Transforming effect of PDGFRA gene mutant on the cell function in gastrointestinal stromal tumor / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To explore the effect of malignant transformation of the L839P, a new mutation site of the PDGFRA gene, on the pathogenesis of gastrointestinal stromal tumors.</p><p><b>METHODS</b>All recombinant plasmids were stably transfected into CHO cells by liposomes. Western blotting was used to detect the expression of PDGFRA protein. The cell growth curve was plotted by cell counting. Flow cytometry was used to detect the cell cycle and apoptosis of CHO cell, respectively. The stably transformed cells were inoculated subcutaneously into the back of nude mice and the mice were used to observe the tumorigenesis. Transient transfection of the mutant-type plasmids of PDGFRA gene and the wild-type plasmids of kit gene into the CHO cells was performed. Western blot was used to detect the expression of kit protein and its phosphorylated forms.</p><p><b>RESULTS</b>PDGFRA protein expressed in the negative control, experimental group and positive control, except the empty vector. The growth curve showed that it was accelerated in the experimental group and positive control. The ratios of cells in proliferative phase were 28.4% (blank), 24.5% (negative control), 43.8% (experimental group) and 40.9% (positive control). Their apoptotic indexes were 1.8%, 1.9%, 1.5% and 1.6%, respectively. After three weeks, tumors were observed in the nude mice of experimental group and positive control, inoculated with the stably transformed cells. Moreover, the expression of phosphorylated protein of kit was enhanced after cotransfection of the mutant-type plasmids of PDGFRA and the wild-type plasmid of kit.</p><p><b>CONCLUSION</b>The PDGFRA mutant L839P is a gain-of-function mutation and has obviously malignant transforming effect on normal cells, and may activate kit protein accelerating the tumorigenesis. Gastrointestinal stromal tumors;</p>

Expression of Oct2 and its significance in lymphoma diagnosis / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the specificity and sensitivity of Oct2 protein expression in lymphoma cells and its significance in diagnosis and classification of lymphoma.</p><p><b>METHODS</b>Formalin-fixed and paraffin-embedded materials from 129 cases of lymphoma and 10 cases of reactive lymphoid hyperplasia (RLH) were studied by EnVision immunohistochemistry for Oct2 protein.</p><p><b>RESULTS</b>Oct2 was mainly expressed in germinal center cells of RLH. It was diffusely expressed in B-cell lymphoma cells. 97.7% cases (85/87) of B-cell lymphoma and 3.8% cases (1/26) of T-cell lymphoma were positive for Oct2 protein. In comparison, the expression rates for CD20 and CD79alpha in B-cell lymphomas were 90.8% (79/87) and 84.7% (61/72) respectively. The difference in expression rates between Oct2 protein and CD20 was not statistically significant (P > 0.05) There was, however, significant difference in expression rates between Oct2 protein and CD79alpha (P < 0.05). The expression rates of Oct2 protein in nodular lymphocyte-predominant Hodgkin lymphoma and classic Hodgkin lymphoma were 3/3 and 46.2% (6/13) respectively. The difference in expression rates of Oct2 protein in these two groups showed no statistical significance (P > 0.05).</p><p><b>CONCLUSION</b>As a relatively sensitive and specific marker for B cells, Oct2 can serve as a useful antibody for the diagnosis and differential diagnosis of lymphoma.</p>

Effect of c-kit gene mutation on prognosis of gastrointestinal stromal tumor / 中华外科杂志

<p><b>OBJECTIVE</b>To evaluate the clinical signification of c-kit gene mutation in gastrointestinal stromal tumor (GIST) and examine whether the presence of mutation of c-kit gene is important as a prognostic factor.</p><p><b>METHODS</b>The c-kit mutation had been detected by PCR-SSCP, DNA sequence, statistical comparison were used for the relationship of c-kit gene mutation and clinical pathology, clinical behavior, recurrence, et al.</p><p><b>RESULTS</b>The presence of c-kit mutation correlated with tumor size, proliferating cell nuclear antigen index, mitotic cell number, presence of necrosis, microscopic invasion to adjacent tissues, recurrence and distant metastasis. The age, sex, location of tumor, cell type, the presence of hemorrhage, and c-kit expression were independently related to the presence of c-kit mutation.</p><p><b>CONCLUSIONS</b>The c-kit gene mutation is an important prognostic factor for GIST.</p>

Pathological observation of airway inflammation after neonatal CVB3 inoculation in rats / 第二军医大学学报

Objective: To observe the effect of coxsackie virus B3 on airway tract and lung morphology, and to study the relation between CVB infection and asthma. Methods: We established CVB3 infective model: 5 d neonatal rats inhaled CVB3 by ultrasonic brume. CVB3-IgM was examined 10 d after inoculating of CVB3, and LW/BW, airway tract and lung pathological change 10 d and 30 d after inoculation of CVB3 were observed. Results: Rats from the virus group had higher D of CVB3-IgM than control's (+2s ) and had higher LW/BW 10 d after inoculation of CVB3 than control (P<0.01). Neonatal rats had acute inflammatory changes 10 d after inoculation of CVB3 and persistent changes in morphology and cytology. Conclusion: Neonatal rats virus model is established. Respiratory infection by CVB3 in neonatal rats has persistent changes in airway tract inflammatory and morphology.

Pathological observation of airway inflammation after neonatal CVB3 inoculation in rats / 第二军医大学学报

Objective: To observe the effect of coxsackie virus B3 on airway tract and lung morphology, and to study the relation between CVB infection and asthma. Methods: We established CVB3 infective model: 5 d neonatal rats inhaled CVB3 by ultrasonic brume. CVB3-IgM was examined 10 d after inoculating of CVB3, and LW/BW, airway tract and lung pathological change 10 d and 30 d after inoculation of CVB3 were observed. Results: Rats from the virus group had higher D of CVB3-IgM than control's (+2s ) and had higher LW/BW 10 d after inoculation of CVB3 than control (P<0.01). Neonatal rats had acute inflammatory changes 10 d after inoculation of CVB3 and persistent changes in morphology and cytology. Conclusion: Neonatal rats virus model is established. Respiratory infection by CVB3 in neonatal rats has persistent changes in airway tract inflammatory and morphology.