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A rare case of sudoriferous cyst of the orbit occurring in an adult, who had facial trauma, is reported. Several factors suggest its adult onset. The only other case reported in an adult is of presumed childhood origin. Very few congenital cases have been reported. A 65-year-old lady presented with recent onset of left-sided ptosis and a painless mass below the left supraorbital margin. The patient had traumatic ptosis after a road traffic accident 13 years ago. The ptosis was surgically repaired, which resulted in symmetrical palpebral apertures. Computed tomographic scan revealed a well-defined cystic mass in the anterior orbit. The mass was removed in toto by anterior orbitotomy. Histopathological examination revealed a single cyst lined by double-layered cuboidal epithelium in some areas and transitional epithelium at others. A periodic acid Schiff (PAS) positive, diastase-resistant glycocalyx lined the inner epithelium. Apical snouting suggested an apocrine nature. This confirmed a diagnosis of sudoriferous cyst.

Behavioral and event-related potential (ERP) measurements were made in an auditory selective-attention paradigm, both before and after a series of inhibition or discrimination training sessions. The presence of distractors caused poor perceptual sensitivity, weak P3 responses, conservative responding, and slow reaction times relative to baseline. Distraction prompted a frontal enhancement of ERP components occurring 100-250 ms after the onset of attended signals (N1, P2, and N2). Training ameliorated behavioral interference from distraction. Participants receiving inhibition training acquired improved inhibitory processing of distractors, ah effect that peaked 200 ms after distractor onset. In a proposed model, distinct excitatory and inhibitory mechanisms work interactively to maintain sensitivity to environmental change in the face of disruption from the contextual integration of irrelevant events.

Although KIT-mutant GISTs can be effectively treated with tyrosine kinase inhibitors (TKIs), many patients develop resistance to imatinib mesylate (IM) as well as the FDA-approved later-line agents sunitinib, regorafenib and ripretinib. Resistance mechanisms mainly involve secondary mutations in the KIT receptor tyrosine kinase gene indicating continued dependency on the KIT signaling pathway. The fact that the type of secondary mutation confers either sensitivity or resistance towards TKIs and the notion that secondary mutations exhibit intra- and intertumoral heterogeneity complicates the optimal choice of treatment in the imatinib-resistant setting. Therefore, new strategies that target KIT independently of its underlying mutations are urgently needed. Homoharringtonine (HHT) is a first-in-class inhibitor of protein biosynthesis and is FDA-approved for the treatment of chronic myeloid leukemia (CML) that is resistant to at least two TKIs. HHT has also shown activity in KIT-mutant mastocytosis models, which are intrinsically resistant to imatinib and most other TKIs. We hypothesized that HHT could be effective in GIST through downregulation of KIT expression and subsequent decrease of KIT activation and downstream signaling. Testing several GIST cell line models, HHT led to a significant reduction in nascent protein synthesis and was highly effective in the nanomolar range in IM-sensitive and IM-resistant GIST cell lines. HHT treatment resulted in a rapid and complete abolishment of KIT expression and activation, while KIT mRNA levels were minimally affected. The response to HHT involved induction of apoptosis as well as cell cycle arrest. The antitumor activity of HHT was confirmed in a GIST xenograft model. Taken together, inhibition of protein biosynthesis is a promising strategy to overcome TKI resistance in GIST. [ABSTRACT FROM AUTHOR]