Comprehensive analysis of signaling lymphocyte activation molecule family as a prognostic biomarker and correlation with immune infiltration in clear cell renal cell carcinoma.

Clear cell renal cell carcinoma (ccRCC) is a common type of kidney cancer and accounts for 2-3% of all cancer cases. Furthermore, a growing number of immunotherapy approaches are being used in antitumor treatment. Signaling lymphocyte activation molecule family (SLAMF) members have been well studied in several cancers, whereas their roles in ccRCC have not been investigated. The present study comprehensively assessed the molecular mechanisms of SLAMF members in ccRCC, performed using The Cancer Genome Atlas database, with analysis of gene transcription, prognosis, biological function, clinical features, tumor-associated immune cells and the correlation with programmed cell death protein 1/programmed death-ligand 1 immune checkpoints. Simultaneously, the Tumor Immune Dysfunction and Exclusion algorithm was used to predict the efficacy of immune checkpoint blockade (ICB) therapy in patients with high and low SLAMF expression levels. The results demonstrated that all SLAMF members were highly expressed in ccRCC, and patients with high expression levels of SLAMF1, 4, 7 and 8 had a worse prognosis that those with low expression. SLAMF members were not only highly associated with immune activation but also with immunosuppressive agents. The level of immune cell infiltration was associated with the prognosis of patients with ccRCC with high SLAMF expression. Moreover, high ICB response rates were observed in patients with high expression levels of SMALF1 and 4. In summary, SLAMF members may serve as future potential biomarkers for predicting the prognosis of ccRCC and emerge as a novel immunotherapy target.

Potential drug targets for tumors identified through Mendelian randomization analysis.

According to the latest cancer research data, there are a significant number of new cancer cases and a substantial mortality rate each year. Although a substantial number of clinical patients are treated with existing cancer drugs each year, the efficacy is unsatisfactory. The incidence is still high and the effectiveness of most cancer drugs remains unsatisfactory. Therefore, we evaluated the human proteins for their causal relationship to for cancer risk and therefore also their potential as drug targets. We used summary tumors data from the FinnGen and cis protein quantitative trait loci (cis-pQTL) data from a genome-wide association study, and employed Mendelian randomization (MR) to explore the association between potential drug targets and nine tumors, including breast, colorectal, lung, liver, bladder, prostate, kidney, head and neck, pancreatic caners. Furthermore, we conducted MR analysis on external cohort. Moreover, Bidirectional MR, Steiger filtering, and colocalization were employed to validate the main results. The DrugBank database was used to discover potential drugs of tumors. Under the threshold of False discovery rate (FDR) < 0.05, results showed that S100A16 was protective protein and S100A14 was risk protein for human epidermal growth factor receptor 2-positive (HER-positive) breast cancer, phosphodiesterase 5A (PDE5A) was risk protein for colorectal cancer, and melanoma inhibitory activity (MIA) was protective protein for non-small cell lung carcinoma (NSCLC). And there was no reverse causal association between them. Colocalization analysis showed that S100A14 (PP.H4.abf = 0.920) and S100A16 (PP.H4.abf = 0.932) shared causal variation with HER-positive breast cancer, and PDE5A (PP.H4.abf = 0.857) shared causal variation with colorectal cancer (CRC). The MR results of all pQTL of PDE5A and MIA were consistent with main results. In addition, the MR results of MIA and external outcome cohort were consistent with main results. In this study, genetic predictions indicate that circulating S100 calcium binding protein A14 (S100A14) and S100 calcium binding protein A16 (S100A16) are associated with increase and decrease in the risk of HER-positive breast cancer, respectively. Circulating PDE5A is associated with increased risk of CRC, while circulating MIA is associated with decreased risk of NSCLC. These findings suggest that four proteins may serve as biomarkers for cancer prevention and as potential drug targets that could be expected for approval.

To Investigate the Occurrence and Development of Colorectal Cancer Based on the PI3K/AKT/mTOR Signaling Pathway.

Colorectal cancer (CRC) is the most common malignancy of the gastrointestinal, however, the underlying mechanisms of CRC remain largely unknown. New evidence suggests that the PI3K/AKT/mTOR pathway is closely related to CRC. PI3K/AKT/mTOR is a classical signaling pathway that is involved in a variety of biological processes, such as regulating cellular metabolism, autophagy, cell cycle progression, cell proliferation, apoptosis, and metastasis. Therefore, it plays a crucial role in the occurrence and development of CRC. In this review, we focus on the role of the PI3K/AKT/mTOR pathway in CRC, and its application of to the treatment of CRC. We review the importance of the PI3K/AKT/mTOR signaling pathway in tumorigenesis, proliferation and progression, and pre-clinical and clinical experience with several PI3K/AKT/mTOR pathway inhibitors in CRC.

MACC1 as a Potential Target for the Treatment and Prevention of Breast Cancer.

Metastasis associated in colon cancer 1 (MACC1) is an oncogene first identified in colon cancer. MACC1 has been identified in more than 20 different types of solid cancers. It is a key prognostic biomarker in clinical practice and is involved in recurrence, metastasis, and survival in many types of human cancers. MACC1 is significantly associated with the primary tumor, lymph node metastasis, distant metastasis classification, and clinical staging in patients with breast cancer (BC), and MACC1 overexpression is associated with reduced recurrence-free survival (RFS) and worse overall survival (OS) in patients. In addition, MACC1 is involved in BC progression in multiple ways. MACC1 promotes the immune escape of BC cells by affecting the infiltration of immune cells in the tumor microenvironment. Since the FGD5AS1/miR-497/MACC1 axis inhibits the apoptotic pathway in radiation-resistant BC tissues and cell lines, the MACC1 gene may play an important role in BC resistance to radiation. Since MACC1 is involved in numerous biological processes inside and outside BC cells, it is a key player in the tumor microenvironment. Focusing on MACC1, this article briefly discusses its biological effects, emphasizes its molecular mechanisms and pathways of action, and describes its use in the treatment and prevention of breast cancer.

Sintilimab combined with chemotherapy successfully treated a patient with advanced submandibular gland tumor.

Primary submandibular gland tumors are relatively rare. Due to its low incidence and broad spectrum phenotypic, biological and clinical heterogeneity types, a wide range of options have been developed to treat this tumor. To date, however, efficacious standard treatment regimens are lacking. Here, the authors present a case of a patient with an advanced submandibular gland tumor. Histological and imaging results diagnosed the case as stage IV submandibular gland adenocarcinoma with multiple metastases. The patient was subjected to systemic platinum-based chemotherapy combined with sintilimab. A primary lesion complete response was observed after six cycles of treatment. This case affirms the efficacy of the PD-1 inhibitor sintilimab combined with platinum-based chemotherapy as a first-line treatment for advanced submandibular gland tumors.

Primary submandibular gland tumors are very uncommon. There is a lack of standard treatment plans due to the low incidence and diverse clinical situations. The authors report a case of an advanced submandibular gland tumor patient who received platinum-based chemotherapy combined with sintilimab as the initial treatment plan. The tumor and multiple lung metastases significantly shrank after six cycles of treatment. This case indicates the regimen is effective for advanced submandibular gland tumor patients.

A systematic pan-cancer analysis identifies RIOK3 as an immunological and prognostic biomarker.

OBJECTIVES: Despite recent research highlighting the critical function of RIO kinase 3 (RIOK3) in a variety of malignancies, a comprehensive evaluation of RIOK3 in human tumors is absent. Our study helps to clarify the molecular mechanism of RIOK3 in carcinogenesis from multiple perspectives. METHODS: Our research looked into the potential oncogenic role of RIOK3 in 33 cancers using TCGA (The Cancer Genome Atlas), GTEx (Genotype-Tissue Expression Project), GEO (Gene Expression Omnibus) datasets, and several bioinformatics tools. RESULTS: RIOK3 expression in tumors is disordered compared to normal tissue, and it is highly linked with the level of MMR (Mismatch repair) gene mutations and DNA methyltransferase expression. According to univariate survival analysis, it could be used as an independent prognostic factor. Further investigation demonstrated that RIOK3 expression was correlated with cancer-associated fibroblast, neutrophil, and endothelial infiltration levels in kidney cancer and was positively correlated with the expression of immune checkpoint markers in different cancers. The functional pathways of RIOK3 also included cell-cell adhesion, protein phosphorylation, and innate immune-related functions. CONCLUSIONS: These findings suggest that RIOK3 could be used as an immunological and prognostic biomarker in various malignant tumors.

The remodeling roles of lipid metabolism in colorectal cancer cells and immune microenvironment.

Lipid is a key component of plasma membrane, which plays an important role in the regulation of various cell biological behaviors, including cell proliferation, growth, differentiation and intracellular signal transduction. Studies have shown that abnormal lipid metabolism is involved in many malignant processes, including colorectal cancer (CRC). Lipid metabolism in CRC cells can be regulated not only by intracellular signals, but also by various components in the tumor microenvironment, including various cells, cytokines, DNA, RNA, and nutrients including lipids. In contrast, abnormal lipid metabolism provides energy and nutrition support for abnormal malignant growth and distal metastasis of CRC cells. In this review, we highlight the remodeling roles of lipid metabolism crosstalk between the CRC cells and the components of tumor microenvironment.

PAICS is related to glioma grade and can promote glioma growth and migration.

Glioma is a common malignant tumour of the brain. In this study, we aimed to investigate diagnostic biomarkers and its role in glioma. Weighted gene co-expression network analysis (WGCNA) and Cytoscape software were used to screen the marker genes in glioma. RT-qPCR and Western blotting methods were performed to determine the expression of PAICS, ERCC1 and XPA genes in glioma tissues. Expression level of PAICS in different grades of glioma was examined by immunohistochemistry. CCK8 and Colony formation assays were used to detect cell proliferation. Cell adhesion assay was used to detect adhesion ability. Wound healing and transwell tests were used to detect cell migration ability. Flow cytometry was used to detect cell cycle and apoptosis. According to the predicted co-expression network, we identified the hub gene PAICS. Furthermore, we observed that PAICS expression level was up-regulated in glioma tissues compared with normal tissues, and the expression level was correlated with the grade of glioma. Moreover, we found PAICS can promote glioma cells proliferation and migration in vitro. Flow cytometry results showed that si-PAICS cells were stalled at the G1 phase compared with the si-NC cells and knocking down PAICS expression can increase apoptotic rate. PAICS can regulate the mRNA and protein levels of nucleotide excision repair pathway core genes ERCC1 and XPA. l-aspartic acid can affect the expression of PAICS and then inhibit glioma cell proliferation. Our results indicated that PAICS can promote glioma proliferation and migration. PAICS may act as a potential diagnostic marker and a therapeutic target for glioma.

Gender Differences of NLRP1 Inflammasome in Mouse Model of Alzheimer's Disease.

Background: There is a significant gender difference in the incidence and symptoms of Alzheimer's disease (AD), but its mechanisms are not completely understood. Recent studies showed that NLRP1 inflammasome was overexpressed in females under some pathological conditions such as nodular melanoma. Whether NLRP1 signals have a gender difference in AD has not been elucidated. This study was designed to investigate gender difference on the expressions of NLRP1 signals including NLRP1, Capase-1 and IL-1ß in the brains of APP/PS1+/- mice. Methods: Female and male APP/PS1+/- mice (30-weeks-old) were used in this study. Amyloid-ß (Aß) plaques were stained with Congo red dye and cell apoptosis was detected by TUNEL staining. Expressions of NLRP1, Capase-1 and IL-1ß were measured by immunofluorescent staining and Western blotting assay. Results: The numbers of Aß plaques in cortex and hippocampus and neuronal apoptosis in cortex were 4 and 2-folds in females than males, respectively (P < 0.001). The average size of Aß plaques in both cortex (females: 3527.11 ± 539.88 µm2 vs. males: 1920.44 ± 638.49 µm2) and hippocampus (females: 1931 ± 308.61 µm2 vs. males: 1038.55 ± 220.40 µm2) were also larger in females than males (P < 0.01). More interestingly, expressions of NLRP1, Caspase-1, and IL-1ß were markedly increased in the cortex of females as compared with males. Conclusions: These findings show that NLRP1 signals are higher in brains of female APP/PS1+/- mice than males, which may be related to the gender differences of AD.

Whole-exome sequencing and immunohistochemistry findings in von Hippel-Lindau disease.

BACKGROUND: von Hippel-Lindau (VHL) disease has a hereditary, autosomal dominant pattern, and multiple tumors can develop in multiple organs of a single patient. However, the exact mechanisms of tumorigenesis are unclear, and further studies are needed to clarify whether the same signaling pathways are involved in different VHL-related tumors. METHODS: Whole-exome sequencing (WES) of tumor and paired peripheral blood samples were performed for a VHL disease pedigree. A bioinformatics analysis was conducted to identify candidate somatic single-nucleotide variants (SNVs) present in all tumor tissues. Sanger sequencing was then used to validate the SNVs identified using WES. Immunohistochemistry was performed to analyze components of the mTOR pathway, which was abnormally activated in tumor tissues. RESULTS: Two hemangioblastomas and two renal cell carcinomas were sequenced. The bioinformatics analysis revealed a VHL somatic variant in all tumors; no other SNV was detected. Immunohistochemistry showed the abnormal expression of the phospho-S6 ribosomal protein in the hemangioblastomas, but not in the renal clear cell carcinomas. CONCLUSION: Except for a SNV in the VHL gene, no other somatic SNVs were detected using WES. The phospho-S6 ribosomal protein in the mTOR pathway is a potential target in VHL-related cerebellum hemangioblastomas.

Robotic enucleation for pediatric insulinoma with MEN1 syndrome: a case report and literature review.

BACKGROUND: A patient with a rare pediatric insulinoma and MEN1 syndrome was treated by robotic enucleation surgery. CASE PRESENTATION: We present a case of a 9-year-old girl presenting with repeated loss of consciousness, concomitant with a pale face, palpitations, and convulsions, which had persisted for 2 years and had been aggravated during the previous 2 months. She was previously misdiagnosed with epilepsy in another hospital. We further examined her while she was hospitalized. By combining her medical history and imaging examination and lab test results, a diagnosis of insulinoma was confirmed. Sanger-directed sequencing on a peripheral blood sample revealed an MEN1 gene mutation, indicating pediatric insulinoma with MEN1 syndrome. The patient underwent minimally invasive insulinoma enucleation surgery under the Da Vinci robot-assisted system with intraoperative ultrasound (IOUS) connected. The surgery was successfully completed within 65 min, and the girl recovered well postoperatively and no longer experienced symptoms of hypoglycemia. CONCLUSION: This is the first report of a case of pediatric insulinoma treated using robotic enucleation. This experience demonstrates the feasibility and safety of combining robotic surgery with the enucleation procedure as an excellent strategy for pediatric insulinoma.

IFI16 regulates HTLV-1 replication through promoting HTLV-1 RTI-induced innate immune responses.

Interferon (IFN)-inducible protein 16 (IFI16) regulates human immunodeficiency virus replication by inducing innate immune responses as a DNA sensor. Human T-lymphotropic virus type 1 (HTLV-1), a delta retrovirus family member, has been linked to multiple diseases. Here, we report that IFI16 expression is induced by HTLV-1 infection or HTLV-1 reverse transcription intermediate (RTI) ssDNA90 transfection. IFI16 overexpression decreases HTLV-1 protein expression, whereas IFI16 knockdown increases it. Furthermore, the knockdown of IFI16 is followed by impaired innate immune responses upon HTLV-1 infection. In addition, IFI16 forms a complex with ssDNA90 and enhances ssDNA90-triggered innate immune responses. Collectively, our data suggest a critical role for IFI16 during HTLV-1 infection by interacting with HTLV-1 RTI ssDNA90 and restricting HTLV-1 replication.

Predicting prognosis in resected esophageal squamous cell carcinoma using a clinical nomogram and recursive partitioning analysis.

BACKGROUND: Development demand of precise medicine in resectable esophageal squamous cell carcinoma (ESCC) require to recognize patients at high risk treated by surgery alone. Thus, our aim was to construct a clinical nomogram and recursive partitioning analysis (RPA) to predict long-term survival in ESCC treated by surgery alone. METHODS: Based on the patients with ESCC who treated by three-incisional esophagectomy and two-field lymphadenectomy alone, we identified and integrated significant prognostic factors for survival to build a nomogram. The nomogram was calibrated for overall survival (OS) and the predictive accuracy and discriminative ability was measured by concordance index (c-index) and Akaike information criterion (AIC). Based on the nomogram, the RPA was performed for risk stratification. RESULTS: A total of 747 patients were included for analysis. Five independent prognostic factors were identified and entered into the nomogram. The calibration curves for probability of 1-, 3-, and 5-year OS showed optimal agreement between nomogram prediction and actual observation. The AIC value of the nomogram was lower than that of the 7th edition staging system, whereas the c-index of the nomogram was higher than that of the 7th edition staging system. The risk groups stratified by RPA allowed significant distinction between survival curves within respective TNM categories. CONCLUSION: The RPA based on a clinical nomogram appears to be suitable for risk stratification in OS for resected ESCC. This practical system may help clinicians in decision making and design of clinical studies.

Nestin expression involves invasiveness of esophageal carcinoma and its downregulation enhances paclitaxel sensitivity to esophageal carcinoma cell apoptosis.

Paclitaxel has been generally used to treat primary and metastatic esophageal carcinoma. It has been shown that nestin is highly expressed in esophageal carcinoma and that there is a strong association of nestin expression with poor prognosis in esophageal carcinoma patients. In this study, using immunohistochemistry, in situ hybridization and Western blotting we demonstrated that nestin was overexpressed in the invasive esophageal carcinoma. To further elucidate whether nestin inhibition could enhance paclitaxel sensitivity to esophageal carcinoma cells, we applied nestin siRNA in esophageal squamous cell carcinoma Eca-109 cells. Flow cytometry and TUNEL staining both showed that combination of paclitaxel treatment and nestin knockdown resulted in greater induction of apoptosis of esophageal carcinoma cells as compared with the cells transfected with control siRNA (also treated with paclitaxel). This study indicates that nestin knockdown enhances chemotherapeutic sensitivity of paclitaxel to esophageal carcinoma, and suggests that silencing of nestin could be a valuble therapeutic approach for enhancing drug sensitivity and thereby improving the treatment outcome of esophageal carcinoma patients.

c-Myc promotes tumor proliferation and anti­apoptosis by repressing p21 in rhabdomyosarcomas.

v-myc avian myelocytomatosis viral oncogene homolog (c-Myc) is an important member protein of the Myc family that is important in cell cycle progression, apoptosis and tumorigenesis. In the present study, the role of c­Myc in rhabdomyosarcoma (RMS) was assessed. Firstly, expression of endogenous c­Myc and cyclin dependent kinase inhibitor 1A (p21) was examined in normal skeletal muscle, RMS specimens and TE671 RMS cells by immunohistochemistry, reverse transcription­quantitative polymerase chain reaction and western blotting. Furthermore, cell cycle progression and apoptosis were assessed in TE671 RMS cells following treatment with a c­Myc inhibitor, 10058­F4. The results demonstrated that c­Myc was overexpressed in clinical RMS tissues and TE671 cells, with the highest expression observed in the most RMS samples. Expression of p21 protein and apoptosis function were increased following treatment with 10058­F4, but no difference was observed in cell cycle progression. In conclusion, the present study indicated that c­Myc promotes RMS development by inhibiting apoptosis through repression of p21 transcription. Further studies will be required to evaluate c­Myc as a target for RMS clinical treatment.

[The expression and clinical significance of MyD88 in laryngeal cancer].

OBJECTIVE: To investigate the myeloid differentiation factor 88 (MyD88) expression in laryngeal carcinoma and its clinical significance. METHOD: Fifty-one patients with laryngeal carcinoma were collected, and all patients were confirmed by pathological diagnosis results. The expression of MyD88 protein was detected by immunohistochemical method in laryngeal cancer and its adjacent tissues to investigate the correlation among MyD88 expression, clinicopathological characteristics and prognosis of patients. RESULT: The positive expression rate of MyD88 in laryngeal cancer tissues was 68.6%, significantly higher than that in normal tissues adjacent to carcinoma of which positive expression rate was 11.8%; MyD88 positive rate had nothing to do with laryngeal cancer patients age, sex, differentiation and tumour location (all P > 0.05), but correlated with clinical stage (P < 0.01) and lymph node metastasis (P < 0.05). In addition, the study also found that the expression of MyD88 quantity was inversely proportional with the five-year survival rate. The survival rate of patients with higher expression of MyD88 was significantly lower than that of patients with lower expression (P < 0.05). CONCLUSION: MyD88 may be an important participant in the pathogenesis of laryngeal carcinoma, MyD88 targeted therapy may improve the prognosis of patients with laryngeal cancer.

Inhibition of Autophagy Increases Proliferation Inhibition and Apoptosis Induced by the PI3K/mTOR Inhibitor NVP-BEZ235 in Breast Cancer Cells.

BACKGROUND: The phosphoinositide 3 kinase (PI3K)/AKT/mammalian target of the rapamycin (mTOR) pathway is a complicated intracellular pathway which leads to cell growth and tumor proliferation and plays a significant role in breast cancer. Multiple compounds targeting this pathway are being evaluated in clinical trials. NVP-BEZ235, a novel and orally available dual PI3K/mTOR inhibitor, showed great antitumor effect and provided a therapy strategy in breast cancer. METHODS: In this study, we detect the effect of NVP-BEZ235 on cell viability, apoptosis, and autophagy in a breast cancer cell line. We also test the effect of NVP-BEZ235 on the expression of PI3K/AKT/mTOR pathway proteins p-AKT, p-mTOR, and p-70S6K. RESULTS: The results showed that the PI3K/AKT/mTOR proteins p-AKT, p-mTOR, and p-70S6K were obviously suppressed by NVP-BEZ235. NVP-BEZ235 inhibited cell proliferation and induced apoptosis and autophagy in breast cancer cells. In combination with autophagy inhibitors or autophagy gene knockdown, enhanced growth inhibition and apoptosis was induced by NVP-BEZ235 in MCF-7 cells. CONCLUSIONS: This study provides a novel treatment strategy that PI3K/AKT/mTOR pathway inhibitors in combination with autophagy inhibitors lead to further apoptosis in breast cancer cells.

miRNA-221 promotes proliferation, migration and invasion by targeting TIMP2 in renal cell carcinoma.

INTRODUCTION: MicroRNAs (miRNAs) play important roles in tumorigenesis. In this study, we investigated the role of miR-221 in the development and progression of clear cell renal cell carcinoma (ccRCC). METHODS: Quantitative real-time PCR (qRT-PCR) was used to measure the expression level of miR-221 in ccRCC tissues and cell lines. Then, we investigated the role of miR-221 to determine its potential roles on renal cancer cell proliferation, migration and invasion in vitro. A luciferase reporter assay was conducted to confirm the target gene of miR-221 and the results were validated in renal cancer cells. RESULTS: In the present study, we found that miR-221 was significantly increased in ccRCC tissues and cell lines. Knocked-down expression of miR-221 remarkably inhibited cell proliferation, migration and invasion of renal cancer cells. Moreover, at the molecular level, our results suggested that TIMP2 as a direct target of miR-221 through which miR-221 promoted tumor cell proliferation, migration and invasion. CONCLUSIONS: These findings suggested that miR-221 play an oncogenic role in the renal cancer cell proliferation, migration and invasion by directly inhibiting the tumor suppressor TIMP2, indicating miR-221 act as a potential new therapeutic target for the treatment of ccRCC.

High serum miR-183 level is associated with poor responsiveness of renal cancer to natural killer cells.

Renal cell carcinoma (RCC) is among the most common subtype of kidney cancers, and the current therapeutic strategies are not efficient. Natural killer (NK) cells are biological agents that can induce apoptosis in a wide range of cancer cells. However, most of RCC patients exhibit resistance against the action of NK cells due to unknown mechanisms. This study is aimed to identify a biomarker that can predict the response of RCC cells to NK cell treatment. We collected 82 RCC patients and 19 healthy volunteers to detect the expression of miR-183 in blood by qPCR assays. The results revealed that serum miR-183 is significantly higher in RCC patients than in healthy controls, and its level is positively associated with the grading of RCC. Furthermore, (51)Cr release assays indicated that the primary RCC cells with low serum miR-183 expression are more sensitive to the cytotoxicity of NK cells. Collectively, we demonstrated that serum miR-183 can be used to predict the response of RCC cells to the cytotoxicity induced by NK cells.

Prognostic value of survivin and EGFR protein expression in triple-negative breast cancer (TNBC) patients.

Triple-negative breast cancer (TNBC) is a particular type of breast cancer which is characterized by its biological aggressiveness, worse prognosis, and lack of prognostic markers or therapeutic targets in contrast with hormonal receptor-positive and human epidermal growth factor receptor 2-positive (HER2+) breast cancers. We aimed to evaluate survivin and epidermal growth factor receptor (EGFR) expression and their prognostic value and determine their relationships with the clinicopathological parameters of TNBC. A total of 136 patients who had undergone a resection of primary TNBC were enrolled at the Third Affiliated Hospital of Harbin Medical University from March 2003 to September 2005. Expression of ER, PR, HER2, EGFR, and survivin was assessed by immunohistochemistry. The association of TNBC and other clinicopathological variables and the prognostic value of survivin and EGFR expression were evaluated. Survivin was expressed in 62 (45.6 %) cases and EGFR was expressed in 82 (60.3 %) cases. Survivin expression was associated with menopausal status (P = 0.011), tumor size (P = 0.037), and lymph node status (P = 0.001). EGFR expression was associated with menopausal status (P = 0.029), lymph node status (P = 0.004), P53 expression (P = 0.001), Ki-67 expression (P = 0.028), and lymphatic vascular invasion (P = 0.037). A multivariate analysis demonstrated that tumor size (hazard ratio (HR) 1.587, 95 % confidence interval (CI) 1.081­2.330, P = 0.018 for disease-free survival (DFS); HR 1.606, 95%CI 1.096­2.354, P = 0.015 for overall survival (OS)), lymph node status (HR 2.873, 95%CI 1.544­5.344, P = 0.001 for DFS; HR 2.915, 95%CI 1.553­5.471, P = 0.001 for OS), tumor grade (HR 1.914, 95%CI 1.218­3.007, P = 0.005 for DFS; HR 1.983, 95%CI 1.228­3.203, P = 0.005 for OS), EGFR (HR 3.008, 95%CI 1.331­6.792, P = 0.008 for DFS; HR 3.151, 95%CI 1.374­7.226, P = 0.007 for OS), and survivin (HR 1.573, 95%CI 1.087­2.277, P = 0.016 for DFS; HR 1.607, 95%CI 1.088­2.374, P = 0.017 for OS) were of prognostic significance for disease-free and overall survival. We draw a conclusion from the present study that survivin and EGFR expression are useful prognostic markers of TNBC and might be useful for molecular targeting therapy of TNBC treatment.