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Classical swine fever (CSF) is a highly infectious and lethal multisystem disease caused by the classical swine fever virus (CSFV). This virus has resulted in huge economic losses in the porcine industry. Rapid detection of CSFV is needed in order to prevent and control the early transmission of CSFV. In this study, nine hybridoma cell lines that secrete monoclonal antibodies against CSFV (anti-CSFV-mAb) were prepared using the cell fusion and cell surface fluorescent immunosorbent assay (CSFIA). A rapid, sensitive, and specific fluorescent microsphere-based lateral flow immunoassay strip (FM-LFIAs) based on the use of paired CSFV-mAbs was developed. The sensitivity of the FM-LFIAs for CSFV detection was 5.28 ng/mL with a linear range from 9.77 to 625 ng/mL. During clinical sample assays, the FM-LFIAs results were consistent with the measurements obtained using the reverse transcription – polymerase chain reaction (RT-PCR), highlighting the practical application of FM-LFIAs for the on-site detection of CSFV.

Background Peroxiredoxin 1 (PRDX1) has been identified as a dual regulator of tumorigenesis. However, its expression, clinical significance, and biological function in nasopharyngeal carcinoma (NPC) remain unknown. This study aimed to explore the role and underlying mechanisms of PRDX1 in NPC. Materials and methods The expression of PRDX1 in NPC tissues was evaluated by immunohistochemistry, and the relationships between the expression of PRDX1 and clinical features and prognosis of NPC patients were analyzed. The effects of PRDX1 on NPC cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT) were examined. A tumor-bearing model of nude mouse was established to verify the function of PRDX1 in vivo. Results PRDX1 expression level was negatively associated with recurrence and metastasis of NPC. PRDX1 knockdown promoted NPC cell proliferation, migration, invasion and EMT in vitro, and enhanced tumor growth in vivo, while PRDX1 overexpression had opposite effects. Furthermore, transcriptome analysis showed that PRDX1 inhibited the activation of PI3K/AKT/TRAF1 signaling in NPC cells. Conclusion PRDX1 inhibits NPC by inhibiting the activation of PI3K/AKT/TRAF1 signaling. PRDX1 is a tumor suppressor in human NPC and may be a prognostic biomarker for NPC patients.

Mammalian embryogenesis begins with a totipotent zygote. Early embryogenesis can be recapitulated by aggregated extended pluripotent stem cells (EPSCs) in a 3D culture system. However, the efficiency of generating blastoids is low and whether other reported totipotent stem cells retained a similar capacity remains unknown. Here we show that spliceosomal repressed totipotent blastomere-like cells (TBLCs) form blastocyst-like structures when aggregated in 3D microwells with around 80% efficiency. TBLC-blastoids resemble blastocyst in morphology and cell-lineage allocation, show similar transcriptional profile with natural blastocyst and contain more TE cells and fewer undefined intermediate cells compared to blastoids from EPSCs. Moreover, TBLC-blastoids can develop beyond the implantation stage in vitro and induce decidualization after transferred into uterus. In summary, we supply an alternative cell type to generate ameliorated blastoids highly efficiently for studying early mouse embryogenesis.

The type B trichothecene mycotoxin deoxynivalenol (DON), colloquially known as “vomitoxin”, is the most commonly detected trichothecene in cereal-based foods, exerting acute and chronic toxic effects on animals and causing serious safety-related concerns. At the cellular and molecular levels, DON can inhibit macromolecule synthesis by binding to ribosomes and may disrupt cell proliferation, differentiation and apoptosis. However, the molecular mechanisms underlying the cytotoxicity of DON remain to be determined. Here, we identified β-catenin, the key signal transducer of the Wnt cascade, as a novel target of DON by quantitative real-time PCR and Western blot analysis in human embryonic kidney 293T and colorectal SW480 cells treated with DON at half IC50 (50 ng/mL for HEK293T and 1 μg/mL for SW480). Further analysis showed that neither posttranslational modification nor nuclear accumulation of β-catenin was affected post DON treatment. Moreover, we found that the β-catenin-dependent canonical Wnt signaling pathway, which regulates many biological processes during embryonic development and adult tissue homeostasis, was involved in DON-induced inhibition of cell proliferation. Then, we determined that the β-catenin/c-Myc axis was essential for this process, as the DON-induced inhibition of cell proliferation was efficiently rescued by restoration of β-catenin or c-Myc levels. Our results advance the current understanding of the molecular toxicological mechanism of DON and provide a new perspective on strategies for the prevention and control of mycotoxins.

Aflatoxin B1 (AFB1), a member of the aflatoxin family, is a common contaminant in foods and feeds, and AFB1 exposure is associated with various clinical conditions. Thus far, research on the toxicity of AFB1 has mainly focused on its induction of liver cancer, but little research has been reported on renal toxicity, especially with regards to the underlying molecular mechanisms. In this study, we found that AFB1 treatment significantly induced kidney damage and reduced kidney weight. The human kidney cell line HEK293T was used to further study the molecular mechanism of the toxicity of AFB1 to kidney cells. We found that AFB1 significantly and dose-dependently induced S phase arrest and upregulated p21 mRNA and protein expression. Upstream of p21, three negative regulators, PLK1, MYC, and PLD1, were significantly downregulated under AFB1 treatment. Consistently, p21 was upregulated, and PLK1, MYC and PLD1 were downregulated in mouse kidney after AFB1 treatment. Interestingly, AFB1 also decreased the physical interaction between PLK1 and MYC and weakened the stability of the MYC protein. Importantly, overexpression of PLK1, MYC and PLD1 significantly blocked the upregulation of p21 and attenuated the S phase arrest caused by AFB1. In summary, AFB1 markedly induces kidney damage and strongly induces S phase arrest by upregulating the expression of p21 via PLK1, PLD1 and MYC, which represents a noval mechanism of the renal toxicity of AFB1.

Cytochrome P450 1A1 (CYP1A1) is abundant in the kidney, liver, and intestine and is involved in the phase I metabolism of numerous endogenous and exogenous compounds. Therefore, exploring the regulatory mechanism of its basal expression in humans is particularly important to understand the bioactivation of several procarcinogens to their carcinogenic derivatives. Site-specific mutagenesis and deletion of the transcription factor binding site determined the core cis-acting elements in the human CYP1A1 proximal and distal promoter regions. The proximal promoter region [overlapping xenobiotic-responsive element (XRE) and GC box sequences] determined the basal expression of CYP1A1. In human hepatocellular carcinoma cells (HepG2) with aryl hydrocarbon receptor (AhR) or specificity protein 1 (Sp1) knockdown, we confirmed that AhR and Sp1 are involved in basal CYP1A1 expression. In HepG2 cells overexpressing either AhR or Sp1, AhR determined the proximal transactivation of basal CYP1A1 expression. Via DNA affinity precipitation assays and ChIP, we found that AhR bound to the promoter and recruited Sp1 to transactivate CYP1A1 expression. The coordinated interaction between Sp1 and AhR was identified to be DNA mediated. Our work revealed a basal regulatory mechanism of an interesting human gene by which AhR interacts with Sp1 through DNA and recruits Sp1 to regulate basal CYP1A1 expression.

Gastric cancer (GC) is a leading cause of cancer-related mortality worldwide, because of the low efficacy of current therapeutic strategies. Estrogen-related receptor γ (ERRγ) was previously showed as a suppressor of GC. However, the mechanism and effective therapeutic method based on ERRγ is yet to be developed. The expression levels of ERRγ, EZH2, and FOXM1 were detected by immunohistochemistry, qRT-PCR, and western blot. The regulatory mechanisms of ERRγ and FOXM1 were analyzed by ChIP, EMSA, and siRNA. The effects of EZH2 inhibitor (GSK126) or/and ERRγ agonist (DY131) on the tumorigenesis of gastric cancer cell lines were examined by cell proliferation, transwell migration, wound healing, and colony formation assays. Meanwhile, the inhibitory effects of GSK126 or/and DY131 on tumor growth were analyzed by xenograft tumor growth assay. The expression of ERRγ was suppressed in tumor tissues of GC patients and positively correlated with prognosis, as opposed to that of EZH2 and FOXM1. EZH2 transcriptionally suppressed ERRγ via H3K27me3, which subsequently activated the expression of master oncogene FOXM1. The combination of GSK126 and DY131 synergistically activated ERRγ expression, which subsequently inhibited the expression of FOXM1 and its regulated pathways. Synergistic combination of GSK126 and DY131 significantly inhibited the tumorigenesis of GC cell lines and suppressed the growth of GC xenograft. The FOXM1 signaling pathway underlying the ERRγ-mediated gastric cancer suppression was identified. Furthermore, combined treatment with EZH2 inhibitor and ERRγ agonist synergistically suppressed GC progression by inhibiting this signaling pathway, suggesting its high potential in treating GC patients.

Deoxynivalenol (DON) is a type B trichothecene mycotoxin that exerts multiple toxic effects on plants, animals and humans. Several reports have shown that DON leads to G2/M cell cycle arrest. However, its molecular mechanism is still unclear. In this study, we showed that DON induced strong G2/M cell cycle arrest in HepG2 cells, and the cell cycle-inhibitory protein p21 was highly upregulated by DON. Further analysis showed that the cell cycle regulating gene EGR1 was highly induced by DON and that EGR1 knockdown abolished the upregulation of p21 and G2/M cell cycle arrest. Furthermore, we showed that the induction of EGR1 was regulated by the stress-responsive transcription factor ATF3. ATF3ΔZip2a/2b, which is a DNA binding domain truncated isoform of ATF3, was upregulated by DON. ATF3 knockdown weakened the expression induction of EGR1 and G2/M cell cycle arrest by DON. Moreover, the upregulation of ATF3ΔZip2a/2 highly depended on the enhanced presence of histones H3K9ac and H3K27ac. H3K9ac and H3K27ac were enriched at the promoter region of ATF3 following the DON treatment, and the knocking down of the genes responsible for H3K9ac and H3K27ac abolished the upregulation of ATF3 by DON. In summary, we found that DON induced G2/M cell cycle arrest by sequentially inducing the expression of ATF3ΔZip2a/2b, EGR1 and p21, and EGR1 played an essential role in this process, which is a novel molecular mechanism of cell cycle arrest by DON and is important for understanding its toxicology.

Chronic stress could induce cancer metastasis by constant activation of the sympathetic nervous system, while cellular mechanism remains obscure. The aim of this research is to explore the metastasis associated negative effect of chronic stress. The analysis of transcriptome sequencing implied that activation of STAT3 signaling pathway by downregulated miR-337-3p might be a potential mechanism to induce epithelial to mesenchymal transition (EMT) of cancer cell and promote metastasis under chronic stress. We also verified this biological process in further experiments. Downregulation of miR-337-3p could downregulate E-cadherin expression and upregulate vimentin expression in vitro and in vivo. STAT3, related signal pathways of which are involved in metastasis regulation, was directly targeted by miR-337-3p. In conclusion, the above results denoted that activation of miR-337-3p/STAT3 axis might be a potential pathway for the increasing metastasis of breast cancer under chronic stress.

Aflatoxin B

The feedback active noise control (ANC) can be seen as a predictor, the conventional method based on filtered-x least mean square (FXLMS) algorithm can only be useful for linear and tonal noise, but for nonlinear and broadband noise, it is useless. The feedback ANC using functional link artificial neural networks (FLANN) based on filtered-s least mean square (FSLMS) algorithm can reduce some nonlinear noise such as chaotic noise, but the noise cancellation performance is not very well, at the same time, it is not useful to random noise. To solve the problem above, a new feedback ANC using wavelet packet FXLMS (WPFXLMS) algorithm is proposed in this paper. By decomposing the broadband noise into several band-limited parts which are predictable and each part is controlled independently, the proposed algorithm can not only suppress the chaotic noise, but also mitigate the random noise. Compared with FXLMS and FSLMS algorithms, proposed WPFXLMS algorithm also holds the best performance on noise cancellation. Numerous simulations are conducted to demonstrate the effectiveness of the proposed WPFXLMS algorithm.

Objectives The objective of the study is to develop a novel tool—the Burnout Battery—for briefly screening burnout among oncology professionals in China and assessing its validity. Methods A multicenter study was conducted in doctors and nurses of the oncology departments in China from November 2014 to May 2015. The Burnout Battery was administered with the Maslach Burnout Inventory-Human Services Survey (MBI-HSS) and the Doctors' Job Burnout Questionnaire. Results Of 538 oncology doctors and nurses who completed all the survey, using MBI-HSS as the standard tool for measuring burnout, 52% had emotional exhaustion, 39.4% had depersonalization, and 59.3% had a low sense of personal accomplishment. Receiver operating characteristic curve analyses showed that the best cut-off of the Burnout Battery was the battery with 3 bars, which yielded best sensitivity and specificity against all the 3 subscales of MBI-HSS. With this cut-off, nearly half of Chinese oncology professionals (46.8%) had burnout. The Burnout Battery correlated significantly with subscales of the MBI-HSS and the Doctors' Job Burnout Questionnaire. In multiple logistic regression analysis, those who worked more than 60 hours per week and who thought clinical work was the most stressful part of their job were more likely to experience burnout. Conclusion Chinese oncology professionals exhibit high levels of burnout. The Burnout Battery appears to be a simple and useful tool for screening burnout. Working long hours and perceiving clinical work as the most stressful part of the job were the main factors associated with burnout.

Background: Death with dignity (DWD) refers to the refusal of life-prolonging measures for terminally ill patients by “living wills” forms in advance. More and more oncology physicians are receiving DWD requests from advance cancer patients in mainland China. Objective: The study objective was to investigate the attitudes of Chinese oncology physicians toward the legalization and implementation of DWD. Methods: A questionnaire investigating the understanding and attitudes toward DWD was administered to 257 oncology physicians from 11 hospitals in mainland China. Results: The effective response rate was 86.8% (223/257). The majority of oncology physicians (69.1%) had received DWD requests from patients. Half of the participants (52.5%) thought that the most important reason was the patients' unwillingness to maintain survival through machines. One-third of participants (33.0%) attributed the most important reason to suffering from painful symptoms. Most oncology physicians (78.9%) had knowledge about DWD. A fifth of respondents did not know the difference between DWD and euthanasia, and a few even considered DWD as euthanasia. The majority of oncology physicians supported the legalization (88.3%) and implementation (83.9%) of DWD. Conclusions: Many Chinese oncology physicians have received advanced cancer patients' DWD requests and think that DWD should be legalized and implemented. Chinese health management departments should consider the demands of physicians and patients. It is important to inform physicians about the difference between DWD and euthanasia, as one-fifth of them were confused about it.

Deoxynivalenol (DON) is a mycotoxin produced by multiple Fusarium species that often contaminates cereals and threatens human and animal health. A wide range of cytotoxic effects, such as the induction of DNA damage, an increase in mitochondrial permeability and the inhibition of macromolecule synthesis, have been reported. However, the effects of DON on cell migration—a fundamental process in living cells critical for normal development, immune responses, and disease processes—and the mechanism underlying these effects are still unclear. Here, we showed that DON significantly inhibited the migration of MRC-5, CCD-18Co, HCT116 and WM793 cells at 50 ng/ml, 50 ng/ml, 400 ng/ml and 250 ng/ml, respectively, which maintained cell viability at 90%. Further analysis showed that DON inhibited the expression of tumour endothelial marker 8 (TEM8), a key gene in cell migration. Furthermore, we showed that DON inhibited the expression of TEM8 through increasing the level of H3K27me3 in the TEM8 promoter. Finally, overexpression of TEM8 or treating by H3K27me3-specific inhibitor GSK126 attenuated the inhibitory effect of DON on cell migration. In summary, low doses of DON at approximately dietary exposure significantly inhibited cell migration by downregulating the expression of TEM8 in a manner mediated by H3K27me3, which may generate increasing concerns for the risk of DON exposure.

The development of biosensors that are portable, low-cost, and quantitative has long been sought for rapid, on-site, and timely detection of avian influenza virus (AIV). In this study, an antibody-based Raman lateral flow immunoassay strip was developed to detect AIV H7N9. This LFIA strip used a novel core-shell structure material, AuAg4−ATP@AgNPs, as a Raman probe. An antibody specific for AIV and goat anti-mouse IgG antibody were immobilized on a nitrocellulose membrane as the test and control lines, respectively. Accumulation of antibody-virus-antibody-Raman probe complex at the test line could be visualized by the naked eye, and the Raman signal could be quantified using a portable Raman instrument. The testing process for the SERS-based LFIA strips could be completed in 20 min, which avoided the time-cost of current methods for AIV analysis. In our SERS-based biosensor, we estimated the limit of detection (LOD) for H7N9 to be 0.0018 HAU. This value is approximately three orders of magnitude more sensitive than the corresponding HA assays. When testing real sample, the results of the strip test were in accordance with those from real-time PCR testing. In conclusion, the SERS-based LFIA strip proposed in this study shows tremendous potential to detect targets quickly and sensitively using an elegantly simple method.

Norepinephrine (NE) has been implicated in epithelial–mesenchymal transition (EMT) of cancer cells. However, the underlying mechanism is poorly understood. The goal of this study was to explore the effect of NE on cancer cell EMT and to investigate the potential mechanism. HT-29 and A549 cells were treated with NE, β-adrenergic receptor (β-AR) antagonist (propranolol) or inhibitor of transforming growth factor-β (TGF-β) receptor type I kinase (Ly2157299). Morphology of cells was observed with optical and electron microscope and immunofluorescence staining. Cellular migration and invasion were tested with transwell migration assay and Matrigel invasion assay, respectively. TGF-β1 and cyclic adenosine monophosphate (cAMP) were quantified. EMT markers and signaling pathway were measured by RT-PCR and western blot. NE stimulated TGF-β1 secretion and intracellular cAMP synthesis, induced morphological alterations in HT-29 and A549 cells, and enhanced their ability of migration and invasion. EMT markers induction was observed in NE-treated cancer cells. The effect of NE could be inhibited by propranolol or Ly2157299. β-AR/TGF-β1 signaling/p-Smad3/Snail and β-AR/TGF-β1 signaling/HIF-1α/Snail were two signaling pathways. These findings demonstrated that TGF-β1 signaling pathway was a significant factor of NE-induced cancer cells EMT. The data also suggested that psychological stress might be a risk factor which enhances the ability of migration or invasion of cancer cells.

Wearable electronic systems have been and will continue to be utilized in both civil and military uses. Strong noise environments derived from large vehicles (e.g. ships, aircrafts, or military tanks) seriously affect the quality of speech communications especially for wearable systems without hermetic packaging. Bone conduction technology through the acquisition of skull vibration is able to obtain voice information, which can effectively avoid the interference of acoustic noise on the speech. In this paper, a high-performance wearable bone-conducted speech enhancement system is developed to reduce the distortion of the environment noises. Both bone-conducted and air-conducted voices are used to train the equalization function of bone-conducted speech to air-conducted speech based on the deep neural network, and spectrum coefficients of linear predictive coding is taken as feature information for conversion model.

The feedback Active Noise Control (ANC) is mainly used to reduce tonal noise, but for broadband noise like chaotic noise, it is less involved other than using filtered-s least mean square (FSLMS) algorithm. Though the feedback ANC based on FSLMS algorithm is successfully used to reduce chaotic noise, there are still some drawbacks such as slower convergence speed, larger steady-state error and heavier computational load. To solving these problems, a novel feedback ANC system using recursive FSLMS (RFSLMS) algorithm is proposed to reduce chaotic noise in this paper. Compared with conventional feedback ANC based FSLMS algorithm, the proposed scheme holds faster convergence speed and less steady-state error. Extensive simulations are conducted to demonstrate the effectiveness of the proposed nonlinear feedback ANC based RFSLMS algorithm.

Sound source location based on General Cross-correlation can be divided into two parts—time delay estimation and location estimation. Considering the cost and calculation speed, the location system based on GCC receives more and more concern from researchers. This paper provides a new approach to improve the accuracy of location estimation using signals from two microphones. For that reverberation carries information of location of acoustic source, we can separate the detail which contains information of sound source under assumption of knowing coordinate of microphones. This method can be applied to many aspects especially for humanoid robot.

In this paper, a variable step-size filtered-x LMS (VSS-FXLMS) algorithm is proposed for a typical narrowband active noise control system. The new algorithm converges much faster than the conventional FXLMS algorithm does, and indicates a convergence rate quite similar to that of the filtered-x recursive least square (FXRLS) algorithm in stationary noise environments. It also considerably outperforms these two existing algorithms in nonstationary situations. The proposed algorithm requires some more computations as compared with the FXLMS algorithm; however, its computational complexity is significantly less than that of the FXRLS algorithm. Numerous simulations for stationary and nonstationary scenarios are conducted to demonstrate the superior performance of the proposed VSS-FXLMS algorithm as compared with the FXLMS and the FXRLS algorithms.

By analyzing the theory of functional link artificial neural network (FLANN) structure based on filtered-s least mean square (FSLMS) algorithm which is usually used in the nonlinear active noise control (NANC) system, it can be found that the controller coefficients of nonlinear parts are multiple related, this problem causes much unbalance to calculate these coefficients and restraints the performance of FSLMS algorithm. To solve this issue, a modified FSLMS (MFSLMS) algorithm is proposed in this paper, it can weaken these multiple relationships greatly by adding a corrective filter before trigonometric expansion. Compared with conventional FSLMS algorithm and its other improved versions, MFSLMS algorithm not only performs better on noise cancellation, but also has less computational complexity. Extensive simulations are conducted to demonstrate the effectiveness of the proposed algorithm.

Avian pathogenic Escherichia coli (APEC) infections are a very important problem in the poultry industry. PhoP-PhoQ is a two-component system that regulates virulence genes in APEC. In this study, we constructed strains that lacked the PhoP or PhoQ genes to assess regulation of APEC pathogenicity by the PhoP-PhoQ two-component system. The PhoP mutant strain AE18, PhoQ mutant strain AE19, and PhoP/PhoQ mutant strain AE20 were constructed by the Red homologous recombination method. Swim plates were used to evaluate the motility of the APEC strains, viable bacteria counting was used to assess adhesion and invasion of chick embryo fibroblasts, and Real-Time PCR was used to measure mRNA expression of virulence genes. We first confirmed that AE18, AE19, and AE20 were successfully constructed from the wild-type AE17 strain. AE18, AE19, and AE20 showed significant decreases in motility of 70.97%, 83.87%, and 37.1%, respectively, in comparison with AE17. Moreover, in comparison with AE17, AE18, AE19, and AE20 showed significant decreases of 63.11%, 65.42%, and 30.26%, respectively, in CEF cell adhesion, and significant decreases of 59.83%, 57.82%, and 37.90%, respectively, in CEF cell invasion. In comparison with AE17, transcript levels of sodA, polA, and iss were significantly decreased in AE18, while transcript levels of fimC and iss were significantly decreased in AE19. Our results demonstrate that deletion of PhoP or PhoQ inhibits invasion and adhesion of APEC to CEF cells and significantly reduces APEC virulence by regulating transcription of virulence genes.

Avian pathogenic Escherichia coli (APEC) is a major bacterial infectious disease that may lead to local or systemic infections in chickens with clinical manifestations. The irp2-fyuA gene cluster has been confirmed to be the main genes involved in the synthesis of HPI. The objective of this study was to determine the influence of the irp2 and fyuA genes in the high pathogenicity island (HPI) of avian pathogenic Escherichia coli (APEC) on its pathogenicity by knocking out these genes. The ΔAE17 (lacking irp2) and ΔΔAE17 (lacking irp2 and fyuA) strains of APEC were constructed. The ΔAE17 and ΔΔAE17 strains showed significantly impaired capacity to adhere onto DF-1 cells. The LD50 results indicated that the virulence of the ΔAE17 and ΔΔAE17 strains was decreased in comparison with that of the AE17 strain. We concluded that the knock-out of the core HPI genes weakened APEC adhesion onto DF-1 cells, inhibited transcription of virulence genes, and reduced pathogenicity in chicks. The effects of genetic deletion of irp2 and fyuA on APEC were more severe than those produced by deletion of irp2 only, indicating that irp2 and fyuA co-regulate APEC pathogenicity.

The objective is to assess how cancer patients know about their diagnosis what they know about their real stage, and the relationship between cancer stage and psychological distress.A questionnaire including the Distress Thermometer was delivered to 422 cancer inpatients. Multivariate logistic regression analysis was used to estimate odds ratios (OR) and 95% confidence intervals (CI).Most of patients (68.7%) knew the bad news immediately after diagnosis. Half of patients knew their diagnosis directly from medical reports. Nearly one third of patients were informed by doctors. Cancer stages, which patients believed, differed significantly from their real disease stages (P0.001). Over half of patients did not know their real disease stages. Patients with stage I-III cancer were more likely to know their real disease stage than patients with stage IV cancer (P0.001). Distress scores of cancer patients were determined by the real cancer stage (P=0.012), not the stage which patients believed.Although most of participants knew the bad news immediately after diagnosis, less than half of them knew their real disease stage. Patient with stage I-III cancer was more likely to know the real disease stage and had a DT score4 than patient with stage IV disease.