Fbxo45 promotes the malignant development of esophageal squamous cell carcinoma by targeting GGNBP2 for ubiquitination and degradation.

Esophageal squamous cell carcinoma (ESCC) is one of the most common and deadly cancers. Fbxo45, a substrate recognition subunit of E3 ligase, is critically involved in tumorigenesis and tumor progression. However, the function of Fbxo45 and the underlying mechanisms have not been elucidated in ESCC. We used cellular and molecular methods to explore the molecular basis of Fbxo45-mediated ESCC development. We found that ectopic overexpression of Fbxo45 promoted the growth of Kyse-150, Kyse30 and ECA-109 cells and inhibited the apoptosis. Moreover, overexpression of Fbxo45 promoted the migration and invasion of ESCC cells. Consistently, knockdown of Fbxo45 exhibited the opposite effects on ESCC cells. Mechanistically, we observed that Fbxo45 binds to GGNBP2 via its SPRY domain and targets GGNBP2 for ubiquitination and degradation. GGNBP2 overexpression exhibited anticancer activity in ESCC cells. Furthermore, Fbxo45 exerted its functions by regulating GGNBP2 stability in ESCC cells. Notably, overexpression of Fbxo45 facilitated tumor growth in mice. Strikingly, Fbxo45 was highly expressed in ESCC tissues, and GGNBP2 had a lower expression in ESCC specimens. High expression of Fbxo45 and low expression of GGNBP2 were associated with poor prognosis in ESCC patients. Fbxo45 was negatively correlated with GGNBP2 expression in ESCC tissues. Therefore, Fbxo45 serves as an oncoprotein to promote ESCC tumorigenesis by targeting the stability of the tumor suppressor GGNBP2 in ESCC.

Primary testicular diffuse large B-cell lymphoma: Case series.

RATIONALE: Primary testicular lymphoma (PTL) is a rare type of extranodal non-Hodgkin's lymphoma (NHL). Although data of PTL in patients with diffuse large B-cell lymphoma (DLBCL) are accumulating, there are still patients respond poorly to prognosis. PATIENT CONCERNS: All patients had disease of the DLBCL subtype and those patients had primary involvement of the testis. In our studies, eleven patients had stage I/II disease, and 3 patients had advanced disease with B symptoms. Four patients exhibited a MYC+, BCL2+, and BCL6- expression pattern, 4 patients had a MYC+, BCL6+, and BCL2- expression pattern, and 3 patients had a MYC+, BCL2+, and BCL6+ expression pattern. Additionally, 43% (7/16) of PT-DLBCL patients had a germinal center B-cell-like (GCB) phenotype, while the others had a non-GCB phonotype. DIAGNOSES: In our case, most patients presented with unilateral painless scrotal swelling and the enlargement of the testicles in the first examination. After hospitalization, all patients underwent preoperative imageological examination of the testis and epididymis and postoperative revealed that all patients were the diffuse infiltration of a large number of anomalous lymphocytes. In addition, no invasion of other sites was observed within 3 months after diagnosis. INTERVENTIONS AND OUTCOMES: Underwent orchiectomy on the affected side was performed by urologists after all patients were diagnosed with PTL. Meanwhile, some patients received at least one course of chemotherapy, or received postoperative combined RT and chemotherapy. Because of it particularity, nineteen instances of lymph node region involvement were discovered in 12 patients since the operation. LESSONS: PT-DLBCL has unique biological characteristics, and its treatment modalities are becoming increasingly standardized. In the future, systematic interventions need to be actively considered in the early stages of PTL.

FOXM 1 induces Vasculogenic mimicry in esophageal cancer through ß-catenin /Tcf4 signaling.

OBJECTIVE: To investigate the role of FOXM1, ß-catenin and TCF4 in esophageal cancer (EC) and their relationship to VM (Vasculogenic Mimicry). METHODS: CCK-8 were performed to examine EC cell proliferation in FOXM1 silenced cells. EC cell migration and invasion were investigated through wound healing and Transwell assays, respectively. The formation of pipe like structures were assessed in 3D cultures. The expression of Foxm1, ß-catenin, Tcf4 and E-cadherin were investigated through western blot, RT-qPCR and immunohistochemistry (IHC) staining. The relationship between FOXM1 expression, clinic-pathological features, and overall survival (OS) were further analyzed. RESULTS: A loss of FOXM1 expression correlated with the OS of ESCC patients. FOXM1 silencing led to a loss of cell growth and suppressed cell migration and invasion in ESCC cells. VM structures were identified in ESCC tissues and human EC cell lines. Mechanistically, FOXM1 was found to promote tumorigenesis through the regulation of ß-catenin, Tcf4, and E-cadherin in EC cells, leading to the formation of VM structures. CONCLUSIONS: These findings highlight FoxM1 as a novel therapeutic target in ESCC.

Expression of CRYAB with the angiogenesis and poor prognosis for human gastric cancer.

Alpha-B crystallin (CRYAB), as a small heat shock protein, has been found to be highly expressed in various human cancers and significantly associated with the unfavorable prognosis of these tumor. Nevertheless, the clinical significance of CRYAB in gastric cancer (GC) angiogenesis remains to be elucidated. In this study, we evaluated the expression of CRYAB and CD34 in GC tissues and corresponding normal gastric specimens to explore whether high level CRYAB is related with the angiogenesis and the poor prognosis in GC.In this study, the expression of CRYAB and CD34 were detected in GC tissues and corresponding normal gastric tissues by immunohistochemical (IHC) technique. Furthermore, the relationship of CRYAB with CD34-evaluated microvessel density (MVD) and poor prognosis was also investigated.CRYAB expression level was significantly higher in GC tissue than in normal gastric mucosa tissue, and clearly mean higher MVD was observed in tumor tissues compared with non-cancerous tissues. Besides, higher MVD value was observed in positive CRYAB expression group than in negative CRYAB expression group. Statistical analysis showed that CRYAB and MVD are associated with clinicopathological features including lymph node metastasis (LNM), tumor differentiation, invasion depth, and TNM stages. Kaplan-Meier method and multivariate survival analysis indicated that high expression of CRYAB, MVD, invasion depth, TNM stages, and tumor differentiation, as well as LNM significantly correlate with poor prognosis of GC patients.High expression of CRYAB may contribute to angiogenesis, invasion and metastasis of GC. These results indicated that CRYAB was expected to be a promising molecular marker for poor prognosis and potential therapeutic target in patients with GC.

Lymphoma of the female genital tract: a clinicopatholngical analysis of 25 cases.

Occurrence of lymphoma of the female genital tract (FGT) is extremely rare, and cohort studies on survival rates of affected patients are sparse. The aim of this study was to retrospectively evaluate the clinicopathological characteristics of patients diagnosed with non-Hodgkin lymphoma of the FGT. This study included 25 women diagnosed with lymphoma of the FGT. Their data on presenting pathological subtype, International Federation of Gynecology and Obstetrics (FIGO) and Ann Arbor staging, International Prognostic Index (IPI) score, treatment, and survival time were collected. Among the 25 patients, the most prevalent histological subtype was diffuse large B-cell lymphoma (23/25). Tumors were most commonly located in the ovary (15/25), with the remainder located in the cervix (7/25) and uterine corpus (3/25). 76% of cases by Ann Arbor were stage III or IV, and 70% of cases by FIGO were stage III or IV. The overall median survival from diagnosis of lymphoma was estimated to be 71 months, with 3-year and 5-year survival rates of 92% and 80%, respectively. The FIGO and Ann Arbor staging and IPI score were significantly correlated with overall survival time.

The Emerging Role of Sperm-Associated Antigen 6 Gene in the Microtubule Function of Cells and Cancer.

Accumulated evidence shows that sperm-associated antigen 6 (SPAG6) gene has multiple biological functions. It maintains the normal function of a variety of cells including ciliary/flagellar biogenesis and polarization, neurogenesis, and neuronal migration. Moreover, SPAG6 is found to be critically involved in auditory transduction and the fibroblast life cycle. Furthermore, SPAG6 plays an essential role in immuno-regulation. Notably, SPAG6 has been demonstrated to participate in the occurrence and progression of a variety of human cancers. New evidence shows that SPAG6 gene regulates tumor cell proliferation, apoptosis, invasion, and metastasis. Therefore, in this review, we describe the physiological function and mechanism of SPAG6 in human normal cells and cancer cells. We also highlight that SPAG6 gene may be an effective biomarker for the diagnosis of human cancer. Taken together, targeting SPAG6 could be a novel strategy for the treatment of human diseases including cancer.

PDS5B regulates cell proliferation and motility via upregulation of Ptch2 in pancreatic cancer cells.

Pds5b (precocious dissociation of sisters 5B) is involved in both tumorigenesis and cancer progression; however, the functions and molecular mechanisms of Pds5b in pancreatic cancer (PC) are unknown. Several approaches were conducted to investigate the molecular basis of Pds5b-related PC progression, including transfection, MTT, FACS, western blotting, wound healing assay, transwell chamber invasion assay, and immunohistochemical methods. Pds5b overexpression inhibited cell growth and induced apoptosis, whereas the inhibition of Pds5b promoted growth of PC cells. Moreover, Pds5b overexpression inhibited cell migration and invasion, while the downregulation of Pds5b enhanced cell motility. Furthermore, reduced Pds5b expression was associated with survival in PC patients. Mechanistically, Pds5b positively regulated the expression of Ptch2 to influence the Sonic hedgehog signaling pathway. Consistently, Ptch2 downregulation enhanced cell growth, migration, and invasion, while inhibiting cell apoptosis. Notably, the downregulation of Ptch2 abolished Pds5b-mediated anti-tumor activity in PC cells. Strikingly, Pds5b expression was positively associated with levels of Ptch2 in PC patient samples, suggesting that the Pds5b/Ptch2 axis regulates cell proliferation and invasion in PC cells. Our findings indicate that targeting Pds5b and Ptch2 may represent a novel therapeutic approach for PC.

Capsaicin induces cytotoxicity in human osteosarcoma MG63 cells through TRPV1-dependent and -independent pathways.

An accumulating body of evidence has shown that capsaicin induces apoptosis in various tumor cells as a mechanism of its anti-tumor activity. However, the effects of capsaicin on osteosarcoma have not been studied extensively. In the current study, we explore the molecular mechanism of capsaicin-mediated tumor suppressive function in osteosarcoma. We found that capsaicin-induced apoptosis and the activation of transient receptor potential receptor vanilloid 1 (TRPV1) in a dose- and time-dependent manner in human osteosarcoma MG63 cells in vitro. Blocking TRPV1 using capsazepine attenuated the capsaicin-induced cytotoxicity, mitochondrial dysfunction, overproduction of reactive oxygen species (ROS) and decrease in superoxide dismutase (SOD) activity. In addition, the results demonstrated that capsaicin induced the activation of adenosine 5'-monophosphate-activated protein kinase (AMPK), p53 and C-jun N-terminal kinase (JNK). In addition, Compound C (antagonist of AMPK) attenuated the activation of p53, which appeared to be TRPV1 independent. Taken together, the present study suggests that capsaicin effectively causes cell death in human osteosarcoma MG63 cells via the activation of TRPV1-dependent (mitochondrial dysfunction, and overproduction of ROS and JNK) and TRPV1-independent (AMPK-p53) pathways. Thus, capsaicin may be a potential anti-osteosarcoma agent.

Xp11.2 translocation/TFE3 gene fusion renal cell carcinoma with a micropapillary pattern: cases report and literature review.

Xp11.2 translocation/transcription factor E3 (TFE3) gene fusion renal cell carcinoma (Xp11.2 translocation RCC) was first classified as a distinct type of renal tumor by the World Health Organization in 2004. However, its morphology and clinical manifestations often overlap with those of conventional RCCs. Moreover, a micropapillary pattern (MPP) comprising small papillary cell clusters surrounded by lacunar spaces has never been described in RCC. We compared the clinicopathological and prognostic characteristics of one patient with Xp11.2 translocation RCC exhibiting an MPP (TFE3-M) to those of four patients with conventional Xp11.2 translocation RCC (TFE3-N); all five tumors resembled conventional RCCs on gross pathology. All patients exhibited similar histologies, clinical manifestations, and prognoses, and all underwent radical nephrectomy. However, their characteristics differed significantly from those of other MPP-comprising neoplasms. Both tumor types were positive for TFE3 and vimentin; however, TFE3-M tumor cells expressed epithelial membrane antigen and human melanoma black-45 but not cluster of differentiation 10 (CD10), whereas the TFE3-N cells expressed P504S, CD10, and vimentin but not cytokeratin 7. Our RT-PCR analysis result showed that TFE3-N and TFE3-M tumor cells were identified expressing ASPSCR1-TFE3 and PRCC-TFE3 fusion genes, respectively. These findings suggest that TFE3-M should be classified as a histological subtype of Xp11.2 translocation RCC, although its relationship with other MPP-exhibiting neoplasms remains unclear. The histological characteristics of Xp11.2 translocation RCCs depend on MiT family transcription factors and their gene fusion partners. Xp11.2 translocation RCC should be considered for malignancies presenting with a particular pattern; such malignancies can be identified reliably by their morphological and immunohistochemical profiles.

WISP2 exhibits its potential antitumor activity via targeting ERK and E-cadherin pathways in esophageal cancer cells.

BACKGROUNDS: Emerging evidence has demonstrated that WISP2 is critically involved in cell proliferation, migration, invasion and metastasis in cancers. However, the function of WISP2 in esophageal squamous cell carcinoma (ESCC) is largely unclear. Therefore, we aim to explore the effects and the potential mechanism of WISP2 on proliferation and motility and invasion of ESCC cells. METHODS: Cell proliferation was detected by MTT assay and apoptosis was measured by FACS in ESCC cells after WISP2 downregulation and overexpression. Cell migration and invasion were analyzed by wound healing assay and transwell migration assay, respectively. The expression of ERK-1/2, Slug and E-cadherin was measured by Western blot respectively. IHC was performed to measure the expression of WISP2 in ESCC tissues. RESULTS: WISP2 overexpression is associated with survival in ESCC patients. WISP2 overexpression inhibited cell growth and induced cell apoptosis, suppressed cell migration and invasion in ESCC cells. Moreover, WISP overexpression retarded tumor growth in mouse model. WISP2 downregulation enhanced cell growth, inhibited apoptosis, promoted cell migration and invasion in ESCC cells. Mechanistically, WISP2 exerts its tumor suppressive functions via regulation of ERK1/2, Slug, and E-cadherin in ESCC cells. CONCLUSIONS: Our findings suggest that activation of WISP2 could be a useful therapeutic strategy for the treatment of ESCC.

Evaluation of the correlativity of gender determining region Y-box 4, N-cadherin, CD44 and E-cadherin expression in the prognosis of esophageal squamous cell carcinoma.

BACKGROUND: SOX4 is highly expressed in many different tumor types, and SOX4 has been reported in the literature to participate in tumor proliferation, damaging and movement by leading Epithelial-Mesenchymal Transition. Cancer vital cells and Epithelial-Mesenchymal Transition have been repeatedly confirmed to participate during the proliferation, damaging and movement of cancer. This research examined the association of the Epithelial-Mesenchymal Transition-related molecules E-cadherin, N-cadherin, CD44, and SOX4 in the ESCC and aimed for providing inspiration for clinical treatment as well as to indicate a new direction for detecting invasion and forecasting the prospect of affected role using ESCC. METHODS: Immunohistochemistry was utilized to observe the expression of the S0X4, N-cadherin, CD44 and E-cadherin proteins. Survival analysis of the positive and negative SOX4, E-cadherin, N-cadherin and CD44 protein expression groups was performed by the Kaplan-Meier approach. OUTCOMES: A confirming relationship was observed among the expression of SOX4, N-cadherin or CD44 and tumor diameter, distant metastasis, deepness of damaging, lymph node metastasis, pTNM stage and histological grade (P<0.05). Spearman correlativity calculation displayed that the expression of the SOX4 protein was obviously responded with the expression of the N-cadherin and CD44 proteins. Moreover, the expression of the N-cadherin and CD44 proteins was also positively correlated. The E-cadherin protein was negatively correlated with SOX4, N-cadherin and CD44 protein expression in ESCC. SOX4, N-cadherin, CD44, E-cadherin, age and distant metastasis were determined to be separate elements that influenced the prognosis of patients with ESCC. CONCLUSIONS: We found that suppression of ESCC providers can suppress the growth of bad tumors and change therapeutic results for ESCC patient since CD44 supports the induction of Epithelial-Mesenchymal Transition in ESCC.

Aberrant expression of MYH9 and E-cadherin in esophageal squamous cell carcinoma and their relationship to vasculogenic mimicry.

PURPOSE: To investigate whether vasculogenic mimicry (VM) exists in esophageal squamous cell carcinoma (ESCC) and to elucidate the relationship among expression of MYH9, E-cadherin and VM. METHODS: The expression of MYH9 (non-muscle myosin heavy chain 9), E-cadherin protein and VM in 120 specimens of esophageal squamous cell carcinoma (ESCC) and 120 specimens of normal esophageal mucosa were detected by using immunohistochemical and histochemical staining. RESULTS: VM channels were identified in 58 (48.33%) of the 120 ESCC specimens and none of the normal esophageal mucosa was found to have VM. The rates of expression of MYH9 and E-cad in ESCC were 57.50% and 40.00%, while rates in the control group were 13.33% and 73.33%, respectively (P<0.05). VM and the expression levels of MYH9 and E-cad were significantly connected with lymph node metastasis, serosa invasion, pTNM staging and 5-year-survival rates of patients with ESCC (P<0.05). VM was positively correlated with MYH9, but negatively correlated with E-cad, and MYH9 was negatively significantly correlated with E-cad. The 5-year-survival rates of patients with ESCC were 6.89% (4/58) in the VM group and 67.74% (42/62) in the non-VM group, 8.00% (4/50) in high MYH9 expression group and 60.00% (42/70) in low MYH9 expression group. However, the 5-year-survival rate in high E-cad expression group was 86.95% (40/46) and that in low E-cad expression group was 8.11% (6/74) (P<0.05). Cox multifactorial regression analysis demonstrated that lymph node metastasis, pTNM stage, VM and expression levels of MYH9 and E-cad were independent risk factors in patients with ESCC (P<0.05). CONCLUSION: ESCC'patients with VM had a poor differentiation and a bad clinical prognosis; Combined detection of VM, MYH9 and E-cad may play an essential role in predicting the invasion, metastasis, and progression of patients with ESCC.

Clinicopathologic features of epithelioid sarcoma: report of seventeen cases and review of literature.

Epithelioid sarcoma (ES) is a rare malignant soft tissue tumor, which is characterized by nodular aggregates of epithelioid cells and immunoreactivity of cytokeratin (CK) as well as epithelial membrane antigen (EMA) and often with CD34. It can be divided into proximal and distal subtypes. Classic ES has a microscopic nodular appearance that is composed of large polygonal epithelioid cells combined with central necrosis, and presents as a subcutaneous or deep dermal mass in the distal extremities of young adults. The proximal variant preferentially occurs in proximal limbs and limb girdles and the midline of the trunk, and is composed of more atypical cells with variable rhabdoid morphology. In this study we investigated the clinicopathologic features of 17 patients diagnosed with ES. In addition, we reviewed relevant literature and discussed some diagnostic and differential diagnostic points of this disease.

[Expression of AXIN and MACC1 in Gastric Carcinoma and Its Clinical Significance].

OBJECTIVE: To investigate the expression of axis inhibition protein (AXIN) and metastasis-associated in colon cancer-1 (MACC1) in gastric carcinoma and their relationship to the clinicopathologic characteristics. METHODS: Expressions of AXIN and MACC1 proteins were examined by immunohistochemistry containing 100 specimens of gastric tissues (gastric carcinoma group) and 60 specimens of normal gastric mucosa tissues (control group,the nearby tissues of the excised specimen of gastric cancer patients,from the tumor of the gastric cancer >5.0 cm,and confirm that there were no cancer cells). RESULTS: The positive rates of AXIN and MACC1 proteins in gastric carcinoma and the control tissues were 37.0% vs. 83.3% and 58.0% vs. 6.7%,respectively. The difference were significant between the two groups (both P<0.05). The expressions of AXIN and MACC1 proteins were significantly related with grades of tumor,depth of invasion,lymph node metastasis,and Duke stages ( P<0.05). Spearman analysis showed that there was a negative relationship between the AXIN expression and MACC1 expression (r=-0.355, P<0.05). Kaplan-Meier survival analysis and log-rank single factor analysis showed that AXIN and MACC1 protein expressions were related to the 5-year survival rate of patients (both P<0.05). Cox regression analysis showed that the positive expression of AXIN and the negative expression MACC1 protein,and Duke stages (Ⅲ-Ⅳ) were the independent prognostic factors of gastric carcinoma. CONCLUSION: The expressions of AXIN and MACC1 proteins are related to the prognosis of gastric carcinoma patients,and are involved in the invasion and metastasis of gastric carcinoma.

Ollier disease: two case reports and a review of the literature.

Ollier disease is a rare tumor with unclear clinicopathological features and pathogenesis. We herein report two cases of Ollier disease in a 15-year-old boy and a 66-year-old man. We analyzed the clinicopathological, radiographical, and histochemical characteristics of Ollier disease in these two cases. Furthermore, we reviewed the literature to better understand the clinicopathological features of this disease. The boy had multiple enchondromas in the metaphysis and upper region of the left femur, and his left leg is short naturally. The 66-year-old man had multiple enchondromas in his left ribs and lower segment of the left femur. He was sent to the hospital because of pathological fracture of the ribs. In addition, he was diagnosed with gastric cancer 4 years before visiting an orthopedic clinic. Ollier disease is a rare bone disease that often renders a typical asymmetrical distribution and is confined to the appendicular skeleton. It is known as a benign bone tumor and has a high risk of malignant transformation into a chondrosarcoma (5%-50%). Correct diagnosis requires radiographic, histochemical, and morphological analyses. Better understanding of the clinical manifestations and pathological features can improve the diagnosis and prevent malignant transformation and deformity, especially in adolescent patient.

Vasculogenic mimicry and expression of slug and vimentin correlate with metastasis and prognosis in non-small cell lung cancer.

Background: Non-small cell lung cancer (NSCLC) has been the leading cause of cancer death in recent years, its morbidity and mortality were increasing yearly. The presence of vasculogenic mimicry (VM) is associated with a high tumor grade, short survival, invasion, and metastasis. Slug is a key regulating factor in the process of EMT. Vimentin is one of the cytoskeleton proteins that plays an important role in EMT. However, associations among VM, Slug and vimentin and their clinicopathologic significance in NSCLC are unclear. In this study, we analyzed associations among VM, Slug and vimentin in NSCLC, and their respective associations with clinicopathologic characteristics and survival in NSCLC. Methods: Positive expression of VM, Slug and vimentin in 198 whole NSCLC tissue samples were detected by immunohistochemical staining. Patients' clinical data were also collected. Results: Levels of VM, Slug and vimentin were significantly higher in NSCLC tissues than in normal lung tissues. Levels of VM, Slug and vimentin were positively associated with tumor grade, distant metastasis (DM), lymph node metastasis (LNM), and tumor-node metastasis (TNM) stage, and inversely with patients overall survival time (OST). In multivariate analysis, high expression of VM, Slug, vimentin, and tumor grade, DM, LNM, TNM stage, were potential to be independent prognostic factors for OST in patients with NSCLC. Conclusion: VM, Slug and vimentin affect NSCLC evolution; and the combined detection of VM, Slug and vimentin are valuable factors for metastasis and prognosis in NSCLC patients.

Correlation of KAI1, CD133 and vasculogenic mimicry with the prediction of metastasis and prognosis in hepatocellular carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) is an aggressive type of tumor with high mortality and poor prognosis, KAI1 is a metastasis suppressor gene which was first found in prostate carcinoma and mapped to chromosome 11p11.2. Vasculogenic mimicry (VM) is a new blood supply phenomenon that exists in highly malignant tumors. CD133 is one of the most common CSC markers for cancer stem cells, and it is related to drug resistance. The purpose of this study was to verify the hypothesis that the above biomarkers have some association with metastasis and prognosis in HCC. METHODS: The levels of KAI1, VM and CD133 in 108 whole tissue samples of HCC were detected by immunohistochemistry and histochemistry. Clinical data were also collected. RESULTS: Levels of CD133 and VM were significantly higher, and the level of KAI1 was significantly lower in HCC tissues than that in normal liver tissues. Levels of CD133 and VM were positively associated with cirrhosis, grade, venous invasion, lymph node metastasis (LNM), intrahepatic metastasis, and tumor-node-metastasis (TNM) stages, and negatively with patients' overall survival (OS). The level of KAI1 was negatively correlated with cirrhosis, grade, venous invasion, lymph node metastasis (LNM), intrahepatic metastasis and TNM stages, and positively with patients' overall survival (OS). In a multivariate analysis, CD133, VM KAI1, and TNM stage were independently correlated with OS in patients with HCC. CONCLUSIONS: KAI1, CD133, and the existence of VM may have important impacts on metastasis and prognosis in HCC.

[Expression of vasohibin-1 and MACC1 in lung squamous cell carcinoma and their clinicopathological significance].

OBJECTIVE: To investigate the expressions of vasohibin-1 and MACC1 in lung squamous cell carcinoma (LSCC) and their associations with the clinicopathological characteristics of the patients. METHODS: The expressions of vasohibin-1 and MACC1 proteins were examined with immunohistochemistry in 160 LSCC tissues and 80 normal lung tissues. RESULTS: The positivity rates of vasohibin-1 and MACC1 proteins were 59.4% and 11.3% in LSCC tissues, respectively, which were significantly higher than the rates in normal lung tissues (57.5% and 8.8%, respectively; P<0.05). The expressions of vasohibin-1 and MACC1 proteins were significantly correlated with the tumor grades, lymph node metastasis, and TNM stages (all P<0.05). Spearman correlation analysis indicated a positive correlation between vasohibin-1 expression and MACC1 expressions (P<0.001). Kaplan-Meier survival analysis showed that LSCC patients with a positive expression of vasohibin-1 had significantly shorter overall survival time than those negative for vasohibin-1; the overall survival time was also significantly shorter in patients positive for MACC1 than in those negative for MACC1 (both P<0.05). Multivariate COX regression analysis indicated that positive expressions of vasohibin-1 and MACC1 protein and TNM stage were independent prognostic factors of LSCC. CONCLUSION: Aberrant expressions of vasohibin-1 and MACC1 may participate in the development and promote invasion and metastasis of LSCC. The combined detection of vasohibin-1 and MACC1 expression may provide important evidence for predicting the progression and prognosis of LSCC.

Quality of life in Chinese family caregivers for elderly people with chronic diseases.

BACKGROUND: Inadequate studies have been conducted in China to examine quality of life in family caregivers. Quality of life in family caregivers for elderly people with chronic diseases was evaluated, and the demographic and characteristic factors of both elderly people and their caregivers were explored. METHODS: The 36-Item Short Form Health Survey (SF-36) was used to assess health-related quality of life in 407 family caregivers caring for elderly people with chronic diseases in six communities on the Mainland China. The explanatory variables included family caregivers' demographic and other caregiving variables related to eldercare. Descriptive statistics and multiple linear regression analysis were used in the data analysis, performed via SPSS 17.0. RESULTS: Mean SF-36 and physical and mental component scores were 66.14 ± 17.50, 70.06 ± 16.49, and 62.22 ± 18.51, respectively. The scores of caregivers' physical function and bodily pain were significantly higher, while the scores of caregivers' role limitations due to physical problems, general health, vitality, social function, mental health and role limitations due to emotional problems were significantly lower. Caregivers' ages, comorbidity, the perceived effects of caregiving on caregivers' social lives and elderly individuals' ages, marital status and Activities of Daily Living scores were significantly associated with the physical component score. In addition, caregivers' age, the affordability of the elderly person's healthcare expenses, the perceived effects of caregiving on caregivers' social lives, and elderly people's marital status and ADL scores were significantly associated with the mental component score. CONCLUSION: Family caregivers for elderly people with chronic diseases showed poorer mental and better physical well-being. Factors of both elderly people and their caregivers impact the caregivers' quality of life. These findings highlight the importance of addressing mental health of family caregivers, and of providing economical support and psychological care for them.

Over-expression of Sox4 and ß-catenin is associated with a less favorable prognosis of osteosarcoma.

The purpose of this study was to examine the association of the expression of Sox4 and ß-catenin with the prognosis of osteosarcoma. A total of 108 cases of conventional osteosarcoma were involved in this study and 28 cases of osteochondroma served as controls. The expression of Sox4 and ß-catenin was detected by using immunohistochemical staining and Western blotting. The results showed that Sox4 and ß-catenin were over-expressed in 67 (62.03%) and 62 (57.41%) of 108 osteosarcoma cases, while in only 3 (10.71%) and 5 (17.86%) of 28 controls, respectively (P<0.05 for all). The expression of Sox4 and ß-catenin was associated with the distant metastasis, pathological grade and Enneking stage of patients with osteosarcoma (P<0.05 for all). The mean overall survival time and the 5-year-survival rate in osteosarcoma patients with Sox4 and ß-catenin over-expressed were significantly reduced as compared with those in Sox4 and ß-catenin low-expression group (P<0.05 for all). Cox multifactor regression analysis revealed that the distant metastasis, Enneking stage, and the expression of Sox4 and ß-catenin were independent risk factors of patients with osteosarcoma (P<0.05 for all). The findings indicated that overexpression of Sox4 and ß-catenin is associated with a poor prognosis of osteosarcoma.