link between two cancers or which may be simply coincidental. Although glioblastoma multiforme and esophageal adenocarcinoma have few clinical similarities there are no known biochemical or genetic links between the two malignancies. This case discussion details the synchronous occurrences of these two lesions and highlights possible clinical, biochemical, and genetic commonalities.

Thalamic glioblastoma with cerebrospinal fluid dissemination in the peritoneal cavity.

Glioblastoma multiforme is one of the commonest primary malignant tumours of the brain with rare incidence of extracranial metastases. Systemic dissemination via the CSF or CSF diversionary shunt procedures is also rare. The reported 9-year-old child was a case of thalamic glioblastoma with hydrocephalus who underwent biventriculoperitoneal shunting before tumour decompression and radiotherapy. The child developed incapacitating ascites 8 months following surgical decompression and 9 months after the shunt diversion which was found to be caused by CSF dissemination of the glioblastoma via the ventriculoperitoneal shunt. The child ultimately succumbed to his disease.