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Giant cell tumor (GCT) is a bone-destructive benign neoplasm characterized by distinctive multinucleated osteoclast-like giant cells with osteolytic properties distributed among neoplastic stromal cells. GCT is locally aggressive with progressive invasion of adjacent tissues and occasionally displays malignant characteristics including lung metastasis. GCT is characterized genetically by highly recurrent somatic mutations at the G34 position of the H3F3A gene, encoding the histone variant H3.3, in stromal cells. This leads to deregulated gene expression and increased proliferation of mutation-bearing cells. However, when GCT complicates Paget disease of bone (GCT/PDB) it behaves differently, showing a more malignant phenotype with 5-year survival less than 50%. GCT/PDB is caused by a germline mutation in the ZNF687 gene, which encodes a transcription factor involved in the repression of genes surrounding DNA double-strand breaks to promote repair by homologous recombination. Identification of these driver mutations led to novel diagnostic tools for distinguishing between these two tumors and other osteoclast-rich neoplasms. Herein, we review the clinical, histological, and molecular features of GCT in different contexts focusing also on pharmacological treatments. [ABSTRACT FROM AUTHOR]

The present study focuses on correlation of in vitro multinucleate giant cell (MGC) forming ability with cytokine production in case of tuberculosis patients before and after treatment. In vitro MGC formation was carried out by treating monocytes with culture supernatant of Con A or PPD stimulated peripheral mononuclear cells. MGC formation was significantly lower for monocytes of untreated patients compared to control monocytes when incubated with respective autologous culture supernatant. MGC forming ability increased significantly for monocytes of treated patients incubated with autologous culture supernatant at the end of two months of treatment. Analysis of the supernatants revealed higher IL-10 levels and lower IFN-γ and IL-2 levels in untreated patients compared to treated patients and controls. The findings suggest that changes in IL-10, IFN-γ and IL-2 levels produced by mononuclear cells of patients before and after treatment might influence the functionality of monocytes and thereby the pathology of tuberculosis. [ABSTRACT FROM AUTHOR]

We analyzed lymphoid cell populations from thyroid multifocal granulomatous folliculitis (palpation thyroiditis) with a panel of antibodies in order to assess the nature of the immunologic process underlying this otherwise clinically insignificant condition as compared with other specific types of thyroiditis. In general, T lymphocytes predominated over B lymphocytes as shown by the extent of the staining with UCHL-1 (CD45RO or CD3 and L26 (CD20) antibodies, respectively. The ratio of kappa-to-lambda-containing plasma cells was 1.4 to 1. Histiocytes, macrophages, and multinucleate giant cells were all found to stain consistently strongly with KPI (CD68) and, when intraluminal, not infrequently also for thyroglobulin, probaby due to colloid phagocytosis. The differing patterns of light chain restriction observed in multifocal granulomatous folliculitis as compared with Riedel's thyroiditis and Graves disease thyroiditis, for instance, may reflect differences in the nature of the underlying immune response.