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Neurilemmoma of the seminal vesicle is an extremely rare tumor. We report a neurilemmoma of right seminal vesicle. A 67-year-old man presented with moderate lower urinary tract symptoms. A magnetic resonance imaging of prostate performed due to high level of prostate specific antigen revealed a 8.1x8.1x7.1 cm, arising from right seminal vesicle. Laparoscopic resection of tumor was performed. The histopathology showed neurilemmoma arising from seminal vesicle.

Carbapenem-resistant Enterobacteriaceae (CRE) is emerging as a major problem in healthcare settings globally, including Thailand, due to limited therapeutic options. We reported the detection, antimicrobial susceptibility profiles, and the presence of carbapenemase genes of CRE isolates obtained from Songklanagarind Hospital between July 2012 and June 2015. A total of 273 non-duplicated CRE isolates was recovered from 248 patients. The predominant organism was Klebsiella pneumoniae (183 [67.0 %]), followed by Escherichia coli (38 [13.9 %]). The susceptibility to 13 antibiotics was performed by disk diffusion assay. Most of the CRE isolates remained susceptible to amikacin. Minimum inhibitory concentrations (MIC) of carbapenems were determined by E-test. The MIC50 and MIC90 were varied among genera and species. Multiplex PCRs for the carbapenemase genes blaIMP, blaVIM, blaOXA-48, blaNDM-1, blaKPC, and blaGES were performed. One hundred and seventy-eight out of these 273 CRE isolates (65.2 %) harbored either single or multiple carbapenemase genes. One hundred and fifty nine isolates harbored the blaNDM-1 gene (113 K. pneumoniae, 25 E. coli, 17 E. cloacae, 2 Citrobacter freundii, 1 Enterobacter aerogenes, and 1 Pantoea agglomerans), 7 isolates carried blaIMP (4 K. pneumoniae, 2 C. freundii, and 1 E. cloacae), 7 isolates possessed blaOXA-48 (1 K. pneumoniae, 5 E. coli, and 1 E. aerogenes), whereas 3 and 2 isolates harbored blaNDM-1 and blaIMP (2 K. pneumoniae and 1 E. cloacae) and blaNDM-1 and blaOXA-48 (1 E. coli and 1 E. cloacae), respectively. In conclusion, this study revealed the detection of CRE, with the majority of K. pneumoniae harboring blaNDM-1 in this setting.

Objective: MicroRNA (miRNA), a short noncoding RNA, is claimed to be a potential blood-based biomarker. We aimed to identify and evaluate miRNAs as diagnostic biomarkers for non-small cell lung cancer (NSCLC). Methods: Profiles of 745 miRNAs were screened in the serum of 8 patients with NSCLC and 8 age- and sex-matched controls using TaqMan low-density arrays (TLDAs) and validated in 25 patients with NSCLC and 30 with other lung diseases (OLs) as well as in 19 healthy persons (HPs). The diagnostic performance of the candidate miRNAs was assessed in 117 cases of NSCLC and 113 OLs using quantitative real-time polymerase chain reaction (qRT-PCR). Differences in miRNA expression between patients with NSCLC and controls were assessed using the Mann-Whitney U test. The area under receiver operating characteristic (ROC) curve (AUC) was obtained based on the logistic regression model. Results: Ten miRNAs were found to be differentially expressed between patients with NSCLC and controls, including miR-769, miR-339-3p, miR-339-5p, miR-519a, miR-1238, miR-99a#, miR-134, miR-604, miR-539, and miR-342. The expression of miR-339-3p was significantly higher in patients with NSCLC than in those with OLs (P < 0.001) and HPs (P = 0.020). ROC analysis revealed an miR-339-3p expression AUC of 0.616 [95% confidence interval (CI): 0.561-0.702]. The diagnostic prediction was increased (AUC = 0.706, 95% CI: 0.649-0.779) in the model combining miR-339-3p expression and other known risk factors (i.e., age, smoking status, and drinking status). Conclusions: MiR-339-3p was significantly upregulated in patients with NSCLC compared with participants without cancer, suggesting a diagnostic prediction value for high-risk individuals. Therefore, miR-339-3p expression could be a potential blood-based biomarker for NSCLC.

Objective: Programmed cell death ligand 1 (PD-L1) and mammalian target of rapamycin (mTOR) are key players in host immune evasion and oncogenic activation, respectively. Evidence of the prognostic role in oral squamous cell carcinoma (OSCC) is conflicting. This study examined the associations of PD-L1 and mTOR expression with 5-year overall survival in OSCC patients. Material and Methods: The expressions of PD-L1 and mTOR proteins were immunohistochemically evaluated on tissue microarrays of 191 patients with OSCC who were treated by surgery at Songklanagarind Hospital, Thailand from 2008 to 2011. Cox regression analysis was used to determine independent prognostic factors. Results: PD-L1 expression was observed in 14.1% of cases while mTOR expression was present in 74.3% of cases. Females were more likely to have tumors with PD-L1 (p-value=0.007) and mTOR expressions (p-value=0.003) than males. In addition, lower clinical stage and well differentiated tumor are more likely to have mTOR expression (p-value= 0.038 and p-value

c-Myc regulates multiple genes involved in cell proliferation in various cancer types including non-small cell lung cancer (NSCLC). Copy number gains of cytoband 17q25.3, along with chromosome 17, have been reported in NSCLC patients, emphasizing the clinical significance as a potential molecular target for therapy. The upregulation of c-Myc has been found to accelerate tumor development associated with duplication of the syntenic human cytoband 17q25.3. This study aimed to explore and compare the correlations of chromosome 17 copy number and c-Myc expression in NSCLC with the paired-normal respiratory epithelium and to examine their role as potential molecular targets for NSCLC therapy.A total of 66 NSCLC tissue samples with paired-normal respiratory epithelium were examined. The copy number of chromosome 17 was determined by human epidermal growth factor receptor 2 (Copy number gains of chromosome 17 were identified in 8 of 60 (13.3%) available NSCLC specimens. No copy number gains of chromosome 17 were demonstrated in the paired-normal respiratory epithelium. The meanBoth biomarkers deserve further investigation to identify NSCLC patients with poorer survival outcomes requiring better therapeutic approaches.

In recent decades, many countries worldwide have implemented some form of Universal Health Coverage (UHC). We sought to evaluate incidence and survival trends of breast, cervical, and colorectal cancer before and after the implementation of UHC in Thailand.The age-standardized incidence rate and 1- and 5-year net survival (NS) were calculated for five Thai provinces, namely Bangkok, Chiang Mai, Khon Kaen, Lampang, and Songkhla for breast, cervix, and colorectal cancer in three study periods (1997-2012): before, during, and after the implementation of UHC.The incidence of breast and colorectal cancer has increased over time, while the incidence of cervical cancer has decreased (17.9-29.9, 9.0-13.6, and 19.6-12.3 per 100,000, respectively). Larger proportion of breast cancer were diagnosed with localized stage after UHC implementation compared to the period prior to UHC (31.5 % vs 19.0 %). Overall, The improvement in survival by cancer site varied in magnitude with a 5-year NS increase from 61.3 % to 75.1 % for breast, 55.4-59.5 % for cervical, and 39.9-47.6 % for colorectal cancer. The amount of increase slightly differed across provinces.Rising incidence for breast and colorectal, and declining cervical cancer may partly be attributable to improved awareness and early detection programs. Additionally, improvement in survival may partly be attributable to increased access to healthcare, availability of treatment, and increased access to cancer screening after UHC was implemented. Thus, continued expansion of UHC package on cancer could potentially contribute to further improvement of cancer control in Thailand.This study provides important evidence on the impact of UHC in cancer burden and survival for breast, cervical, and colorectal cancer in Thailand. This study serves as an example for other countries where UHC has been recently implemented and guide policymakers in allocating resources towards UHC and cancer control programs.

Previous studies have reported the diagnostic and prognostic value of serum microRNA (miR)-145 and vascular endothelial growth factor (VEGF) levels in various types of cancer; however, their clinical use in non-small cell lung cancer (NSCLC) remains unclear. The present study included 215 patients, 106 with NSCLC and 109 with other lung diseases (OLDs). miR-145 expression levels were determined using reverse transcription-quantitative PCR (RT-qPCR) and VEGF levels were measured using an ELISA. The diagnostic performance was assessed using a receiver operating characteristic curve and area under the curve (AUC) analysis. A Kaplan-Meier survival curve and Cox regression analysis were employed to evaluate the prognostic significance of the markers. The biological function of miR-145 was examined in A549 and H1792 cell lines. The effects of miR-145 on cell proliferation of NSCLC cells were evaluated by flow cytometry, and the expression levels of miR-145 and cell cycle-related genes were determined by RT-qPCR. The results revealed that miR-145 and VEGF exhibited fair diagnostic performance [AUC, 0.61 (95% CI, 0.55-0.68) and AUC, 0.64 (95% CI, 0.57-0.71), respectively]. Combining age and smoking status with miR-145 and VEGF provided the best model for differentiating patients with NSCLC from those with OLDs (AUC, 0.76; 95% CI, 0.69-0.83). Furthermore, low serum miR-145 levels were associated with poor overall survival [hazard ratio (HR), 0.48; 95% CI, 0.27-0.85], whereas high VEGF levels were not associated with poor overall survival (HR, 1.47; 95% CI, 0.81-2.68). In addition, the results of the in vitro experiments indicated that miR-145 decreased cell proliferation via the induction of cell cycle arrest. In conclusion, the findings of the present study suggested that combining miR-145 and VEGF levels with clinical risk factors may be a potential diagnostic scheme for NSCLC. In addition, serum miR-145 may be used as a prognostic marker. These results indicated that miR-145 may function as a tumor suppressor in NSCLC.

Background: Non-small cell lung cancer (NSCLC) remains a leading cause of cancer death worldwide, for which better knowledge in molecular prognostic factors is needed to improve clinical outcome. This study aimed to investigate the clinical significance of c-Myc, ALK, ROS1, BRAF, and PD-L1 in NSCLC patients. Methods: Formalin-fixed paraffin-embedded tissue specimens were obtained from 124 NSCLC patients. Of these, 66 matched specimens of normal respiratory epithelial and tumor tissue from patients with stages I-III, who underwent surgical resection, and 58 NSCLC specimens from stage IV patients were recruited into this analysis. Immunohistochemistry staining along with semiquantitative criteria were used to evaluate the expression of the interested proteins. Results: Of the 66 patients with stages I-III, positive expression of c-Myc was detected in 12 specimens (18.2%) of NSCLC tissue, whereas none of the normal respiratory epithelial tissue was found to have c-Myc expression ( P Conclusions: NSCLC tissue significantly expressed more c-Myc and PD-L1, compared with the matched normal respiratory epithelium, emphasizing the important role of these key drivers in tumorigenesis. Therapeutic approach to precisely inhibit the targetable molecular pathways should be considered on an individual patient basis to improve survival outcome.

Objective: The study aimed to determine the frequency of intron 3 16 base pair (bp) duplication polymorphism and intron 6 G to C substitution (G>C) of the TP53 gene and to evaluate the association these two intronic variants with the risk of esophageal cancer (EC).Material and Methods: A case-control study was conducted to evaluate the frequency and association of cancer. Cases were patients with squamous cell carcinoma of esophagus and controls were age and sex-matched non-cancer patients. Blood samples were also obtained from healthy blood donors. Polymerase chain reaction (PCR) was used to detect intron 3 16 bp duplication and PCR-restriction fragment length polymorphism was applied to detect intron 6 G>C. Logistic regression was used for the analysis.Results: Heterozygous intron 3 16 bp duplication (Del/Ins) was found in 10.1% (31/308) of blood donors, 9.3% (28/302) of controls and 8.6% (26/301) of EC cases. Intron 6 G>C was found in 0.3% (1/308) of blood donors, in 2.6% (8/310) of controls and 3.9% (12/307) of EC cases. Both variants displayed no significant association with risk of esophageal cancer (odd ratio (OR) = 1.16 [95% confidence interval (CI) = 0.64–2.11] for intron 3 16 bp duplication and OR = 0.81 [95% CI = 0.47-4.61] for intron 6 G>C.Conclusion: Southern Thai population have low frequency of intron 3 16 bp duplication polymorphism and intron 6 G>C variant, both of which are not likely to be associated with esophageal cancer susceptibility.

MicroRNAs (miRNAs) are small, non-coding RNA molecules that regulate gene expression at the post-transcriptional level. Since aberrant expression of miRNAs has been proposed as usage for blood-based biomarkers, hence reliable techniques for miRNA isolation as well as stability of miRNAs in various stored conditions needs to be explored. This present study aimed to investigate the efficacy of the Trizol-based isolation technique and the stability of miRNAs in stored serum and cDNA derivatives. Total RNA, including miRNAs, was isolated from human serum and a comparison of the efficiency of the Trizol®LS reagent isolation method against the miRNeasy®mini kit was conducted. Expression of RNU6, miR-145, and miR-20a was determined by quantitative real-time polymerase chain reaction (qRT-PCR). We showed that Trizol®LS isolation yielded significantly lower RNA concentrations than that of the miRNeasy®mini kit by approximately 35%. Purity of the isolated RNAs by both methods was similar. RNU6, miR-145, and miR-20a degraded at room temperature, but all genes were stable at 4ºC, -20ºC and -80ºC for a 72-hrs period, in both serum and cDNA storage conditions. In the stored cDNA derivatives, we observed the stability of RNU6, miR-145, and miR-20a for 3 months at -20ºC, and all genes also resisted 4 repeated freeze-thaw cycles at -20ºC. In conclusion, the Trizol-based method is efficient as well as economical to use for quantification of circulating miRNAs. In addition, we proposed that the storage of miRNA-derived cDNAs may be an alternative choice to avoid the stability effect.

Objective: 14-3-3 gamma (γ) is known to modulate the development and progression of many cancers. However, the evidence in lung cancer is still unclear. In this study, effects of 14-3-3γ on tumor cell migration and invasion were investigated. Material and Methods: A 14-3-3γ expression vector was made and transfected into A549 cells. In-vitro scratch assay and transwell assay were applied to assess migration and invasion, respectively. Western blotting was used to detect expression of proteins related to epithelial–mesenchymal transition.Results: Closing rate of scratch wounds, both in classical and non-classical scratch assay, was significantly increased in 14-3-3γ-overexpressing cells in comparison to the controls. Similarly, by transwell assay, a significant increase in the invasion and migration was shown in the 14-3-3γ-overexpressing cells in comparison to the null vector cells, by approximately 79.2% (p-value=0.002) and 131.2% (p-value

Background This study aimed to identify differentially expressed proteins in the serum of advanced non-small cell lung cancer (NSCLC) patients responding to carboplatin (CAR) plus paclitaxel (PTX) chemotherapy compared to non-responders. Materials and methods Serum from 8 responders and 6 non-responders was subjected to proteomic analysis by label-free liquid chromatography tandem mass spectrometry and validated by western blotting. CAR/PTX-resistant human H1792 and A549 cells were used for evaluating gene expression. Results Fifty-two proteins were differentially expressed between responders and non-responders. Alpha 1 antitrypsin antibody, alpha 1 acid glycoprotein (A1AG1), afamin, protein S100-A9 and immunoglobulin heavy constant gamma 3 (IGHG3) were validated. IGHG3 was elevated (p=0.037) while A1AG1 was reduced (p=0.003) in responders as compared to non-responders. Gene expression of IGHG3 and ORM1 in resistant cells showed consistent results with the proteomics profiles. Conclusion Serum expression levels of IGHG3 and A1AG1 proteins may be useful to recruit an NSCLC subpopulation that can benefit from CAR plus PTX standard therapy.

Antineoplastic drugs (AD) are important chemical risks for healthcare workers. Precautions against AD exposure include the use of appropriate personal protective equipment (PPE). Evaluation of PPE usage during patient care processes has not been reported in Thailand. We aimed to evaluate the level of PPE usage and factors predicting PPE usage among nurses and nurse assistants in Thailand. A cross-sectional survey was conducted in a university hospital and two general hospitals. The questionnaires covered demographic characteristics, self-reported use of PPE and 7 predictive factors. Mixed-effects modeling was used to determine the association between standardized score of predictive factors and PPE usage score. The response rate was 78.6% and 884 participants were left for analysis after data cleaning. Among nurses (n = 499), higher PPE usage score was associated with self-efficacy (β = 0.28, 95% CI 0.21, 0.34), workplace safety climate (β = 0.27, 95% CI 0.20, 0.34), and conflict of interest (β = − 0.07, 95% CI − 0.14, − 0.01). Among nurse assistants (n = 385), higher PPE usage score was associated with self-efficacy (β = 0.27, 95% CI 0.18, 0.36), interpersonal influence (β = 0.14, 95% CI 0.04, 0.24), workplace safety climate (β = 10.29, 95% CI 0.19, 0.38), and conflict of interest (β = − 0.14, 95% CI − 0.24, − 0.03). Several factors were associated with PPE usage among nurses and nurse assistants. Improved PPE usage against AD can be promoted through interventions that modify those factors.

Synergistic loss of E-cadherin and acquisition of vimentin are characteristic feature of epithelial–mesenchymal transition (EMT) which confers an invasive phenotype of epithelial cancer cells. The aim of the study was to evaluate the prognostic significance of E-cadherin and vimentin expression individually and in combination as a measure of epithelial–mesenchymal transition (EMT) in oral squamous cell carcinoma (OSCC). Expression of E-cadherin and vimentin through immunohistochemical analysis was examined in 200 patients with surgically resected OSCC. Combined E-cadherin and vimentin expression was evaluated to determine the EMT status. Kaplan–Meier curves and log-rank test were used to compare differences in survival. Cox regression analysis was performed to identify independent prognostic factors. E-cadherin expression was negative in 28 (14%) tumors, and vimentin expression was positive in 87 (43.5%) tumors. Moreover, 99 (49.5%), 87 (43.5%), and 14 (7.5%) tumors exhibited no, partial, and complete EMT, respectively. Both individual protein expression were significant prognostic factors [Negative E-cadherin, hazard ratio (HR) = 1.74, 95% confidence interval (CI) = 1.04–2.93; positive vimentin, HR = 1.64, 95% CI = 1.12–2.41]. For EMT status, the HR increased with EMT progression [partial EMT, HR = 1.64, 95% CI = 1.09–2.49; complete EMT, HR = 2.88, 95% CI = 1.44–5.79], of which, the complete EMT had higher HR than was individual protein expression. Combined E-cadherin and vimentin expression as a measure of EMT showed a superior prognostic significance compared with individual protein expression.

Since the introduction of image pattern recognition and computer vision processing, the classification of cancer tissues has been a challenge at pixel-level, slide-level, and patient-level. Conventional machine learning techniques have given way to Deep Learning (DL), a contemporary, state-of-the-art approach to texture classification and localization of cancer tissues. Colorectal Cancer (CRC) is the third ranked cause of death from cancer worldwide. This paper proposes image-level texture classification of a CRC dataset by deep convolutional neural networks (CNN). Simple DL techniques consisting of transfer learning and fine-tuning were exploited. VGG-16, a Keras pre-trained model with initial weights by ImageNet, was applied. The transfer learning architecture and methods responding to VGG-16 are proposed. The training, validation, and testing sets included 5000 images of 150 × 150 pixels. The application set for detection and localization contained 10 large original images of 5000 × 5000 pixels. The model achieved F1-score and accuracy of 0.96 and 0.99, respectively, and produced a false positive rate of 0.01. AUC-based evaluation was also measured. The model classified ten large previously unseen images from the application set represented in false color maps. The reported results show the satisfactory performance of the model. The simplicity of the architecture, configuration, and implementation also contributes to the outcome this work.

Tumor-promoting cytokines are a cause of tumor progression; therefore, identifying key regulatory microRNAs (miRNAs) for controlling their production is important. The aim of this study is to identify promising miRNAs associated with tumor-promoting cytokines in non-small cell lung cancer (NSCLC). We identified circulating miRNAs from 16 published miRNA profiles. The selected miRNAs were validated in the serum of 32 NSCLC patients and compared with 33 patients with other lung diseases and 23 healthy persons using quantitative real-time PCR. The cytokine concentration was investigated using the enzyme-linked immunoassay in the same sample set, with clinical validation of the miRNAs. The correlation between miRNA expression and cytokine concentration was evaluated by Spearman's rank correlation. For consistent direction, one up-regulated miRNA (miR-145) was found in four studies, and seven miRNAs were reported in three studies. One miRNA (miR-20a) and four miRNAs (miR-25-3p, miR-223, let-7f, and miR-20b) were reported in six and five studies. However, their expression was inconsistent. In the clinical validation, serum miR-145 was significantly down-regulated, whereas serum miR-20a was significantly up-regulated in NSCLC, compared with controls. Regarding serum cytokine, all cytokines [vascular endothelial growth factor (VEGF), interleukin-6 (IL-6), and transforming growth factor β (TGF-β)], except tumor necrosis factor-α (TNF-α), had a higher level in NSCLC patients than controls. In addition, we found a moderate correlation between the TGF-β concentration and miR-20a (r = -0.537, p = 0.002) and miR-223 (r = 0.428, p = 0.015) and a weak correlation between the VEGF concentration with miR-20a (r = 0.376, p = 0.037) and miR-223 (r = -0.355, p = 0.046). MiR-145 and miR-20a are potential biomarkers for NSCLC. In addition, the regulation of tumor-promoting cytokine, through miR-20a and miR-223, might be a new therapeutic approach for lung cancer.

Background/aim 14-3-3γ is involved in the metastasis of lung cancer cells. However, its functional roles in tumor cell invasion and the underlying mechanisms are still not understood. In this study, the roles and molecular mechanisms of 14-3-3γ in epithelial-mesenchymal transition (EMT), migration, and invasion were investigated using A549 and H358 non-small cell lung cancer (NSCLC) cell lines. Materials and methods siRNA against 14-3-3γ was used to suppress 14-3-3γ expression. Expression levels of proteins were detected by western blotting. Activity of matrix metalloproteinases (MMP)-2 and MMP9 was determined by gelatin zymography. Cell migration and invasion were analyzed using the Transwell assay. Results Knockdown of 14-3-3γ resulted in a significant reduction of expression of EMT-associated proteins in NSCLC cell lines, and led to significant reduction in invasion and migration by approximately 59% and 39% in A549 cells, and 65% and 62% in H358 cells, respectively. In addition, MMP2 and MMP9 activity was significantly reduced in both NSCLC cell lines after down-regulation of 14-3-3γ. Conclusion Our results suggest that knockdown of 14-3-3γ may be a potential strategy for suppressing metastasis of lung cancer by inhibiting MMP2 and MMP9 through regulation of EMT.

Non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancers and it is the leading cause of cancer death globally. Vascular endothelial growth factor (VEGF) plays an important role in cancer progression, including lung cancer. Therefore, it would be interesting to determine key modulators that can suppress VEGF production. This study aimed to identify miRNAs regulating VEGF using systematic reviews and bioinformatics tools. We further validated miRNA expression and VEGF level using qRT-PCR and ELISA, respectively. A total 17 studies were selected using systematic review. 97 miRNAs were found to be up-regulated in serum of NSCLC compared to controls. miR-145 was selected to further validate in clinical samples. Serum miR-145 expression in NSCLC (10.77±3.40) was lower than patient with other lung diseases (25.10±7.90) with p-value of 0.019. The VEGF level in serum of NSCLC was significantly higher than other lung diseases and healthy persons with p-value of 0.003 and 0.002, respectively. However, a weak negative correlation of miR-145 and VEGF in serum of NSCLC was observed without significant difference. In conclusion, the expression of miR-145 and VEGF in NSCLC patients may be involved with lung tumorigenesis; however, the VEGF is not regulated by miR-145 in lung cancer.

The 14-3-3 protein has been shown to be involved in the cancer process. However, there is no understanding of the relationship between 14-3-3γ (14-3-3 gamma) expression and prognosis in advanced non-small cell lung cancer. In this study, we therefore investigated the association between protein levels by immunohistochemistry and clinicopathological features of advanced NSCLC patients. Survival curves were estimated using the Kaplan-Meier method and tested by log-rank. Multivariate analysis was conducted with the Cox's regression model to determine independence of factors. p values less than 0.05 were considered significant. A total 153 patients were studied, with 54.3% being stage III and 45.8% stage IV. Fifty-one cases (33.3%) were squamous cell carcinomas, and 98 cases (64.1%) were adenocarcinomas. High 14-3-3γ expression was seen in 59.5% and significantly correlated with lymph node metastasis (p=0.010) and distant metastasis (p=0.017). On Kaplan-Meier analysis, high 14-3-3γ expression was associated with poorer survival with a marginal trend toward significance (p=0.055). On multivariate analysis, age, treatment, and 14-3-3γ expression proved to be independent prognostic parameters. In vitro experiments indicated that 14-3-3γ overexpression also played a potential role in cancer invasion. In conclusion, our data suggest that 14-3-3γ overexpression is associated with invasion and a poor prognosis. Therefore, 14-3-3γ may be a potential prognostic marker of advanced non-small cell lung cancer.

Background: The proteins p16, p53, Bcl-2, and Bax are important cell cycle and apoptotic regulators involved in carcinogenesis and found to have prognostic significance in various cancers. However, the data for squamous cell carcinoma of oral cavity (OSCC) and of oropharynx (OPSCC) are conflicting. Objective: We sought to determine if expression of p16, p53, Bcl-2, and Bax expression are associated with 5-year overall survival (OS) of patients with OSCC and OPSCC. Methods: One-hundred thirty-seven cases of OSCC and 140 cases of OPSCC diagnosed from January 2002 to December 2004 at Songklanagrind Hospital, Songkhla, Thailand, were analyzed using a Cox proportional hazards model for 5-year OS in relation to immunohistochemical detection of Bcl-2, Bax, p53, and p16 proteins. Results: The frequencies of p16, p53, Bcl-2, and Bax expression in OSCC were 13%, 45%, 4%, and 66%, and in OPSCC were 18%, 53%, 22%, and 75%, respectively. In univariate analysis, clinical variables including T stage, N stage and treatment were significantly associated with survival. In multivariate Cox regression, Bax overexpression was significantly associated with poor survival both in OSCC (HR 1.77, 95% CI 1.04-3.01) and in OPSCC (HR 2.21, 95% CI 1.00-4.85). We found no significant association of p16, Bcl-2, and p53 expression with survival. Conclusion: The expression pattern of p16, p53, Bcl-2, and Bax are similar in OSCC and OPSCC. Only Bax expression has prognostic significance for both tumor sites.

This study aimed to investigate tumor microvessel density (MVD) and lymphatic vessel density (LVD) using the Chalkley method as predictive markers for the risk of axillary lymph node metastasis and their relationship to other clinicopathological parameters in primary breast cancer cases. Forty two node-positive and eighty node-negative breast cancers were immunostained for CD34 and D2-40. MVD and LVD were counted by the Chalkley method at x400 magnification. There was a positive significant correlation of the MVD with the tumor size, coexisting ductal carcinoma in situ (DCIS) and lymph node metastases (P0.05). In multivariate analysis, the MVD (2.86-4: OR 5.87 95%CI 1.05-32;4: OR 20.03 95%CI 3.47-115.6), lymphovascular invasion (OR 3.46, 95% CI 1.13-10.6), and associated DCIS (OR 3.1, 95%CI 1.04-9.23) independently predicted axillary lymph node metastasis. There was no significant relationship between LVD and axillary lymph node metastasis. However, D2-40 was a good lymphatic vessel marker to enhance the detection of lymphatic invasion compared to H and E staining. In conclusion, MVD by the Chalkley method, lymphovascular invasion and associated DCIS can be additional predictive factors for axillary lymph node metastases in breast cancer. No relationship was identified between LVD and clinicopathological variables, including axillary lymph node metastasis.

Loss of 14-3-3σ expression through DNA methylation has been associated with carcinogenesis and the prognosis for various cancer types. Detection of methylation of the gene in serum may be useful for diagnostic utility. The present study aimed to investigate the correlation between 14-3-3σ methylation level in 36 paired tumor tissues of non-small cell lung cancer (NSCLC) and matched serum using methylation-specific polymerase chain reaction. The prognostic significance of 14-3-3σ expression in 167 NSCLC was also evaluated using immunohistochemistry. Methylation of the 14-3-3σ gene was identified in all samples. The methylation level in the serum (mean 87.7%, range 64.6-100%) was higher compared with tumor (mean 46.7%, range 25.3-56.3%). However, no significant correlation between methylation levels in tissues and serums was observed (Spearman's correlation, -0.036; P=0.837). In the 167 tumor tissues, the majority of the cases (83.8%) exhibited negative expression. Adenocarcinoma is more likely to exhibit negative expression (91.4%) compared with squamous cell carcinoma (70.2%). No significant difference was identified in the overall survival according to 14-3-3σ expression status and 14-3-3σ expression did not demonstrated independent prognostic significance. In conclusion, NSCLC harbors certain levels of 14-3-3σ methylation in the tumor and the sera of patients. The clinical value of serum 14-3-3σ methylation should be further elucidated. Immunohistochemical expression 14-3-3σ protein has limited value on prognostic significance.

We report the first establishment of in vitro cultivation and genotypic characterization of Leishmania siamensis isolated from an autochthonous disseminated dermal and visceral leishmaniasis in a Thai acquired immunodeficiency syndrome (AIDS) patient. The molecular identification has shown that the parasite was identical to L. siamensis, a recently described Leishmania species reported in the southern provinces of Thailand. The phylogenetic analysis has confirmed L. siamensis as closely related to the zoonotic Leishmania species L. enrietti.

Background: Head and neck cancers are prevalent in Thailand, in particular in the southern region of the country. However, survival with a large data set has not been reported. The purpose of the present study was to evaluate the survival figures and the prognostic factors in a cohort of patients treated in a university hospital located in the south of Thailand. Patients and Methods: Consecutive new cases of primary carcinoma of the oral cavity, oropharyx, hypopharynx and larynx, treated at Songklanagarind Hospital during 2002 to 2004, were analyzed. The 5-year overall survival rates were obtained by the Kaplan-Meier method. Prognostic factors were identified through multivariate Cox regression analysis. Results: A total 1,186 cases were analyzed. Two-thirds (66.6%) of the cases were at advanced stage (stage III & IV) at presentation. The five-year overall survivals for the whole cohort, oral cavity, oropharynx, hypopharynx and larynx were 24.1%, 25.91%, 19.2%, 13.4%, 38.0% respectively. Stage and treatment type were strong prognostic factors for all sites. An age ≥ 80 years was associated with poor survival in oral cavity and larynx cancer. Conclusions: The results revealed remarkably poor outcomes of the patients in the series, indicating a strong need to increase the proportion of early stage presentations and maximize the treatment efficacy to improving outcomes. Very old patients are of particular concern for treatment care of oral cavity and larynx cancer.

Objective: 14-3-3σ protein is well known for its tumor suppressive function in breast cancer. However, recent evidence has raised the possibility that the 14-3-3σ protein may also have an oncogenic function in certain cancer types. The aim of this study was to investigate the oncogenic function of 14-3-3σ in adenocarcinoma cell lines of the lung (A549, H358) and colon (HT-29).Material and Methods: siRNA against 14-3-3σ was used to suppress 14-3-3σ expression. Cell proliferation, cell-cycle distribution and expression of related molecules were determined by MTT, flow cytometry, and western blotting, respectively.Results: Down-regulation of 14-3-3σ significantly reduced the proliferation of A549 and H358 by 35.0% and 31.0%, respectively, and significantly induced cell cycle arrest at the G0/G1 and G2/M phases, respectively. Increased p21 expression by 43.0% was only observed in si-14-3-3σ-H358 cells. The si-14-3-3σ-HT-29 cells showed no alteration of cell proliferation and cell-cycle distribution but harbored reduced p53 expression by 56.0% and p27 expression by 67.0%.Conclusion: 14-3-3σ may have an oncogenic function in lung adenocarcinoma but play a different role in colon cancer.

Context.—The pathologic protocol for sentinel lymph node evaluation has yet to be standardized. Results from previous studies are troublesome to compare because they have been conducted on different sets of subjects with cancer. Objective.—To compare the detection of sentinel lymph node metastases by using step-sectioning methods at 20-μm and 150-μm intervals for the same patient with primary breast cancer. Design.—A total of 186, initially tumor-negative sentinel lymph nodes from a group of 80 patients with breast cancer were included. For all nodes, each paraffin block was cut serially to produce a total of 10 levels: 5 consecutive levels of sections for each of the 20-μm and 150-μm intervals. The nodal findings obtained at these intervals on hematoxylin-eosin and cytokeratin slides were compared by using the McNemar test. Results.—The overall detection rate for sentinel lymph node metastasis at intervals of 20 μm and 150 μm was 27.5% (22/80) and 20% (16/80), respectively. The overall agreement between the 20-μm and 150-μm sections was 82.5%. No macrometastasis was missed by either method. At the 20-μm interval, 2 cases of micrometastasis were missed, while 10 cases of isolated tumor cells were missed at the 150-μm interval. However, no statistical difference was observed for the final sentinel lymph node results with either method. (McNemar test, P = .18 for case-based results and P = .052 for nodal-based results). Conclusions.—The 20-μm and 150-μm interval step-sectioning methods produce comparable results for detection of metastatic deposits in sentinel lymph nodes.

Objective . The objective was to determine the prognostic significance of the immunohistochemical expressions of Bax, Bcl-2, and p53 in squamous cell carcinoma of the uterine cervix treated by radiotherapy alone. Methods . One hundred and seventy-four cases of squamous cell carcinoma of the cervix (stage Ib–IVa) diagnosed between January 1996 and December 1998 were investigated for Bax, Bcl-2, and p53 expressions and were correlated to the patients' survival. Results . The mean age of the patients was 54.1 with a range of 29–82 years. There were 23 cases with stage I (13.2%), 99 stage II (56.9%), 51 stage III (29.3%), and 1 case with stage IV (0.6%). The 5-year disease-free survival (DFS) was 70.50% and overall survival (OS) was 65.95%. Bax, Bcl-2, and p53 expressions were seen in 68.4%, 25.9%, and 77.6% of cases, respectively. In multivariate analysis by Cox's regression, age, stage, Bax, and Bcl-2 expressions appeared to be independent prognostic predictors of DFS. Bax expression was associated with good survival (hazard ratio, 0.47) while Bcl-2 expression was associated with poor survival (HR, 2.51). In addition, a combination of Bcl-2+/Bax+ was significantly associated with poorer DFS compared to Bcl-2−/Bax+ (HR 3.55). However, none of the markers or combinations was associated with OS. Conclusions . Evaluation of Bax and Bcl-2 expressions and their co-expression provide independent prognostic information for the clinical course of the disease and therefore could be developed as a prognostic indicator for cervical cancer.

The association of lifestyle habits and polymorphism of ADH2 and ALDH2 genes with the risk of esophageal cancer in Thai population was investigated in a hospital-based case-control study: 202 cases and 261 controls. The results of multivariate logistic analysis showed that alcohol consumption >60g/day, smoking >10 cigarettes/day and chewing betel >or=10 quids/day significantly increased risk (odds ratio (OR) 5.84, 95% confidence interval (CI) 3.15-10.83; 4.65, 95% CI 1.99-10.84; and 4.68, 95% CI 2.05-10.72, respectively). ADH2*1/*1 also increased the risk significantly (OR 1.56, 95% CI 1.01-2.39) while ALDH2 did not (OR of ALDH2*1/*2 1.57, 95% CI 0.89-2.76). However, the combined at risk genotypes, ADH2*1/*1 and ALDH2*1/*2 increased risk to four-fold. In addition, significant gene-environment interaction was found. Heavy drinkers >60g/d harboring ADH2*1/*1 or ALDH2*1/*2 had about an 11-fold increased risk.

p53 expression related to the aggressive infiltrative histopathological feature of basal cell carcinoma Aims: To determine whether the p53 protein expression which is involved in the genesis and progression of various malignant tumours may relate to age, sites or the aggressive histopathological feature of the basal cell carcinoma. Methods and results: One hundred and fifty-eight basal cell carcinoma specimens from Songklanakarind Hospital, southern Thailand, collected from January 1992 to December 2000, were examined by immunohistochemistry using polyclonal anti-p53-CM1 (Novocastra Laboratories, Newcastle, UK; dilution 1:700). p53 protein expression was demonstrated in 48.7% of cases. The multivariate analysis showed that the aggressive infiltrative histopathological type was significantly associated with p53 expression (odds ratio 2.95, 95% confidence interval 1.10–7.90), whereas age, sun-exposure site, cellular response and fibrosis were not. Conclusions: The p53 expression is found to be related to the aggressive histopathological feature, which may be of predictive value for the behaviour of basal cell carcinoma. However, this result does not support the relation between sun exposure inducing basal cell carcinoma and p53 protein expression.

Background Breast cancer is the second most common cause of cancer death in Thai women. Cancer registry data reveal a high prevalence of late-stage disease at diagnosis. The factors resulting in delay in Thailand have not yet been investigated. Objectives To determine the extent of, and the factors contributing to, delay in breast cancer care. Design Women with breast cancer who were first treated at Songklanagarind Hospital between June 1994 and June 1996 were interviewed with retrospective chart audits of care. Measures Dependent variables included patient delay (symptom recognition to first care) and system delay (first care to treatment). Independent variables tested included demographic factors, help-seeking behavior, and cancer knowledge. Nonparametric rank sum tests were used for univariate analysis, and Cox regression was used for multivariate analysis. Results Ninety-four cases were included in the study. The median patient and system delays were 4 weeks; 26.6% and 24.4% of patients, respectively, experienced patient and system delay >12 weeks. Only marital status (unmarried compared with married women) was significantly associated with patient delay (hazard ratio [HR] 2.78, 95% CI 1.23-6.25). Contacting a provincial hospital instead of a university hospital as first medical care (hazard ratio 2.50, 1.23-5.26), being given a diagnosis rather than being told nothing (HR 2.04, 1.14-3.57) and being given treatment rather than being immediately referred (HR 4.55, 2.22-9.09) were associated with system delay. Conclusions Patient delay and system delay in breast cancer care are important weaknesses of disease control in Thailand. Educational programs should target unmarried women, who are at higher risk of delay. System delay in hospitals outside the university needs to be improved by a good referral system.

Determine the incidence of FGFR3 mutations in Thai patients with bladder transitional cell carcinoma (TCC), and evaluate their correlation with pathological characteristics.One hundred twenty two frozen tissue samples from TCC patients were analyzed for mutations in exons 7, 10, and 15 of FGFR3 by polymerase chain reaction and direct DNA sequencing.FGFR3 mutations were detected in 22 of 122 cases (18%) studied, all of which were found within previously identified hotspots, including S249C (13 cases; 59%) and R248C (4 cases; 18%) in exon 7, and Y375C (5 cases; 23%) in exon 10, but no mutations in exon 15. Sixty-five patients (53%) were categorized as non-muscle-invasive TCC (pTa-pT1). The incidence of mutations is significantly higher in non-muscle-invasive tumors (28%) compared to the muscle-invading group (7%) (p0.01). Patients with grade (G) 1 TCC have significantly higher mutation frequency (40%) compared to other grades (4%) (p0.01). When T stage and grade were considered together, mutations were most commonly found in Ta-T1/G1 TCC (18/45 cases, 40%). Mean follow-up period was 45.1 months. Two-year and four-year overall survival (OS) was 70% and 56% respectively. Three-year OS in non-muscle-invasive TCC (80%) is significantly higher than that of muscle invading TCC (41%) (p0.01). However three-year OS in cases with an FGFR3 mutation (73%) is not significantly different from cases without a mutation (61%). In 16 cases with an FGFR3 mutation and recurrent disease, no mutations were detected in metachronous disease.The overall incidence of FGFR3 mutations in Thai patients with TCC was lower than similar reports from other ethnic groups. In the presented cases, although FGFR3 mutations were frequently detected in low-grade, non-muscle-invasive TCC, identical mutation was not conserved in metachronous disease, thereby precluding the use of this marker in detection of tumor recurrence.