Objective To study the relation between Tiam1 gene(T lymphoma invasion/metastasis 1)and carcinomas of larynx metastasized to lymph node.Method Using reverse transcription polymerase chain (RT-PCR) mRNA overexpression of Tiam1 gene in 30 cases of carcinoma of larynx tissue,12 lymph nodes and 10 cases of normal larynx tissue was studied.Result The frequency of TIAM1 overexpression was 75% (6/8) in primary carcinomas of larynx with metastasis but only 18.7%(4/22) in those without metastasis(P=0.0072).Overexpression of TIAM1 in metastasized lymph nodes was observed in 100% (8/8) of lymph nodes with metastasis but in only 25%(1/4) of the lymph nodes without metastasis of carcinoma(P=0.0182).The frequency of TIAM1 overexpression was 33.3% (10/30) in primary carcinomas of larynx.Conclusion Our data suggest that the overexpression of the TIAM1 gene correlates with lymph node metastasis of carcinomas of larynx.

Objective To investigate the frequency of ocular complication and the quality of patient's life after radiation therapy in nasopharyngeal carcinoma ( NPC ) . Methods 254 NPC patients who initially received radiation were followed and analysed. Visual acuity, automational visual field, slit-lamp microscopic findings, pattern visual evoked potential ( P-VEP ) and fundal findings were determined before, during and after radiation therapy. The severity of retinal impairment was assessed according to the international criteria on late tissue effects. Results The radiation dose was more than 70 Gy in 241 (94.9%)NPC patients, giving a radiation retinopathy incidence of 8. 7 % (22) patients after a mean of 46. 8 ? 14. 4 months. After being diagnosed as radiation retinopathy, 16 patients received combined-modality therapy of the modern medicine and Chinese traditional medicine. The disease condition was controlled in 56% (9) patients but progressed into optic neuropathy in 7 patients, 3 of whom developed radiation encephalopathy in 14 to 20 months after onset of retinopathy. The morbidity of radiation retinopathy was not associated with the patient' s age, but was related to the radiation dose. The retinopathy rate was as high as 13.6% in the 75-79 Gy group, which is significantly higher than 5.6% in the 70-74 Gy group ( P

OBJECTIVE: To investigate the effects of situation of misdiagnosis of nasopharyngeal carcinoma (NPC) on distant metastasis. METHOD: The history of diagnosis and treatment of 85 newly diagnosed cases with nasopharyngeal carcinoma were studied by using itemized questionnaire purposely; 433 patients with different prognosis were analyzed retrospectively for the misdiagnoses and mistreatment, including surgical biopsy in the neck. RESULT: (1) The rate of misdiagnosis of 85 patients was 72.64%, and the percentage decreased as the level of the hospitals increased; the majority of the patients (77.36%) were diagnoses within 1 month after the first symptom had appeared; the number of diseases misdiagnosed was 20, most common of which were lymphnoditis, tuberculosis of lymph node and secretory tympanitis; (2) Our data showed that among 433 patients analysed retrospectively, 60 cases had undergone surgical biopsy in the neck, 75% of whom had never received nasopharyngeal biopsy; 43 cases had underwent nasopharyngeal biopsy after the pathological diagnosis as metastatic carcinoma of neck biopsy (71.67%) and the rest (20.0%) received radiotherapy directly or after negative nasopharyngeal biopsy for merely 1 to 4 times; of those 43 cases who were diagnosed as NPC by nasopharyngeal biopsy, 79.17% got positive results at first sampling. (3) Rate of misdiagnosis and mistreatment including surgical biopsy in the neck of patients who had been tumor-free for 5 years or above was significantly lower than that of those who experienced distant metastasis after or before treatment (P < 0.05). CONCLUSIONS Misdiagnosis and mistreatment including biopsy by surgery of neck is common even in high-grade hospitals; it is doctor that is responsible for this situation; the high occurrence rate of misdiagnosis and mistreatment, biopsy by neck surgery, especially the delayed treatment after the neck biopsy are the factors that contribute to distant metastasis of NPC.
Diagnostic Errors ; Humans ; Nasopharyngeal Neoplasms ; diagnosis ; pathology ; therapy ; Neoplasm Metastasis ; Neoplasm Staging ; Prognosis ; Retrospective Studies ; Treatment Outcome

OBJECTIVE: To investigate the pathogenesis of unknown nosebleed patients. METHOD: The ELISA test were used to detected plasma Urokinase-type plasminogen activator (uPA) and Urokinase-type plasminogen activator receptor (uPAR) level in 19 cases unknown factor nosebleed patients and 36 health persons. RESULT: The results showed uPAR and uPA level in nosebleed group (before treatment) uPAR (0.14 +/- 0.04) microg/L, uPA (0.24 +/- 0.09) microg/L; (after treatment) uPAR (0.08 +/- 0.02) microg/L, uPA (0.18 +/- 0.07) microg/L. And normal group uPAR (0.07 +/- 0.03) microg/L, uPA (0.17 +/- 0.05) microg/L. The uPAR and uPA level in nosebleed group before treatment is higher than that in normal group (P <0.05). There is no significant difference between nosebleed group after treatment and normal group (P>0.05). CONCLUSION The reasons of uPAR and uPA level high in unknown factor nosebleed patients were not clear, maybe relation to vascular endothelial cell, smooth muscle cell and neutrophil-monocytic release more uPAR and uPA. So uPAR and uPA density of nostril accumulation is more high in its microenvironment, that fibrinolytic system activated increase and result in its hyperactivity, and happened nosebleed when blood be in hypocoagulable state.
Adolescent ; Adult ; Case-Control Studies ; Epistaxis ; blood ; etiology ; Female ; Humans ; Male ; Middle Aged ; Receptors, Urokinase Plasminogen Activator ; blood ; metabolism ; Urokinase-Type Plasminogen Activator ; blood ; metabolism ; Young Adult

OBJECTIVE: This study was to explore the expression and clinicopathologic features of Tyrosine kinase receptors B (TrkB) and its ligand brain-derived neurotrophic factor (BDNF) in nasopharyngeal carcinoma (NPC). METHOD: Immunohistochemistry was adopted to detect the expression level of TrkB and BDNF in NPC patients. RESULT: Both TrkB and BDNF were expressed in NPC as well as in chronic inflammation. The active expression rate of TrkB in NPC was 82.5% (47/57) and BDNF was 52.6% (30/57), both of which were higher than those in chronic inflammation (P < 0.05). The degree of TrkB expression was more marked in T3 + T4, III + IV stage NPC than that in T1 +T2, I + II stage NPC (P < 0.05). TrkB abnormal expression rate of nasopharyngeal carcinoma with lymph node metastasis was higher than that of NPC without lymph node metastasis (P < 0.05). No statistical significance for degrees of TrkB expression in pathologic type grades was found (P > 0.05). There were no statistical significance for degrees of BDNF expression in T stage, clinical stage and lymph node metastasis in NPC (P > 0.05). The expression of TrkB was unrelated to the expression of BDNF (r = 0.049, P > 0.05). CONCLUSION The high expression rate of TrkB and BDNF maybe plays an important role in development of NPC. It is suggested that TrkB and its ligand BDNF may act as an important index for forecasting the development and metastasis of NPC.
Adolescent ; Adult ; Aged ; Brain-Derived Neurotrophic Factor ; metabolism ; Female ; Humans ; Lymphatic Metastasis ; Male ; Middle Aged ; Nasopharyngeal Neoplasms ; metabolism ; pathology ; Neoplasm Staging ; Receptor, trkB ; metabolism ; Young Adult

Objective To investigate risk factors of postoperative pulmonary infection in patients with liver cancer. Methods A total of 120 patients with primary liver cancer patients were divided into infected group(12 cases) and non-infected group(108 cases), two groups of patients in sex, age, underlying disease, whether ascites before surgery, surgery transfusion amount of time, blood loss, intraoperative, duration of mechanical ventilation index differences were com-pared and line Logistic regression analysis of its risk factors. Results In 120 cases of hepatocellular carcinoma 12 cases of postoperative pulmonary infection, the rate was 10.0%. The differences of age, underlying disease, whether ascites preoperative, operative time, blood loss, intraoperative blood transfusion, duration of mechanical ventilation in non-in-fected group and the infection group were statistically significant (P<0.05). Conclusion Age>60 years, underlying dis-ease, preoperative ascites, long operation time, blood loss volume, blood transfusion volume, length of mechanical venti-lation independent are risk factors for lung infections in patients with liver cancer after surgery.

OBJECTIVE: To discover the relationship of transcriptional levels and promoter methylation status of CHFR gene in human nasopharyngeal carcinoma,to discuss the significance and epigenetic mechanism of CHFR inactivation in NPC, and to evaluate the feasibility of detecting methylated CHFR in nasopharyngeal swab as a means for diagnosis of NPC. METHOD: Transcriptional levels of CHFR was evaluated by RT-PCR. Methylation specific PCR was used to detect the methylation status of CHFR in NPC cells, normal nasopharyngeal epithelia, primary tumors and their paired nasopharyngeal swabs. Detailed methylation status was confirmed by bisulfite sequencing. NPC cells were treated by the methyltransferase inhibitor 5-aza-dC and the reactivation of CHFR was evaluated by RT-PCR. RESULT: CHFR transcription was inactivated in NPC. The methylation frequency in NPC primary tumors and their paired swabs were 65.5% and 63.8%, respectively, with a 86.2% concordance. Bisulfite sequencing revealed a dense methylation in NPC cells and primary tumors, but all the normal nasopharyngeal epithelia were unmethylated. CHFR expression were restored after 5-aza-dC treatment. CONCLUSION CHFR is epigenetically inactivated by promoter methylation in NPC. Detecting methylated CHFR can be served as a useful non-invasive means for diagnosis of NPC.
Aged ; Carcinoma ; Cell Cycle Proteins ; genetics ; DNA Methylation ; Epigenesis, Genetic ; Female ; Gene Silencing ; Humans ; Male ; Middle Aged ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms ; genetics ; pathology ; Neoplasm Proteins ; genetics ; Neoplasm Staging ; Poly-ADP-Ribose Binding Proteins ; Promoter Regions, Genetic ; Ubiquitin-Protein Ligases

[Abstrca t] Objective To investigate the inactivation of PMS 2 gene mediated by promoter methylation and its regulatory mechanism in nasopharyngeal carcinoma (NPC).Methods Fifty-four NPC tissues, 16 normal nasopharyngeal epithelia ( NNE) , 5 NPC cell lines ( CNE1, CNE2, TWO3, HNE1 and HONE1) and 1 normal nasopharyngeal epithelial cell line (NP69) were collected.Methylation-specific PCR (MSP) was used to detect the PMS2 promoter methylation, semi-quantitative reverse transcription PCR ( qRT-PCR) was applied to determine its mRNA expression , and immunohistochemistry ( IHC) was used to detect the protein expression of PMS 2.The expressions of PMS 2 mRNA in CNE1 and CNE2 cells before and after treated with methyltransferase inhibitor 5-aza-2-deoxycytidine were analyzed by qRT-PCR.The impact of methylation and demethylation on the mRNA expression of PMS 2, and the association of mRNA and protein expression of PMS 2 with clinicopathological features of nasopharyngeal cancer were analyzed .Results Methylation of PMS2 gene was detected in all of the five NPC cell lines , but not in normal nasopharyngeal epithelial NP69 cells.The methylation rate of PMS2 gene in NPC tissues was 63%(34/54), significantly higher than that of the normal nasopharyngeal epithelia (0/16, P<0.001).The expression levels of PMS2 mRNA and protein were significantly down-regulated in the 54 NPC tissues when compared with those in the 16 NNE tissues (P<0.001), and were also significantly lower in the 34 methylated NPC tissues than those in the 20 unmethylated NPC tissues (P<0.001).After treatment with 5-aza-2-deoxycytidine, the expression of PMS2 mRNA was restored in the CNE1 and CNE2 cells.However, the expressions of PMS2 mRNA and protein were not significantly correlated with patients′age, gender, TNM stage, histopathologic type or lymph node metastasis (P>0.05 for all).Conclusions Promoter methylation -mediated inactivation of PMS2 gene participates in carcinogenesis and development of NPC .PMS2 may be a candidate tumor suppressor in the treatment for patients with inactivation of PMS 2 promoter methylation .

[Abstrca t] Objective To investigate the inactivation of PMS 2 gene mediated by promoter methylation and its regulatory mechanism in nasopharyngeal carcinoma (NPC).Methods Fifty-four NPC tissues, 16 normal nasopharyngeal epithelia ( NNE) , 5 NPC cell lines ( CNE1, CNE2, TWO3, HNE1 and HONE1) and 1 normal nasopharyngeal epithelial cell line (NP69) were collected.Methylation-specific PCR (MSP) was used to detect the PMS2 promoter methylation, semi-quantitative reverse transcription PCR ( qRT-PCR) was applied to determine its mRNA expression , and immunohistochemistry ( IHC) was used to detect the protein expression of PMS 2.The expressions of PMS 2 mRNA in CNE1 and CNE2 cells before and after treated with methyltransferase inhibitor 5-aza-2-deoxycytidine were analyzed by qRT-PCR.The impact of methylation and demethylation on the mRNA expression of PMS 2, and the association of mRNA and protein expression of PMS 2 with clinicopathological features of nasopharyngeal cancer were analyzed .Results Methylation of PMS2 gene was detected in all of the five NPC cell lines , but not in normal nasopharyngeal epithelial NP69 cells.The methylation rate of PMS2 gene in NPC tissues was 63%(34/54), significantly higher than that of the normal nasopharyngeal epithelia (0/16, P<0.001).The expression levels of PMS2 mRNA and protein were significantly down-regulated in the 54 NPC tissues when compared with those in the 16 NNE tissues (P<0.001), and were also significantly lower in the 34 methylated NPC tissues than those in the 20 unmethylated NPC tissues (P<0.001).After treatment with 5-aza-2-deoxycytidine, the expression of PMS2 mRNA was restored in the CNE1 and CNE2 cells.However, the expressions of PMS2 mRNA and protein were not significantly correlated with patients′age, gender, TNM stage, histopathologic type or lymph node metastasis (P>0.05 for all).Conclusions Promoter methylation -mediated inactivation of PMS2 gene participates in carcinogenesis and development of NPC .PMS2 may be a candidate tumor suppressor in the treatment for patients with inactivation of PMS 2 promoter methylation .

OBJECTIVETo identify a novel human leukocyte antigen (HLA) allele HLA-B*13:92 and analyze 3D model of HLA molecule.

METHODSPolymerase chain reaction sequencing-based (PCR-SBT) was used in routine HLA typing, the B locus typing results of one sample was one base mismatch with B*13:01:01, B*58:01:01 at locus 189, The Group Specific Sequencing Products (GSSP) which target at B*13 and B*58 were used to confirm difference between the new allele and highest homologous allele, then the new allele was modeled by Swiss-model to its 3D structure.

RESULTSThe sequencing results showed that the new allele with highest homologous allele B*13:01:01 was the difference in the second exon at position 189 C>A (codon 39 GAC>GAA), 39 Asp (D) was changed to Glu (E). The amino acid substitution at residue 39 of the HLA polypeptide was located in α-helices of antigenic peptide-biding region.

CONCLUSIONThis allele is a new HLA-B allele found in Chinese Guangxi Zhang population and has been designated as HLA-B*13:92 by the World Health Organization (WHO) HLA Nomenclature Committee.