Ribosomal RNA synthesis is a key molecular process for understanding the mechanisms that drive cell proliferation. In this process, the upstream binding factor (UBF) is involved in regulating rDNA transcription at the nucleolus, together with RNA polymerase I. Recently, UBF was demonstrated to be a substrate for selective cleavage by specific proteases during apoptosis. Here we studied the expression of UBF in several cases of Hodgkin's disease (HD) by immunostaining and found it to be absent or clearly diminished in a high proportion of Reed-Sternberg cells and Hodgkin cells compared to small reactive lymphocytes. This result contrasted with labeling of those cells by the AgNOR technique, a marker of cell proliferation dependent on increased amounts of several proteins related to ribosome assembly. Disappearance of UBF and preservation of other NOR proteins is consistent with the pattern of selective proteolysis by caspases described in early stages of apoptosis. This correlates well with our results observed on induction of apoptosis in Jurkat cells treated with anti-FAS/APO-1 serum and with those in aged germinal center B-cells, in which UBF was no longer seen although the staining signal of other NOR proteins was maintained. These results support the concept that the rate of apoptosis is higher in neoplastic cells of HD than in the benign reactive lymphocyte population. Differential proteolysis of NOR proteins, as revealed by double staining of UBF and AgNOR, may prove valuable for identification of early stages of apoptosis in cytological and histopathological samples.
Because sarcomas of the anterior lower neck region occur so infrequently, they are not usually considered in the diVerential diagnosis of Riedel's thyroiditis. Riedel's thyroiditis itself may be confused on clinical grounds alone with malignant neoplasms because of its invasive features. Sarcomatoid carcinoma is the main entity to be discarded in this regard. This is accomplished through histological examination by the finding of carcinomatous areas and/or reactivity with epithelial markers. These features also set apart sarcomatoid carcinoma from true sarcomas. This report concerns a patient with a sarcoma of the anterior lower neck region which was initially suspected to be Riedel's thyroiditis or sarcomatoid carcinoma on clinical and radiological grounds. A peroperative biopsy was interpreted by two independent pathologists as consistent with Riedel's thyroiditis. The subsequent clinical course and postmortem examination demonstrated a high grade sarcoma with metastasis to both lungs and the pleura, and invasion of adjacent neck structures. Nevertheless, some areas of the postmortem material showed a microscopic pattern similar to mediastinal fibrosis, raising the possibility of the malignant transformation of a fibrosclerotic lesion. (J Clin Pathol 2001;54:570-572) Keywords: Riedel's thyroiditis; sarcomatoid carcinoma; fibrous histiocytoma; diVerential diagnosis On 1 August 1994, a 65 year old white man was referred to our hospital with hoarseness of six months duration. The patient was also found to have stridor and dyspnea related to exercise. There was no antecedent of radiotherapy or thyroid pathology and past medical history was unremarkable except for chronic bronchitis.Scintigraphic study showed no uptake of tracer in the right thyroid lobe, isthmus, and lower pole of left lobe, which was coincident with a palpable mass at the same level.A computer assisted tomography scan revealed diVuse enlargement of the thyroid gland, which was more conspicuous in the right lobe and caused displacement, compression, and stenosis of the trachea. Displacement of the carotid sheath on the right and endothoracic growth were noted. Ultrasonography showed diVuse enlargement without nodularity.A barium swallow detected stenosis and displacement of the oesophagus. Indirect laryngoscopy revealed limitation of vocal cord movements and paralysis of the right vocal cord. Laryngeal and oesophageal mucosa were normal and the skin was not involved. The only abnormal laboratory test result was an erythrocyte sedimentation rate of 65 in the first hour.At surgery, a large fibrous mass of stony hard consistency was found firmly adherent to the trachea and invading the skeletal muscles and right carotid sheath. Remnants of the thyroid gland could be identified on the left side only. Resection was not possible. Biopsies from both sides of the mass overlying the trachea were taken, and tracheal intubation was performed. Peroperative biopsy was interpreted as consistent with Riedel's thyroiditis. Microscopic examination of th...
A hexameric 48‐atom cluster core (Mg6S12N6O24; see picture) and the novel azadisulfite dianion [O2S(μ‐NPh)SO2]2− are the main features of [(thf)Mg{O2S(μ‐NPh)SO2}]6, which is formed by reaction of an excess of SO2 with [(thf)MgNPh]6. The dimer [(thf)MgNPh]2 is trapped by cycloaddition to two molecules of tBuNSO in the complex [(thf)2Mg{OS(NtBu)(NPh)}]2.
Exquisite regulation of telomere length is essential for the preservation of the lifetime function and self-renewal of stem cells. However, multiple oncogenic pathways converge on induction of telomere attrition or telomerase overexpression and these events can by themselves trigger malignant transformation. Activation of NFκB, the outcome of telomere complex damage, is present in leukemia stem cells but absent in normal stem cells and can activate DOT1L which has been linked to MLL-fusion leukemias. Tumors that arise from cells of early and late developmental stages appear to follow two different oncogenic routes in which the role of telomere and telomerase signaling might be differentially involved. In contrast, direct malignant transformation of stem cells appears to be extremely rare. This suggests an inherent resistance of stem cells to cancer transformation which could be linked to a stem cell’specific mechanism of telomere maintenance. However, tumor protection of normal stem cells could also be conferred by cell extrinsic mechanisms.
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