Publications by authors named "K Mellert"

Chordomas are very rare malignant neoplasms of the bone occurring almost exclusively along the spine. As the tumours are thought to arise from notochordal remnants, the vast majority of chordomas express the gene, resulting in detectable nuclear amounts of its gene product brachyury. This T-Box transcription factor is commonly recognised as being essential in chordoma cells, and limiting expression is thought to be the key factor in controlling this tumour.

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Article Synopsis
  • Richter's syndrome (RS) is a severe form of cancer resulting from the evolution of chronic lymphocytic leukemia (CLL) into a high-grade B-cell malignancy, characterized by decreased reliance on BCL-2, a key protein that prevents apoptosis (cell death).
  • Studies comparing CLL and RS revealed that RS cells display lower apoptotic priming and may depend on different anti-apoptotic proteins, complicating treatment strategies like using BH3 mimetics that target cell death pathways.
  • Transcriptomic analyses showed that as CLL transforms into RS, there is a downregulation of pro-apoptotic factors and changes in mitochondrial structure that contribute to enhanced resistance to apoptosis, making it harder to target RS directly.
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In the past few years, numerous new insights have been gained in the field of giant cell tumor of bone (GCTB). On the one hand, the detection of the highly characteristic histone mutation in the H3F3A gene in GCTB is becoming increasingly important in diagnostics in differentiating GCTB from other giant cell-rich lesions of bone as well as for defining rare variants of GCTB without osteoclastic giant cells. On the other hand, the effects of the H3F3A mutation were shown to have an impact on the epigenetic profile of tumor-driving stromal cells, providing new insights into tumorigenesis of GCTB.

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Giant cell tumor of bone (GCTB) is an osteolytic tumor driven by an -mutated mononuclear cell with the accumulation of osteoclastic giant cells. We analyzed tissue from 13 patients with recurrence and 25 patients with denosumab therapy, including two cases of malignant transformation. We found a decrease in the total number of cells ( = 0.

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Giant cells (GCs) are thought to originate from the fusion of monocytic lineage cells and arise amid multiple backgrounds. To compare GCs of different origins, we immunohistochemically characterised the GCs of reactive and neoplastic lesions ( = 47). We studied the expression of 15 molecules including HLA class II molecules those relevant to the cell cycle, bone metabolism and lineage affiliation.

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