No abstract

Solitary fibrous tumours are uncommon spindle cell neoplasms generally associated with serosal surfaces, especially the pleura (‘localized fibrous mesothelioma’). Recently, these tumours have been documented in extraserosal sites. We report two solitary fibrous tumours, including one occurring in the paediatric age group, arising in two previously unreported locations, parapharyngeal space and epiglottis. These cases expand the range of sites where this tumour may originate and confirm the tendency of extrapleural cases to involve the upper respiratory tract and adjacent structures.

Endophthalmitis is a feared complication of trauma, surgical procedures and septicemia. Although uncommon, its potential for significant visual loss is well recognized. Especially over the past decade, complicated surgeries and medical techniques have increased and seriously ill patients are being sustained in ever increasing numbers. New pathogens are being recognized and known ones reclassified thanks to advances in molecular analysis. Continuously evolving PCR methodologies also add a new dimension to the diagnosis of infectious endophthalmitis. As well, medical literature is now truly international, encompassing studies from around the world that expand our understanding of ocular infectious disease. This report reviews some of these changes as they relate to endophthalmitis and particularly to the spectrum of organisms involved.

These results suggest that c-myc amplification can occur at an early stage in tumor progression and that amplification does not always persist in the nodal metastasis.

Summary Breast cancer-induced activated fibroblasts support tumor progression. However, the role of normal fibroblasts in tumor progression remains controversial. In this study, we used modified patient-derived organoid cultures and demonstrate that constitutively secreted cytokines from normal breast fibroblasts initiate a paracrine signaling mechanism with estrogen receptor-positive (ER + ) breast cancer cells, which results in the creation of an interleukin (IL)-1β-enriched microenvironment. We found that this paracrine signaling mechanism is shared between normal and activated fibroblasts. Interestingly, we observed that in reconstructed tumor microenvironment containing autologous ER + breast cancer cells, activated fibroblasts, and immune cells, tamoxifen is more effective in reducing tumor cell proliferation when this paracrine signaling is blocked. Our findings then suggest that ER + tumor cells could create a growth-promoting environment without activating stromal fibroblasts and that in breast-conserving surgeries, normal fibroblasts could be a significant modulator of tumor recurrence by enhancing the proliferation of residual breast cancer cells in the tumor-adjacent breast tissue.