Biomedical subjects

Ming-Tsang Wu

Publications and source records attributed to Ming-Tsang Wu.

At least 19 recordsLinked to original sources

PubMed2007

Anatomical subsite discrepancy in relation to the impact of the consumption of alcohol, tobacco and betel quid on esophageal cancer.

The carcinogenetic impact of risk factors on esophageal cancer (EC) may differ according to the portion of the esophagus where the tumor occurs. It is unclear why more esophageal squamous cell carcinomas (SCC) developed in the middle location. We carried out a multicenter case-control study in Taiwan to assess anatomical subsite risk discrepancy for this neoplasm in regard to the consumption of alcohol, tobacco and betel quid. Four hundred forty seven incident patients with pathology-proven SCC of the esophagus (107 were upper-third [U/3-EC], 199 middle-third [M/3-EC] and 141 lower-third [L/3-EC] cases), as well as 1,022 gender, age and study hospital matched controls were analyzed by unordered polytomous logistic regression. All consumption of the three substances was related to the development of each subsite of EC, with a heterogeneously higher risk for current smokers (adjusted odds ratio (AOR) = 6.2) found in M/3-EC and for current chewers, in U/3-EC (AOR = 4.9). The joint risk of contracting lower two-third EC for drinking and smoking appeared to significantly surpass those estimated by a multiplicative interaction model. Concomitant exposure to these two agents brought the risks of EC at all three subsites up to 10- to 23.9-fold and additional tobacco-free betel quid to a 30.3- to 75.0-fold. In conclusion, tumor subsite discrepancy risk is related to prolonged exposure to tobacco and betel quid with inflorescence. Alcohol interacts with tobacco in a stronger supra-multiplicative way in the middle portion of the esophagus, probably explaining why esophageal SCC occurs more commonly at this anatomical location.

Adult↗

PubMed2007

Lifetime cigarette smoke and second-hand smoke and cervical intraepithelial neoplasm--a community-based case-control study.

BACKGROUND: Both active cigarette smoking and human papillomavirus (HPV) infection are known risk factors for cervical intraepithelial neoplasm (CIN). The association between second-hand smoke (SHS) and CIN has not been conclusively determined. We conducted a community-based case-control study to estimate the relationship between SHS and CIN. METHODS: Potential study subjects were selected through Pap smear screening in Kaohsiung County, Taiwan. A total of 171 subjects with either their first case of inflammation (benign epithelial lesion) or > or = CIN1 by biopsy confirmation were assigned to a case group; 513 normal subjects with negative findings by Pap smears or biopsies were assigned to a control group. RESULTS: Non-smoking women exposed to more than 20 pack-years of cigarette smoke had a significantly greater risk of developing > or = CIN2 than unexposed non-smokers (adjusted OR=7.2, 95% CI=2.5-20.6). Among the women without HPV infections, the greater the severity of disease found in the groups (normal, inflammation, CIN1, to > or = CIN2), the more likely it was for the women to be exposed to SHS, a significant increasing trend (p=0.037). CONCLUSIONS: In addition to HPV infection and active cigarette smoking, exposure to SHS is a major risk factor for CIN among Taiwanese women.

Adult↗

PubMed2006

Interactive effects of lifetime alcohol consumption and alcohol and aldehyde dehydrogenase polymorphisms on esophageal cancer risks.

In our previous study, we found that polymorphisms of alcohol and aldehyde dehydrogenase (ADH1B and ALDH2) are important risks for esophageal squamous cell carcinoma in a Taiwanese population. In this study, we increased the sample size to investigate the modifying effect of lifetime alcohol consumption on the association between ADH1B and ALDH2 genotypes and the risks of esophageal cancer. A multicenter hospital-based case-control study was conducted between August 2000 and June 2004. Three hundred and thirty newly-diagnosed esophageal squamous cell carcinoma patients and 592 controls were recruited from National Taiwan University Hospital in Taipei and Kaohsiung Veterans General Hospital and Kaohsiung Medical University Hospital in Kaohsiung, Taiwan. Controls were matched to the case patients by gender and age within 4 years (case:control = 1:1-4). Polymorphisms of ADH1B and ALDH2 were genotyped by the method of PCR-RFLP. Individuals with ADH1B*1/*1 genotype had a 3.99-fold risk (95% CI = 2.13-7.48) of developing esophageal cancer, compared with those with ADH1B*2/*2 genotype, after adjusted for appropriate covariates. Individuals with ALDH2*1/*2 and ALDH2*2/*2 had 4.99-fold risk (95% CI = 3.11-7.99) and 4.24-fold risk (95% CI = 1.52-11.84), respectively, of developing esophageal cancer, compared with those with ALDH2*1/*1, after adjusted for appropriate covariates. We also found a modifying effect of lifetime alcoholic consumption on the association between genotypes of ADH1B and ALDH2 on esophageal cancer risk. These results suggest that ADH1B and ALDH2 polymorphisms play a pivotal role on esophageal cancer and that the effect of these polymorphisms was modified by the amount of alcohol consumed.

Adult↗

PubMed2006

The expression of CD66a and possible roles in colorectal adenoma and adenocarcinoma.

BACKGROUND: The aim of our study was to analyze the expression and possible role of CD66a in colorectal adenoma and adenocarcinoma and the relationship between its expression and pre-operation serum carcinoembryonic antigen (CEA) level and tumor stage in patients with colorectal adenocarcinomas. METHODS: Paraffin-embedded sections from 184 patients including 42 colorectal adenomas with low-grade dysplasia, 43 adenomas with high-grade dysplasia, and 99 adenocarcinomas were collected for this study. Immunohistochemical analysis was performed, and the expression and the location of CD66a were evaluated and were correlated with beta-catenin nuclear expression. RESULTS: The expression of CD66a was found not only in the apical membrane of neoplastic glands but also in secretion within the lumen of the neoplastic glands including adenomas and adenocarcinomas. Expressions of secreted CD66a were of higher level in adenocarcinoma than in adenoma with high-grade dysplasia and adenoma with low-grade dysplasia (p < 0.0001). High expression of secreted CD66a was also associated with tumor stage, invasion, and pre-operation serum CEA level of patients with colorectal adenocarcinoma. CONCLUSIONS: This study implied that CD66a can function both as an epithelial cell adhesion protein or alternatively as secreted CD66a. In addition, a high expression of CD66a was significantly correlated with tumor invasion, stage, and pre-operation serum CEA level.

Adenocarcinoma↗

PubMed2006

Association of vitamin D receptor FokI polymorphism with prostate cancer risk, clinicopathological features and recurrence of prostate specific antigen after radical prostatectomy.

To investigate the effect of vitamin D receptor (VDR) FokI polymorphism on susceptibility to prostate cancer and the outcome of the disease in a Taiwanese population, we genotyped a total of 416 prostate cancer patients, 502 age-matched male controls and 189 non age-matched symptomatic benign prostatic hyperplasia. Although we did not find a significant association between VDR FokI genotypes and overall prostate cancer risk, we found that in men aged less than or equal to the median age of 73 years with VDR FokI F allele specifically had an increased risk of prostate cancer with a marginal significant trend (OR, 2.08; 95% CI, 1.00-4.34, p for trend = 0.056). The FF genotype was also highly associated with more aggressive prostate cancer (Gleason score 8-10) (OR, 2.47; 95% CI, 1.20-5.08) than did the Ff and ff genotypes. After adjusting other covariates, we found that in patients who had localized prostate cancer for which a radical prostatectomy was performed (n = 131), the VDR FokI FF genotype was associated with worse prostate-specific antigen (PSA) recurrence-free survival (hazard ratio = 3.25, 95% CI = 1.32-8.00, p = 0.010). Our findings suggest that the VDR FF genotype may increase the risk of early-onset prostate cancer and is associated with more aggressive disease. Furthermore, the VDR polymorphism could be used as a prognostic marker for localized prostate cancer after radical prostatectomy.

Aged↗

PubMed2006

Residential exposure to petrochemicals and the risk of leukemia: using geographic information system tools to estimate individual-level residential exposure.

The authors conducted a population-based, case-control study in Kaohsiung, southern Taiwan, Republic of China, to investigate the association between residential petrochemical exposure and leukemia risk among subjects 29 years of age and younger. Between November 1997 and June 2003, 171 cases and 410 controls matched for age and sex were recruited. Since assessment of petrochemical impacts depends on accurate exposure estimates, the authors developed a procedure using geographic information system tools to assign subjects' exposure. The resulting individual-level exposure estimates (the exposure opportunity score) are an integrated exposure measure that accounts for subjects' mobility, length of stay at each residence, distance to petrochemical plant(s), monthly prevailing wind direction, and multiple petrochemical pollution sources. Different conditional logistic regression models were fitted for subjects aged 0-19 and 20-29 years to evaluate separately childhood versus adulthood leukemia. No overall association was observed for the younger age group. However, residential petrochemical exposure was a significant risk factor for leukemia for the older age group. For one unit of increase in the log-transformed exposure opportunity score, the adjusted odds ratio was 1.54 (95 percent confidence interval: 1.14, 2.09). This study illustrates the utility of geographic information system tools for providing refined exposure estimates for residential exposure to petrochemical pollution.

Adolescent↗

PubMed2006

Positive association between STAT3 and Ki-67 in cervical intraepithelial neoplasia.

Signal transducer and activator of transcription 3 (STAT3) has been regarded as an oncogene in many types of cancers. However, its role in cervical carcinogenesis is not well determined. The purpose of this study was to evaluate the expression patterns of STAT3 in cervical intraepithelial neoplasia (CIN), normal cervix (NC), and squamous cell carcinoma (SCC) to explore its possible role in cervical carcinogenesis. Paraffin-embedded sections from 83 patients including 20 CIN 1, 10 CIN 2, 26 CIN 3, and 27 comparative cases of 10 NC and 17 stage Ib SCC were collected in this study. Immunohistochemistry was performed to analyze the expression patterns of STAT3, and the results obtained were categorized by a semiquantitative method and were further correlated with the CIN histopathologic grade and the proliferation marker, Ki-67, using the chi2 test. Our results showed that nuclear STAT3 expression was predominantly in the squamous epithelial cells, and that high-grade CIN and stage Ib SCC lesions had a higher nuclear STAT3 expression when compared with NC and CIN 1. Furthermore, the nuclear STAT3 expression in CIN was significantly correlated with Ki-67 expression (p = 0.025), but not CIN lesion grade. In summary, our results indicate that an altered STAT3 expression in CIN is correlated with cell proliferation but may not have a direct contribution to cervical carcinogenesis.

Adult↗

PubMed2006

Associations between exposure to polycyclic aromatic hydrocarbons and temporal change of urinary 1-hydroxypyrene levels in Taiwanese coke-oven workers.

OBJECTIVES: Our aim is to analyze the association between polycyclic aromatic hydrocarbon (PAH) exposure and the temporal change of urinary 1-hydroxypyrene (1-OHP). METHODS: Two personal air samples, eight spot urine samples, and questionnaires were used to collect PAH exposure, urinary 1-OHP, demographic data, and environmental pollutants. RESULTS: Topside-oven workers had significantly higher levels of PAH exposure and 1-OHP than side-oven workers. Urinary 1-OHP was a biomarker for PAH exposure. In topside-oven workers, the trend of 1-OHP increased sharply and reached the top in the sixth day after work and declined dramatically on days off. In side-oven workers, such a trend was not found, and those who smoked showed a slight increase in urinary 1-OHP levels on days off. CONCLUSIONS: We suggest that the pattern of temporal change of urinary 1-OHP levels is different between topside-oven and side-oven workers.

Adult↗

PubMed2005

Effects of arsenic exposure among semiconductor workers: a cautionary note on urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine.

Arsenic is a notorious environmental toxicant and was found to cause oxidative stress in cultured cells and animals. However, little work has been done in human studies, especially for the population occupationally exposed to arsenic. In order to investigate the effect of occupational exposure to arsenic in oxidative stress, we measured urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo) from 90 semiconductor workers including 50 exposed and 40 nonexposed subjects. A highly sensitive and specific isotope dilution LC-MS/MS method was used for quantification of 8-oxodGuo. The levels of inorganic arsenic (iAs3+, iAs5+), monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA) in urine were determined by high-performance liquid chromatography-flow injection atomic absorption spectrometry (HPLC-FIAAS). Results showed that the mean urinary concentrations of total arsenic and 8-oxodGuo were significantly higher for exposed workers compared with the nonexposed workers. In addition, elevated urinary 8-oxodGuo concentrations of exposed workers were correlated with urinary levels of MMA (r = 0.44, P < 0.005) and the extent of primary methylation (the ratio of MMA to inorganic arsenic) (r = 0.40, P < 0.005). These findings suggested that occupational exposure to arsenic could result in the induction of oxidative stress. The presence and/or formation of MMA could play an important role in arsenic-involved injuries.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2005

Sperm DNA damage correlates with polycyclic aromatic hydrocarbons biomarker in coke-oven workers.

OBJECTIVES: The aim was to determine whether occupational exposure to polycyclic aromatic hydrocarbons (PAHs) in men has adverse effect on semen quality. METHODS: Forty-eight coke-oven workers, including 16 topside-oven (TO) workers and 32 sideoven (SO) workers, were studied. Ambient PAHs exposure, urinary 1-hydroxypyrene (1-OHP) levels, and parameters of semen quality were determined. RESULTS: TO workers had significantly higher ambient PAHs exposure (3,436.1+/-3,411.0 vs. 1,123.1+/-1,829.3 ng/m3, P < 0.01), urinary 1-OHP levels (207.8+/-176.4 vs. 54.0+/-44.8 microg/g, P < 0.001), frequency of oligospermia (18.8 vs. 0%, P < 0.05), and morphological abnormality in sperm (32.3 vs. 14.6%, P < 0.01) than SO workers. Among cigarette smokers, TO workers had significantly higher rates of DNA denaturation in spermatozoa (alphaT) and percentage of sperm with increased DNA denaturation (COMP alphaT) levels than SO workers (246.2+/-49.5 vs. 198.1+/-30.3 for alphaT; 34.8+/-14.4 vs. 19.3+/-13.9% for COMP alphaT, P < 0.05). There was a positive correlation between urinary 1-OHP and alphaT, COMP alphaT, and abnormal sperm morphology and a tenfold increase in urinary 1-OHP associated with a 2.35-fold increase in alphaT, as well as a 1.07-fold increase in percentage of sperm with abnormal morphology. CONCLUSIONS: A potential risk of sperm dysfunction should be considered for workers occupationally exposed to high levels of PAHs. Cigarette smoking may aggravate this risk. Urinary 1-OHP can be used as a biomarker predicting sperm dysfunction.

Adult↗

PubMed2005

The associations of p53 overexpression with p53 codon 72 genetic polymorphism in esophageal cancer.

Variations in p53 codon 72 have been identified as significant predisposing factors for various cancers, but molecular mechanisms remain unclear. We investigated associations of p53 overexpression with codon 72 variants and other factors with esophageal cancer. Status of p53 overexpression was determined by immunohistochemical staining. Codon 72 polymorphisms and mutation of p53 was identified by PCR-RFLP and direct sequencing from exons 4 to 9, respectively. We evaluated 126 patients who underwent esophagectomy in the National Taiwan University Hospital, and found that the status of p53 overexpression was significantly influenced by presence of codon 72 polymorphisms. After adjustment for other possible confounders, the incidence of p53 overexpression was significantly decreased in patients with Pro/Pro genotype with an odds ratio (OR) of 0.21 (95% CI: 0.067-0.64) (p = 0.0065) compared with incidence in patients with Arg/Arg genotype. The incidence of p53 overexpression was additively increased with environmental exposure to cigarette smoke, alcohol, and areca quid. When compared with individuals exposed to only one of these environmental risk factors, patients who had exposure to two or three risk factors had ORs of 6.11 (95% CI: 1.80-20.75) and 6.22 (95% CI: 1.81-21.34) for p53 overexpression, respectively. Elderly patients (age >70 years) were also more likely to have p53 overexpression, with an OR of 5.63 (95% CI: 1.53-20.64) compared with overexpression among patients aged less than 55 years. Forty-one patients received further evaluation of p53 mutation. There was also a higher incidence of, but without reaching a statistical significance, p53 mutation in patients with p53 overexpression (OR[95% CI]: 2.18 [0.52-9.6]) and codon 72 Arg/Arg genotype (OR [95% CI] of 0.8 [0.13-4.2], comparing genotypes of Pro/Pro and Arg/Pro with Arg/Arg). Our data provide the first observations that the presence of p53 codon 72 variants can be a significant factor influencing p53 overexpression in esophageal cancer, with overexpression also influenced by combined or prolonged environmental exposures.

Aged↗

PubMed2005

Relationship between genetic polymorphisms of alcohol and aldehyde dehydrogenases and esophageal squamous cell carcinoma risk in males.

AIM: To investigate the association between the genetic polymorphisms of ADH2 and ALDH2, lifetime alcohol consumption and esophageal cancer risk in the Taiwanese men. METHODS: Between August 2000 and June 2003, 134 pathologically-proven esophageal squamous cell carcinoma male patients and 237 male controls were recruited from Kaohsiung Medical University Hospital and Kaohsiung Veterans General Hospital in southern Taiwan. ADH2 and ALDH2 polymorphisms were genotyped using PCR-RFLP. RESULTS: Compared to those with ADH2*2/*2, individuals with ADH2*1/*2 and ADH2*1/*1 had 2.28- and 7.14-fold, respectively, increased risk of developing esophageal cancer (95%CI = 1.11-4.68 and 2.76-18.46) after adjusting for alcohol consumption and other covariates. The significant increased risk was also noted among subjects with ALDH2*1/*2 (adjusted OR (AOR) = 5.25, 95%CI = 2.47-11.19), when compared to those with ALDH2*1/*1. The increased risk of esophageal cancer was made greater, when subjects carried both ADH2*1/*1 and ALDH2*1/*2, compared to those with ADH2*1/*2 or ADH2*2/*2 and ALDH2*1/*1 (AOR = 36.79, 95%CI = 9.36-144.65). Furthermore, we found a multiplicative effect of lifetime alcoholic consumption and genotypes (ADH2 and ALDH2) on esophageal cancer risk. CONCLUSION: Our findings suggest that polymorphisms of ADH2 and ALDH2 can modify the influence of alcoholic consumption on esophageal cancer risk.

Aged↗

PubMed2005

The association between microsomal epoxide hydrolase genotypes and esophageal squamous-cell-carcinoma in Taiwan: interaction between areca chewing and smoking.

One hundred and forty-five ESCC patients and 352 controls were recruited from three hospitals in Taiwan to determine the association between esophageal squamous-cell-carcinoma (ESCC) and microsomal epoxide hydrolase (mEH) genotypes at Thy113His and His139Arg. Stratified by their exposures, the His113His genotype was a significant protective factor for ESCC in areca chewers and tobacco smokers. Stratified by His113 polymorphisms, the risk of contracting ESCC for participants with His113His who chewed areca and smoked was >50% less than for those with Thy113Thy. We suggest that the mEH His113His genotype can differentiate the association between smoking, areca chewing, and ESCC.

Adult↗

PubMed2005

Association of GSTP1 polymorphism and survival for esophageal cancer.

PURPOSE: Activity of glutathione S-transferase (GST) is associated with detoxification of xenobiotics and the maintenance of cell viability. Genetically variant GSTs produce different enzymatic activities. The clinical significance of this variation is still puzzling. We investigated whether genetic polymorphisms of GST including GSTP1, GSTM1, and GSTT1 affect survival among esophageal cancer patients. EXPERIMENTAL DESIGN: From 1996 to 2002, 233 patients with pathologically proven esophageal cancer were recruited from the Department of Surgery, National Taiwan University Hospital. GST genotypes, including GSTT1, GSTM1, and GSTP1, were determined by PCR or PCR-RFLP. The influence of the genetic polymorphisms on patient survival was estimated using the method of Kaplan-Meier survival function and Cox proportional hazards models. RESULTS: The mean survival times (months) of the GSTP1 Ile/Ile, Ile/Val, and Val/Val were 11, 10, and 7, respectively (P < 0.05). The more the patients carried GSTP1 variant Val alleles, the poorer the survival rate (adjusted hazard ratio, 1.36; 95% confidence interval, 1.01-1.84; Ptrend = 0.045). In contrast, no association of GSTT1 or GSTM1 genotypes with survival rate was noted. CONCLUSION: The presence of the GSTP1 variant allele (Val) is associated with a poorer prognosis of esophageal cancer.

Adult↗

PubMed2005

Independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer in Taiwan.

A multicenter case-control study was conducted in northern and southern Taiwan to clarify the independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer. A total of 513 patients with newly diagnosed and histopathologically confirmed squamous cell carcinoma of the esophagus and 818 gender, age and study hospital-matched controls were included. We found a significant dose-response relationship between the duration and intensity of consumption of the 3 substances and the development of this neoplasm in this site. Although the amount of alcohol consumed had a stronger effect on the risk of esophageal cancer than the number of years it was consumed, however, the number of years one smoked had a stronger effect on the risk than the amount of cigarettes consumed. The strongest risk factor of esophageal cancer was alcohol intake, with highest risk (OR = 13.9) being for those who consumed more than 900 g/day-year. Combined exposure to any 2 of 3 substances brought the risks up to 8.8-19.7 fold and, to all 3 substances, to 41.2-fold. A multiplicative interaction effect for alcohol drinkers who smoked on cancer risk was detected, whereas an additive interaction effect was found among drinkers who chewed. The combined effect of all 3 substances accounted for 83.7% of the attributable fraction of contracting esophageal cancer in this population. In conclusion, these results suggest that the intensity and the length of time alcohol and tobacco are used play different roles in the etiology of esophageal cancer. Alcohol separately interacts with tobacco and betel quid in a differently synergistic way in determining the development of this site of cancer.

Adult↗

PubMed2005

Safrole-DNA adducts in tissues from esophageal cancer patients: clues to areca-related esophageal carcinogenesis.

Epidemiological studies have demonstrated that areca quid chewing can be an independent risk factor for developing esophageal cancer. However, no studies are available to elucidate the mechanisms of how areca induces carcinogenesis in the esophagus. Since the areca nut in Taiwan contains a high concentration of safrole, a well-known carcinogenic agent, we analyzed safrole-DNA adducts by the 32P-postlabelling method in tissue specimens from esophageal cancer patients. In total, we evaluated 47 patients with esophageal cancer (16 areca chewers and 31 non-chewers) who underwent esophagectomy at the National Taiwan University Hospital between 1996 and 2002. Of the individuals with a history of habitual areca chewing (14 cigarette smokers and two non-smokers), one of the tumor tissue samples and five of the normal esophageal mucosa samples were positive for safrole-DNA adducts. All patients positive for safrole-DNA adducts were also cigarette smokers. Such adducts could not be found in patients who did not chew areca, irrespective of their habits of alcohol consumption or cigarette smoking (p<0.001, comparing the areca chewers with non-chewers). The genotoxicity of safrole was also tested in vitro in three esophageal cell lines and four cultures of primary esophageal keratinocytes. In two of the esophageal keratinocyte cultures, adduct formation was increased by treatment with safrole after induction of cytochrome P450 by 3-methyl-cholanthrene. This paper provides the first observation of how areca induces esophageal carcinogenesis, i.e., through the genotoxicity of safrole, a component of the areca juice.

Aged↗

PubMed2005

The role of p-STAT3 (ser727) revealed by its association with Ki-67 in cervical intraepithelial neoplasia.

OBJECTIVES: Constitutive activation of signal transducer and activator of transcription 3 (STAT3) has been described in many types of cancers. However, the role of phospho-STAT3 (p-STAT3) at serine residue 727 is in large part undetermined. Our purposes of this study were to evaluate the expression patterns of p-STAT3 (ser727) in cervical intraepithelial neoplasia (CIN) and to explore its possible role in the progression of cervical cancer. METHODS: Paraffin-embedded sections from 56 patients including 20 CIN 1, 10 CIN 2, and 26 CIN 3 were collected in this study. Immunohistochemical analysis was performed, and the expression patterns of p-STAT3 (ser727) were categorized by semiquantitative method and further correlated with the CIN histopathologic grade using the chi(2) test with Bonferroni adjustment for multiple comparisons and with the proliferation marker Ki-67 expression using Fisher's Exact Test. RESULTS: The categorized high p-STAT3 (ser727) expression group in nuclei of dysplastic cells was significantly higher in CIN 3 (76.92%), in comparison with CIN 1/2 (13.33%, P < 0.001). Moreover, both the nuclear and cytoplasmic p-STAT3 (ser727) expressions were correlated with Ki-67 nuclear staining (P < 0.001 and < 0.001, respectively). CONCLUSIONS: Our result revealed that aberrant expression levels of p-STAT3 (ser727) were significantly correlated with CIN lesion grade and cell proliferation. Evaluation of p-STAT3 (ser727) expression may provide additional prognostic information for the clinical course of the disease and therefore to be developed as a prognostic indicator for cervical cancer.

Biomarkers, Tumor↗

PubMed2005

Citalopram-induced serotonin syndrome: a case report.

Serotonin syndrome is a disorder resulting from excess stimulation of serotonin and is associated with drug interaction, single-drug therapy, and overdose. We report a case involving a 32-year-old man who developed sudden agitation, diaphoresis, subjective fever, tremor, and insomnia. These symptoms were related to doubling the dose of citalopram in combination antidepressant therapy. Discontinuation of the agent resulted in early notable clinical resolution after 1 week. This is a rare report of serotonin syndrome induced by citalopram polytherapy. Although serotonin syndrome is rare, clinicians need to recognize it early.

Adult↗