Reza Ataei; Alireza Khooei; Mohammad Gharedaghi
Volume 5, Issue 2 , March 2010, , Pages 53-59
Abstract
Background and Objectives: Giant cell Tumor of bone (GCT) is often regarded as a benign tumor, but its clinical course is unpredictable, has a high rate of recurrence, and even can metastases and transform to a malignant tumor. Histological features of the tumor often could not predict its future ...
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Background and Objectives: Giant cell Tumor of bone (GCT) is often regarded as a benign tumor, but its clinical course is unpredictable, has a high rate of recurrence, and even can metastases and transform to a malignant tumor. Histological features of the tumor often could not predict its future biologic behavior, so it is just called ''Giant cell tumor'' without indicating malignancy or benignicity. Several methods are suggested to predict the biologic behavior of this tumor. This study evaluated the relation between Bax & bcl-2 as proteins involved in cell proliferation and death (apoptosis) with histopathologic features and clinical course of GCT. Materials & Methods: Paraffin- embedded tissue specimens of 40 GCTs of conventional, aggressive, recurrent, malignant, & metastatic types were evaluated by immunohistochemistry for Bax & bcl-2 markers. Clinicopathologic features and immunohistochemical results were statistically analyzed and presented in tables & diagrams. Results:Age, sex, and pattern of skeletal involvement were the same as other worldwide reports. Expression of Bax & bcl-2 markers were significantly higher in malignant GCTs but no statistically significant difference was found in other subtypes for bcl-2 while there was statistically significant difference between subgroups for Bax. Conclusion:Considerable expression of Bax & bcl-2 markers in a GCT could signal its malignant course, but low expression is not valuable in predicting the clinical course. In addition, it seems that secondary tumor nodules in lung are just simple implantation not true malignant metastases
Alireza Azizzadeh Delshad; Marjan Heshmati; Taki Tiraihi
Volume 3, Issue 2 , March 2008, , Pages 67-74
Abstract
Background and Objective: As apoptotic cell death is extremely involved in physiological development and many pathological situations such as cancer and neurodegenerative diseases, the understanding of its molecular machinery can be useful in designing new therapeutic strategies. The present ...
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Background and Objective: As apoptotic cell death is extremely involved in physiological development and many pathological situations such as cancer and neurodegenerative diseases, the understanding of its molecular machinery can be useful in designing new therapeutic strategies. The present study investigated the temporal expression of the proapoptotic protein Bax in adult spinal motoneurons. Materials and Methods: Following unilateral mid-thigh sciatic transection in adult rats, the incidence and nature of spinal motoneuron loss were evaluated by means of light microscopic cell count and electron microscopy 1 day, 1 week, 1 month and 3 months post-operatively. In all groups the temporal expression of Bax was immunohistochemically determined and the findings were compared with the results of the cell count. Results: Following axotomy the related motoneurons underwent chromatolytic changes which increased up to one month and diminished in the 3-month group. One day following axotomy the number of motoneurons did not show any significant reduction, but thereafter a progressive cell loss occurred, which was most prominent after three months. Electron microscopic study confirmed the ultrastructural apoptotic nature of cell death. Bax immunohistochemistry indicated an increasing immunoreactivity up to one month post-axotomy, but in 3-month group it was clearly diminished. Conclusion: Following transection of a peripheral nerve in adult animals, related motoneurons undergo chromatolytic changes which in some neurons may proceed to apoptotic cell death. Although the proapoptotic protein Bax has long been believed as the main apoptotic factor, other Bax-independent pathways may also participate in the axotomy-induced neuronal apoptosis which must not be ignored.
