Allergic fungal sinusitis with massive intracranial extension presenting with tearing.

A 24-year-old male presented with tearing, and subsequent workup and imaging showed a mass with fluid involving the nasopharynx, the paranasal sinuses, and the posterior dehiscence of the left frontal sinus intracranially compressing the frontal lobe significantly. Microscopic examination confirmed the diagnosis of allergic fungal sinusitis. Endoscopic drainage and sinostomy was performed by the otolaryngology (ear-nose-throat) service. The patient was followed 9 months postoperatively and did well with resolution of the epiphora. Although epiphora alone is an unusual presentation of allergic fungal sinusitis, ophthalmologists need to be aware of this entity, as it may invade the orbit through the sinus cavities or compress on the nasolacrimal duct before it causes other mass-related symptoms. Radiology and the characteristic histopathologic findings are the most useful in establishing the correct diagnosis.

Antiangiogenic drugs synergize with a membrane macrophage colony-stimulating factor-based tumor vaccine to therapeutically treat rats with an established malignant intracranial glioma.

Combining a T9/9L glioma vaccine, expressing the membrane form of M-CSF, with a systemic antiangiogenic drug-based therapy theoretically targeted toward growth factor receptors within the tumor's vasculature successfully treated >90% of the rats bearing 7-day-old intracranial T9/9L gliomas. The antiangiogenic drugs included (Z)-3-[4-(dimethylamino)benzylidenyl]indolin-2-one (a platelet-derived growth factor receptor beta and a fibroblast growth factor receptor 1 kinase inhibitor) and oxindole (a vascular endothelial growth factor receptor 2 kinase inhibitor). A total of 20-40% of the animals treated with the antiangiogenic drugs alone survived, while all nontreated controls and tumor vaccine-treated rats died within 40 days. In vitro, these drugs inhibited endothelial cells from proliferating in response to the angiogenic factors produced by T9/9L glioma cells and prevented endothelial cell tubulogenesis. FITC-labeled tomato lectin staining demonstrated fewer and constricted blood vessels within the intracranial tumor after drug therapy. Magnetic resonance imaging demonstrated that the intracranial T9 glioma grew much slower in the presence of these antiangiogenic drugs. These drugs did not affect in vitro glioma cell growth nor T cell mitogenesis. Histological analysis revealed that the tumor destruction occurred at the margins of the tumor, where there was a heavy lymphocytic infiltrate. Real-time PCR showed more IL-2-specific mRNA was present within the gliomas in the vaccinated rats treated with the drugs. Animals that rejected the established T9/9L glioma by the combination therapy proved immune against an intracranial rechallenge by T9/9L glioma, but showed no resistance to an unrelated MADB106 breast cancer.