Kang Suek Suh

Comparison of Polymerase Chain Reaction With Histopathologic Features for Diagnosis of Tuberculosis in Formalin-Fixed, Paraffin-Embedded Histologic Specimens

Objective.-To investigate the relationship between various histopathologic features and the results of the tuberculosis (TB)-polymerase chain reaction (PCR) method in routinely submitted histologic specimens for the histopathologic diagnosis of TB. Design.-We used 95 formalin-fixed, paraffin-embedded tissue blocks from 81 patients who were clinically suspected of having TB. We assessed the presence of histopathologic features including well-formed granuloma, poorly formed granuloma, caseous necrosis, and Langhans-type giant cells. We performed nested PCR for IS6110 and Ziehl-Neelsen staining for acid-fast bacilli (AFB). Results.-Of the 81 patients studied, 53 patients had chronic granulomatous inflammation, whereas 28 patients had only chronic inflammation without definite granulomatous inflammation. Of the 53 cases with chronic granulomatous inflammation, 17 (32%) were AFB positive and 36 (68%) were TB-PCR positive. Among cases with chronic granulomatous inflammation, the percentage that were positive and negative by TB-PCR differed significantly with the presence of various histopathologic features. All of the 13 cases with well-formed granuloma, caseous necrosis, and Langhans-type giant cells were TB-PCR positive; however, 10 (36%) of the 28 cases with chronic inflammation without granulomatous lesions were also TB-PCR positive. Conclusions.-TB-PCR is a rapid, sensitive method for the diagnosis of TB in routinely processed formalin-fixed, paraffin-embedded histologic specimens and is readily available in histopathology laboratories. We recommend use of TB-PCR when TB is suspected clinically, especially in cases of chronic inflammation without definite evidence of granulomatous inflammation.

Malignant Osteoclast-like Giant Cell Tumar of the Kidney with Osteosarcomatous Transformation

Malignant giant cell tumor of osseous or extraosseous origin is extremely rare, and diagnosis is reserved for those lesions that display bizarre mitosis and cytological atypia or an association with sarcoma.1 Heller et al first reported malignant giant cell tumor of the kidney without accompanying sarcoma or carcinoma.2 Their case showed a high mitotic index, variable cytological atypia in mononuclear stromal cells and widespread metastasis of perirenal tissue. We report an unusual case of malignant giant cell tumor of the kidney with osteosarcomatous transformation. CASE REPORT

Expressions of transforming growth factor (TGF)-β1 and TGF-β type II receptor and their relationship with apoptosis during chemical hepatocarcinogenesis in rats

The expression of transforming growth factor (TGF)-beta1, which regulates cell proliferation, is tightly associated with that of TGF-beta type II receptor (TGR2), and has been regarded as an important change during hepatocarcinogenesis. Our aim in this study was to investigate the expression and localization of TGF-beta1 and TGR2 and to determine their relationships with apoptosis in chemical hepatocarcinogenesis of the rat produced by Solt and Farbers method. Northern blot analysis showed that a slight increase of TGF-beta1 transcripts and a decrease of TGR2 transcripts during hepatocarcinogenesis. Immunohistochemistry revealed that TGF-beta1-positive preneoplastic hepatocytes increased with time, and that this correlated with a reduction TGR2 expressing preneoplastic lesions. Hepatocellular carcinoma (HCC) tissues showed higher levels of TGF-beta1 transcripts and protein and lower levels of TGR2 transcripts and protein compared to the paired adjacent liver parenchyme. TUNEL revealed that apoptotic cells increased with time and were more numerous in the adjacent liver parenchyme than in preneoplastic lesions and HCC tissues. Our data suggest that the down regulation of TGR2 in preneoplastic lesions and HCC tissues might contribute to resistance to the growth inhibitory effects of TGF-beta1, and to the roles of TGF-beta1 in the development and progression of preneoplastic lesions and HCC in a chemically induced rat hepatocarcinogensis model.