Association of caffeine intake with all-cause and cardiovascular mortality in diabetes and prediabetes.

BACKGROUD: The association between caffeine intake and mortality in prediabetes and diabetes is not well defined. This study was designed to investigate the association between caffeine intake and all-cause mortality and cardiovascular disease (CVD) mortality in adults with prediabetes and diabetes in the United States. METHODS: This analysis included 18,914 adult patients with diabetes and prediabetes from the National Health and Nutrition Examination Survey (NHANES) 2003-2018. Follow-up extended to December 31, 2019. Weighted Cox proportional hazards regression models were used to estimate the hazard ratios (HR) and 95% confidence intervals (CI) for all-cause mortality and CVD mortality. RESULTS: During 142,460 person-years of follow-up, there were 3,166 cases of all-cause mortality and 1,031 cases of CVD mortality recorded. In the fully adjusted models, caffeine intake showed a significant dose-response association with the risk of all-cause mortality and CVD mortality in individuals with diabetes and prediabetes. When comparing extreme quartiles of caffeine intake, the multivariable-adjusted hazard ratio for all-cause mortality was 0.78 (0.67-0.91) (P for trend = 0.007); however, there was no significant association with the risk of CVD mortality. Results remained consistent in stratified analyses by sex, age, race/ethnicity, education level, family income-poverty ratio, BMI, hypertension, smoking status, alcohol intake, and HEI-2015. CONCLUSIONS: This study suggests that caffeine intake is significantly inversely associated with the risk of all-cause mortality in individuals with diabetes and prediabetes. In individuals with prediabetes, there is also a significant inverse association between caffeine intake and CVD events, but this association is not present in those with diabetes.

INPP5E Regulates the Distribution of Phospholipids on Cilia in RPE1 Cells.

BACKGROUND: Primary cilia are static microtubule-based structures protruding from the cell surface and present on most vertebrate cells. The appropriate localization of phospholipids is essential for cilia formation and stability. INPP5E is a cilia-localized inositol 5-phosphatase; its deletion alters the phosphoinositide composition in the ciliary membrane, disrupting ciliary function. METHODS: The EGFP-2xP4MSidM, PHPLCδ1-EGFP, and SMO-tRFP plasmids were constructed by the Gateway system to establish a stable RPE1 cell line. The INPP5E KO RPE1 cell line was constructed with the CRISPR/Cas9 system. The localization of INPP5E and the distribution of PI(4,5)P2 and PI4P were examined by immunofluorescence microscopy. The fluorescence intensity co-localized with cilia was quantified by ImageJ. RESULTS: In RPE1 cells, PI4P is localized at the ciliary membrane, whereas PI(4,5)P2 is localized at the base of cilia. Knocking down or knocking out INPP5E alters this distribution, resulting in the distribution of PI(4,5)P2 along the ciliary membrane and the disappearance of PI4P from the cilia. Meanwhile, PI(4,5)P2 is located in the ciliary membrane labeled by SMO-tRFP. CONCLUSIONS: INPP5E regulates the distribution of phosphoinositide on cilia. PI(4,5)P2 localizes at the ciliary membrane labeled with SMO-tRFP, indicating that ciliary pocket membrane contains PI(4,5)P2, and phosphoinositide composition in early membrane structures may differ from that in mature ciliary membrane.

Dynamic changes of endothelial and stromal cilia are required for the maintenance of corneal homeostasis.

Primary cilia are distributed extensively within the corneal epithelium and endothelium. However, the presence of cilia in the corneal stroma and the dynamic changes and roles of endothelial and stromal cilia in corneal homeostasis remain largely unknown. Here, we present compelling evidence for the presence of primary cilia in the corneal stroma, both in vivo and in vitro. We also demonstrate dynamic changes of both endothelial and stromal cilia during corneal development. In addition, our data show that cryoinjury triggers dramatic cilium formation in the corneal endothelium and stroma. Furthermore, depletion of cilia in mutant mice lacking intraflagellar transport protein 88 compromises the corneal endothelial capacity to establish the effective tissue barrier, leading to an upregulation of α-smooth muscle actin within the corneal stroma in response to cryoinjury. These observations underscore the essential involvement of corneal endothelial and stromal cilia in maintaining corneal homeostasis and provide an innovative strategy for the treatment of corneal injuries and diseases.

A crosswalk on the genetic and conventional strategies for enhancing astaxanthin production in Haematococcus pluvialis.

Astaxanthin is a naturally occurring xanthophyll with powerful: antioxidant, antitumor, and antibacterial properties that are widely employed in food, feed, medicinal and nutraceutical industries. Currently, chemical synthesis dominates the world's astaxanthin market, but the increasing demand for natural products is shifting the market for natural astaxanthin. Haematococcus pluvialis (H. pluvialis) is the factory source of natural astaxanthin when grown in optimal conditions. Currently, various strategies for the production of astaxanthin have been proposed or are being developed in order to meet its market demand. This up-to-date review scrutinized the current approaches or strategies that aim to increase astaxanthin yield from H. pluvialis. We have emphasized the genetic and environmental parameters that increase astaxanthin yield. We also looked at the transcriptomic dynamics caused by environmental factors (phytohormones induction, light, salt, temperature, and nutrient starvation) on astaxanthin synthesizing genes and other metabolic changes. Genetic engineering and culture optimization (environmental factors) are effective approaches to producing more astaxanthin for commercial purposes. Genetic engineering, in particular, is accurate, specific, potent, and safer than conventional random mutagenesis approaches. New technologies, such as CRISPR-Cas9 coupled with omics and emerging computational tools, may be the principal strategies in the future to attain strains that can produce more astaxanthin. This review provides accessible data on the strategies to increase astaxanthin accumulation natively. Also, this review can be a starting point for new scholars interested in H. pluvialis research.

Hsa-miR-301a-3p inhibited the killing effect of natural killer cells on non-small cell lung cancer cells by regulating RUNX3.

BACKGROUND: Non-small cell lung cancer (NSCLC) is the most commonly diagnosed solid tumor. Natural killer (NK) cell-based immunotherapy is a promising anti-tumor strategy in various cancers including NSCLC. OBJECTIVE: We aimed to investigate the specific mechanisms that regulate the killing effect of NK cells to NSCLC cells. METHODS: Reverse transcription-quantitative PCR (RT-qPCR) assay was applied to measure the levels of hsa-microRNA (miR)-301a-3p and Runt-related transcription factor 3 (RUNX3). Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of IFN-γ and TNF-α. Lactate dehydrogenase assay was applied to detect the killing effect of NK cells. Dualluciferase reporter assay and RNA immunoprecipitation (RIP) assay were carried out to confirm the regulatory relationship between hsa-miR-301a-3p and RUNX3. RESULTS: A low expression of hsa-miR-301a-3p was observed in NK cells stimulated by IL-2. The levels of IFN-γ and TNF-α were increased in NK cells of the IL-2 group. Overexpression of hsa-miR-301a-3p reduced the levels of IFN-γ and TNF-α as well as the killing effect of NK cells. Furthermore, RUNX3 was identified to be a target of hsamiR-301a-3p. hsa-miR-301a-3p suppressed the cytotoxicity of NK cells to NSCLC cells by inhibiting the expression of RUNX3. We found hsa-miR-301a-3p promoted tumor growth by suppressing the killing effect of NK cells against NSCLC cells in vivo. CONCLUSIONS: Hsa-miR-301a-3p suppressed the killing effect of NK cells on NSCLC cells by targeting RUNX3, which may provide promising strategies for NK cell-based antitumor therapies.

Emphasis on the clinical relationship between alpha-fetoprotein and hepatoid adenocarcinoma of the stomach: a retrospective study.

BACKGROUND: Hepatoid adenocarcinoma of the stomach (HAS) is a highly malignant and rare extrahepatic tumor. The prognosis is controversial because of its rarity and the lack of multi-center cohort studies, especially on the influence of serum Alpha-fetoprotein (AFP) level on prognosis. We aimed to analyze the clinicopathological characteristics and prognosis of HAS, particularly the effect of serum AFP on the prognosis of HAS. METHODS: We retrospectively reviewed clinical data of one HAS patient treated at our institution in 2019 and of 252 patients reported between 1984 and 2020 in research databases. RESULTS: Among these patients, 60.1% were > 60 years, 51% had lesions in the gastric antrum, and 51.0% (73/143) had the ulcerative lesion type. The preoperative elevated levels of serum alpha-fetoprotein (AFP) were detected in most patients (76.7%). Lymph-node (84.6%) and preoperative liver metastasis (39.1%) were often found. The high-AFP group was characterized by a higher rate of stage IV (P = 0.000682) and liver metastasis (P = 0.000068). The 1-, 3-and 5-year progression-free survival(PFS) rates were 41%, 18%, and 0%, and the 1-, 3-, and 5-year overall survival (OS) rates were 64%, 26%, and 21%, respectively. The survival analysis showed that OS was significantly shorter for HAS with high-AFP (> 300 ng/ml) than with low-AFP (≤ 300 ng/ml) (P = 0.023). The univariate analysis indicated that the OS of HAS was associated with tumor location, pTNM stage, lymph-node metastasis, surgical resection, and serum AFP > 300 ng/ml. However,the prognostic factors for PFS was only pTNM stage and surgical resection. The multivariate analysis confirmed that the independent prognostic factor affecting OS of HAS included pTNM stage and surgical resection. CONCLUSIONS: Liver metastasis was increasingly more likely with increasingly higher serum AFP, but the prognosis of HAS is not necessarily poor. Serum AFP level is an important prognostic indicator in HAS and should be monitored.

Oncology nursing on the move: a contemporary issue on Chinese oncology nursing in cancer care.

Cancers have become the primary cause of death among Chinese residents, seriously affecting their health and life. Oncology nursing is a specialized nursing practice focusing on cancer education, prevention, screening, early detection, and palliative and hospice care. China has made tremendous progress in developing oncology nursing. However, to ensure more individuals can get cancer care, the country's healthcare system still confronts several problems in oncology nursing that need to be addressed to ensure that more individuals can receive cancer care. This article reviews the current development of oncology nursing in China, especially in pain symptom control, palliative care, end-of-life care, education and training. The challenges faced in oncology nursing in China and the suggestions for developing oncology nursing in China are also discussed and proposed in this review. The growth of research on oncology nursing by Chinese nursing scholars and concerned policymakers is anticipated to ultimately improve oncology nursing and the quality of life of patients with cancer in China.

PCDH1 promotes progression of pancreatic ductal adenocarcinoma via activation of NF-κB signalling by interacting with KPNB1.

Uncontrolled growth, distant metastasis and chemoresistance are critical characteristics of pancreatic ductal adenocarcinoma (PDAC), and they result in high mortality; however, the mechanisms triggering these effects have not been fully investigated. In this study, we analysed a dataset in the Cancer Genome Atlas (TCGA) and identified PCDH1, a rarely studied transmembrane protein, as a novel prognostic marker in PDAC patients. We demonstrated that PCDH1 expression was upregulated in PDAC tissues, and its expression levels were associated with the depth of tumour invasion and lymph node metastasis. Patients with high PCDH1 levels showed poor overall survival (OS). We also investigated the biological significance of PCDH1 in PDAC cell growth, metastasis, and side population (SP) phenotype acquisition and explored the internal molecular mechanisms of PCDH1 action. Our results demonstrated that PCDH1 enhanced p65 nuclear localization by interacting with KPNB1, a well-characterized nuclear transporter, thereby activating the NF-κB signalling pathway and increasing its functional effects during PDAC progression. Hence, our results indicate that PCDH1 can be used as a negative prognostic marker and may be a potential therapeutic target for PDAC patients.

A novel four-gene signature predicts immunotherapy response of patients with different cancers.

BACKGROUND: Immune checkpoint blockade (ICB) therapy has demonstrated favorable clinical efficacy, particularly for advanced or difficult-to-treat cancer types. However, this therapy is ineffective for many patients displaying lack of immune response or resistance to ICB. This study aimed to establish a novel four-gene signature (CD8A, CD8B, TCF7, and LEF1) to provide a prognostic immunotherapy biomarker for different cancers. METHODS: Transcriptome profiles and clinical data were obtained from The Cancer Genome Atlas database. Multivariate Cox regression analysis was used to establish a four-gene signature. The R package estimate was used to obtain the immune score for every patient. RESULTS: Risk scores of the novel four-gene signature could effectively divided all patients into high- and low-risk groups, with distinct outcomes. The immune score calculated via the estimate package demonstrated that the four-gene signature was significantly associated with the immune infiltration level. Furthermore, the four-gene signature could predict the response to atezolizumab immunotherapy in patients with metastatic urothelial cancer. CONCLUSIONS: The novel four-gene signature developed in this study is a good prognostic biomarker, as it could identify many kinds of patients with cancer who are likely to respond to and benefit from immunotherapy.

Long Noncoding RNA FOXD2-AS1 Promotes Pancreas Adenocarcinoma Cell Invasion and Migration by Sponging miR-30a-3p to Upregulate COX-2.

INTRODUCTION: FOXD2-AS1 is known to promote the development of several cancers. However, its role in pancreatic adenocarcinoma (PAAD) is unclear. METHODS: Expression of FOXD2-AS1 and miR-30a-3p in PAAD patients was analyzed with RT-qPCR. A follow-up study was performed to analyze the prognostic value of FOXD2-AS1 for PAAD. Overexpression assays were performed to analyze the crosstalk between FOXD2-AS1 and miR-30a-3p. Cell invasion and migration were analyzed by transwell assays. RESULTS: Analysis of the TCGA dataset revealed that FOXD2-AS1 was upregulated in PAAD tissues compared to the non-cancer tissues (1.89 vs. 0.2 TPM), indicating potential involvement of FOXD2-AS1 in PAAD. Our own data also showed FOXD2-AS1 was overexpressed in PAAD. Moreover, high FOXD2-AS1 levels predicted poor survival. It is predicted that miR-30a-3p can bind FOXD2-AS1, while their overexpression did not affect each other's expression. Correlation analysis revealed a significant correlation between FOXD2-AS1 and COX-2. In addition, FOXD2-AS1 overexpression increased COX-2 level, while miR-30a-3p played an opposite role. FOXD2-AS1 and COX-2 overexpression increased PAAD cell invasion and migration. MiR-30a-3p played an opposite role and inhibited the effects of FOXD2-AS1 and COX-2 overexpression. CONCLUSION: FOXD2-AS1 may promote PAAD cell invasion and migration by sponging miR-30a-3p to upregulate COX-2.

Atherogenic index of plasma is related to coronary atherosclerotic disease in elderly individuals: a cross-sectional study.

BACKGROUND: Dyslipidaemia plays an important role in coronary atherosclerotic disease (CAD). The relationship between the atherogenic index of plasma (AIP) and CAD in elderly individuals was explored in this study. METHODS: Elderly individuals (age ≥ 65 years) who underwent coronary angiography from January 2016 to October 2020 were consecutively enrolled in the study. RESULTS: A total of 1313 individuals, including 354 controls (non-CAD) and 959 CAD patients, were enrolled. In univariate analysis of all populations, the adjusted AIP (aAIP) in the CAD group was 1.13 (0.96, 1.3), which was significantly higher than that in the controls [1.07 (0.89, 1.26)]. However, in subgroup analyses, this phenomenon was only present in males. In addition, further study showed that aAIP was positively related to CAD severity. In binary logistic regression analyses, after adjusting for sex, age, smoking status, primary hypertension (PH), type 2 diabetes mellitus (T2DM), heart rate (HR), white blood cell (WBC) and platelet (PLT), AIP remained independently related to CAD in elderly individuals and was superior to traditional and other nontraditional lipid indices. Subgroup analyses showed that AIP independently influenced CAD risk in males. Ultimately, sensitivity analyses were performed excluding all coronary emergencies, and the final results were similar. CONCLUSIONS: AIP was positively related to the risk and severity of CAD in elderly individuals and was superior to traditional and other nontraditional lipid profiles. However, this association only exists in elderly males.

RNA-binding protein RBM6 acts as a tumor suppressor gene to inhibit the progression of hepatocellular carcinoma.

PURPOSE: To investigate whether RBM6 can serve as a suppressor gene in hepatocellular carcinoma (HCC) and affect its progression. METHODS: QPCR and Western blot were carried out to measure RBM6 expression in tissue samples collected from HCC patients with different tumor sizes or in different stages. The relationship between overall survival (OS) and RBM6 expression in patients with HCC was analyzed using Kaplan-Meier survival method. Meanwhile, the effects of different factors on HCC progression were evaluated through Cox regression analysis. After over-expression of RBM6 in HepG2 and HB611 cells, the cell viability, cell migration and invasion abilities and apoptosis rate were assessed by cell counting kit-8 (CCK-8), transwell assay, and flow cytometry analysis, respectively. RESULTS: RBM6 expression, markedly down-regulated in HCC tissues, showed a great relevance to tumor size, TNM stage, and histological grade, and the survival rate of patients in high RBM6 expression group was higher than those in low RBM6 expression group. Besides, Cox regression analysis revealed that RBM6 expression, tumor size, TNM stage and histological grade were four independent factors affecting the OS of HCC patients. Moreover, in vitro cell experiments demonstrated that overexpression of RBM6 significantly attenuated the cell viability as well as the invasive ability while enhanced cell apoptosis. CONCLUSIONS: The low expression of RBM6 contributes to the improvement of the survival of patients with HCC. Therefore, RBM6 can serve as a tumor-suppressing gene to repress cell proliferation, migration and invasion and promote cell apoptosis, thereby affecting the progression of HCC.

Association between vein diameters, reflux characteristics, and clinical severity in patients with chronic venous insufficiency in Northwest China.

OBJECTIVE: Our goal was to summarize the relationship between vein diameters, reflux characteristics, and clinical severity in consecutive patients with chronic venous insufficiency (CVI) in Northwest China. METHODS: We evaluated 531 consecutive patients with CVI (249 women) who presented to the Department of Ultrasound of Xijing Hospital from September 2017 to July 2019. Reflux times and the mean diameters of the great saphenous, the small saphenous, and the calf perforator veins based on duplex ultrasound scans obtained in the standing position were recorded. Venous-specific assessment tools-the Heaviness, Achiness, Swelling, Throbbing, Itching (HASTI) score, the Venous Clinical Severity Score (VCSS), and the Clinical, Etiological, Anatomical, Pathophysiological (CEAP) class-were analyzed. Regression analysis was used to investigate the relationship between the clinical scores, vein diameters, and reflux times. A P value of less than .05 was considered statistically significant. RESULTS: We analyzed 531 consecutive patients with 728 limbs. The mean age was 55.24 ± 11.38 years; the mean body mass index (BMI) was 24.75 ± 3.49 kg/m2. Three hundred thirty-four patients (62.9%) presented with unilateral limb findings and 197 (37.1%), with bilateral limb involvement. No significant changes were noted in age and BMI across CEAP classes (F = 2.322 and F = 3.917, respectively; P > .05 for both). Both the HASTI score (r2 = 0.8741; P < .001) and the VCSS (r2 = 0.9257; P < .001) correlated with the CEAP class. The HASTI score strongly correlated with the mean diameters of the great saphenous and small saphenous veins (r2 = 0.9252, r2 = 0.6304, respectively; P < .001 for both) similarly to VCSS (r2 = 0.9396, r2 = 0.7195, respectively; P < .001 for both). The HASTI score and VCSS correlated equally with the mean diameters of the calf perforator veins (r = 0.7773 and r = 0.7781, respectively; P < .001 for both). In those with C6, both great saphenous vein (F = 4.608; P < .001) and small saphenous vein reflux times (F = 14.97; P < .001) were significantly higher than those in C1. Both the HASTI score and VCSS strongly associated with the reflux times of the great saphenous (r2 = 0.7706 and r2 = 0.8181, respectively; P < .001 for both) and small saphenous veins (r2 = 0.6470 and r2 = 0.7865, respectively; P < .001 for both). CONCLUSIONS: This analysis is one of the few epidemiologic studies of patients with CVI in Northwest China. Age and BMI did not correlate with CEAP class. Both the HASTI score and VCSS correlated strongly with the CEAP classification; vein diameters and reflux time in both the great saphenous vein and the small saphenous vein, indicating the validity of these outcome tools to venous hemodynamics and to CVI in general.

Prognostic significance of platelet-to-lymphocyte ratio in patients with nasopharyngeal carcinoma: a meta-analysis.

Aim: Several studies reported the association of platelet-to-lymphocyte ratio (PLR) and prognosis in nasopharyngeal carcinoma (NPC), but the results remain controversial. Therefore, we investigated the prognostic value of PLR in NPC through meta-analysis. Materials & methods: A comprehensive literature search of PubMed, Embase and Web of Science was performed. Results: A total of 9 studies comprising of 3459 patients with NPC were included. The data demonstrated that an increased PLR predicted poor overall survival, progression-free survival and distant metastasis-free survival. There was no significant association between PLR and sex, age, T stage, N stage, tumor node metastasis (TNM) stage or intensity-modulated radiotherapy. Conclusion: This meta-analysis revealed that PLR might be a potential predicative biomarker of poor prognosis in patients with NPC.

CTRP3 inhibits high glucose-induced human glomerular mesangial cell dysfunction.

C1q/tumour necrosis factor-related protein-3 (CTRP3) is a member of CTRP family, and its blood level is reduced in human and rodent models of obesity and diabetes. However, the role of CTRP3 in diabetic nephropathy remains unclear. This study was designed to examine the effects of CTRP3 on cell proliferation and extracellular matrix (ECM) accumulation in human glomerular mesangial cells (MCs) in response to high glucose (HG), and explore the potential molecular mechanisms. Our results demonstrated that the expression of CTRP3 was significantly decreased by HG stimulation in MCs. In addition, CTRP3 overexpression inhibited MCs proliferation, reactive oxygen species level, and ECM production in HG-stimulated MCs. Mechanistically, CTRP3 overexpression inhibited the activation of the Janus kinase 2/signal transducers and activators of transcription 3 (JAK2/STAT3) pathway in HG-stimulated MCs. Taken together, these findings indicated that CTRP3 attenuated HG-induced MC proliferation and ECM production through the inactivation of the JAK2/STAT3 signaling pathway. Thus, CTRP3 may be a potential therapeutic target for the treatment of diabetic nephropathy.

Duckweed (Lemna minor) as a model plant system for the study of human microbial pathogenesis.

BACKGROUND: Plant infection models provide certain advantages over animal models in the study of pathogenesis. However, current plant models face some limitations, e.g., plant and pathogen cannot co-culture in a contained environment. Development of such a plant model is needed to better illustrate host-pathogen interactions. METHODOLOGY/PRINCIPAL FINDINGS: We describe a novel model plant system for the study of human pathogenic bacterial infection on a large scale. This system was initiated by co-cultivation of axenic duckweed (Lemna minor) plants with pathogenic bacteria in 24-well polystyrene cell culture plate. Pathogenesis of bacteria to duckweed was demonstrated with Pseudomonas aeruginosa and Staphylococcus aureus as two model pathogens. P. aeruginosa PAO1 caused severe detriment to duckweed as judged from inhibition to frond multiplication and chlorophyll formation. Using a GFP-marked PAO1 strain, we demonstrated that bacteria colonized on both fronds and roots and formed biofilms. Virulence of PAO1 to duckweed was attenuated in its quorum sensing (QS) mutants and in recombinant strains overexpressing the QS quenching enzymes. RN4220, a virulent strain of S. aureus, caused severe toxicity to duckweed while an avirulent strain showed little effect. Using this system for antimicrobial chemical selection, green tea polyphenols exhibited inhibitory activity against S. aureus virulence. This system was further confirmed to be effective as a pathogenesis model using a number of pathogenic bacterial species. CONCLUSIONS/SIGNIFICANCE: Our results demonstrate that duckweed can be used as a fast, inexpensive and reproducible model plant system for the study of host-pathogen interactions, could serve as an alternative choice for the study of some virulence factors, and could also potentially be used in large-scale screening for the discovery of antimicrobial chemicals.

Immunohistochemical analysis of human arrest-defective-1 expressed in cancers in vivo.

The arrest-defective-1 (ARD1) gene has been reported to be important in yeast cell cycle regulation, and recent studies have shown that human arrest-defective-1 (hARD1) is related to cancer cell proliferation. To investigate the expression pattern of hARD1 protein in cancer tissues, immunohistochemical analysis was performed to analyze the hARD1 expression pattern in 400 cases of 19 types of common cancer and 133 non-cancer samples from 11 tissue types. hARD1 protein was expressed extensively in cancer tissues including glandular carcinoma and squamous cancer, and the positive rate was 71.5% (15/20) in urinary bladder cancer, 62.5% (30/48) in breast cancer and 57.1% (8/14) in cervical carcinoma. The average hARD1-positive rate was 52.3% in cancers and 31.5% in non-cancers, for which the difference was significant (p<0.005). Comparing the staining intensity of different fields in the same section, the hARD1 protein was highly accumulated in cancer cells when compared to the cells adjacent to cancer. The positive rate of breast and intestinal cancer was obviously higher than corresponding non-cancers (p<0.05 and 0.01). These findings suggest that the accumulation of hARD1 protein may be related to carcinogenesis of various types of cancer.