scholarly journals CMIP Promotes Proliferation and Metastasis in Human Glioma

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Bin Wang ◽  
Zheng-sheng Wu ◽  
Qiang Wu
Keyword(s):  
Tumor Grade ◽  
Karnofsky Performance Score ◽  
Human Glioma ◽  
Performance Score ◽  
Free Survival ◽  
Migration Assay ◽  
Normal Tissues ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

Glioma is one of the most common primary malignant brain tumors and the outcomes are generally poor. The intrinsic mechanisms involved in glioma development and progression remain unclear. Further studies are urgent and necessary. In this study, we have proven that CMIP (C-Maf-inducing protein) promotes cell proliferation and metastasis in A172 cells through knockdown of CMIP and in U251 cells through overexpression of CMIP by using MTT assay, cell colony formation assay, cell migration assay, and cell invasion assay. Furthermore, we discovered that CMIP upregulates MDM2, which is involved in the promoting role of CMIP in human glioma cells. For clinical study, 99 glioma tissues and 59 normal tissues were analyzed. CMIP expression was higher in glioma tissues than in normal tissues. In glioma tissues, CMIP is found to correlate positively with tumor grade but no significant correlation is found with patients’ age, gender, or Karnofsky performance score (KPS). Moreover, CMIP also correlates with low relapse-free survival (RFS) rate and overall survival (OS) rate in glioma patients. Therefore, CMIP is oncogenic and could be a potential target for human glioma diagnosis and therapy.

scholarly journals OS14 - 208 The prognostic role of pre-operative complete blood count (CBC) in progression-free survival in patients with meningioma

2016 ◽  
Vol 43 (S4) ◽  
pp. S6-S6
Author(s):  
S. Karimi ◽  
P.D. Tonge ◽  
L. Gonen ◽  
R. Tabasinejad ◽  
G. Zadeh ◽  
...  
Keyword(s):  
Complete Blood Count ◽  
Tumor Resection ◽  
Progression Free Survival ◽  
Final Analysis ◽  
Tumor Grade ◽  
Prognostic Information ◽  
Free Survival ◽  
Univariate Analyses

Factors which might influence outcome in patients with meningioma are not well-understood. Previous studies have examined associations of laboratory blood values including hemoglobin levels with patient outcomes in cancer. We hypothesized those changes in CBC before tumor resection can be used as one of the prognostic factors for tumor recurrence/progression in meningioma. To address this, we gathered the clinical and pre-operative CBC results for final analysis from 226 patients (64 males and 162 females) who underwent craniotomy for primary meningioma (grades: 157 WHO GI, 59 GII, 10 GIII) at our institution between 2001 and 2015.Individual parameters were analyzed for correlation with progression-free survival. The median recurrence free survival (RFS) was not reached and follow-up ranged 0.3-14 years. Fifty-six patients (25%) had anemia and 30% of the patients showed leukocytosis using standard cut-offs. On univariate analyses, low hemoglobin (Hb) level, as well as high leukocytes (Lkc), neutrophil (Neutro) and monocyte counts correlated with worse RFS. As expected, tumor grade was correlated with RFS. Low Hb level, high Lkc and Neutro counts were all significantly associated with RFS after adjusting for grade. Strikingly, 32% of patients with pre-operative anemia experienced a recurrence at 5 years, compared with only 11% of non-anemic patients. Conclusion: In this exploratory study, we find that pre-operative CBC data, which is readily available, may contain prognostic information relevant to subsequent risk of recurrence or progression in meningioma. While the biological mechanism for these associations is not clear, they represent hypotheses for further investigation.

Role of Extent of Resection in the Long-Term Outcome of Low-Grade Hemispheric Gliomas

2008 ◽  
Vol 26 (8) ◽  
pp. 1338-1345 ◽  
Author(s):  
Justin S. Smith ◽  
Edward F. Chang ◽  
Kathleen R. Lamborn ◽  
Susan M. Chang ◽  
Michael D. Prados ◽  
...  
Keyword(s):  
Tumor Volume ◽  
Progression Free Survival ◽  
Extent Of Resection ◽  
Malignant Progression ◽  
Low Grade ◽  
Karnofsky Performance Score ◽  
Long Term Outcome ◽  
Free Survival

Purpose The prognostic role of extent of resection (EOR) of low-grade gliomas (LGGs) is a major controversy. We designed a retrospective study to assess the influence of EOR on long-term outcomes of LGGs. Patients and Methods The study population (N = 216) included adults undergoing initial resection of hemispheric LGG. Region-of-interest analysis was performed to measure tumor volumes based on fluid-attenuated inversion-recovery (FLAIR) imaging. Results Median preoperative and postoperative tumor volumes and EOR were 36.6 cm3 (range, 0.7 to 246.1 cm3), 3.7 cm3 (range, 0 to 197.8 cm3) and 88.0% (range, 5% to 100%), respectively. There was no operative mortality. New postoperative deficits were noted in 36 patients (17%); however, all but four had complete recovery. There were 34 deaths (16%; median follow-up, 4.4 years). Progression and malignant progression were identified in 95 (44%) and 44 (20%) cases, respectively. Patients with at least 90% EOR had 5- and 8-year overall survival (OS) rates of 97% and 91%, respectively, whereas patients with less than 90% EOR had 5- and 8-year OS rates of 76% and 60%, respectively. After adjusting each measure of tumor burden for age, Karnofsky performance score (KPS), tumor location, and tumor subtype, OS was predicted by EOR (hazard ratio [HR] = 0.972; 95% CI, 0.960 to 0.983; P < .001), log preoperative tumor volume (HR = 4.442; 95% CI, 1.601 to 12.320; P = .004), and postoperative tumor volume (HR = 1.010; 95% CI, 1.001 to 1.019; P = .03), progression-free survival was predicted by log preoperative tumor volume (HR = 2.711; 95% CI, 1.590 to 4.623; P ≤ .001) and postoperative tumor volume (HR = 1.007; 95% CI, 1.001 to 1.014; P = .035), and malignant progression-free survival was predicted by EOR (HR = 0.983; 95% CI, 0.972 to 0.995; P = .005) and log preoperative tumor volume (HR = 3.826; 95% CI, 1.632 to 8.969; P = .002). Conclusion Improved outcome among adult patients with hemispheric LGG is predicted by greater EOR.

scholarly journals Inflammatory Microenvironment-Mediated E-Cadherin Decrease Induces Migration in LNCaPs

Proceedings ◽  
2018 ◽  
Vol 2 (25) ◽  
pp. 1540
Author(s):  
Iroda Saydullaeva ◽  
Bilge Debeleç Bütüner ◽  
Kemal Sami Korkmaz
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Early Stage ◽  
Host Factors ◽  
Lncap Cells ◽  
Migration Assay ◽  
Inflammatory Microenvironment ◽  
Mechanistic Insight ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

Infection and chronic inflammation contribute to about 1 in 4 of all cancer cases. Emerging evidence suggests that the host factors in the tumor microenvironment may interact with underlying inflammatory prostate cancer cells to make them aggressive. In this study, we hypothesized that soluble factors secreted by immune cells activated by inflammation can induce EMT in prostate cancer and thus promote metastasis. We identify that macrophage-secreted cytokines including TNFα act as mediators for potentiating LNCaP cell proliferation in migration assay. Hence, our data indicate a mechanistic insight of how inflammation may contribute to development of prostatic disease at an early stage through increasing cell proliferation and metastasis of LNCaP cells.

CSN5 promotes carcinogenesis of thyroid carcinoma cells through ANGPTL2

Endocrinology ◽  
2020 ◽  
Author(s):  
Peiyi Xie ◽  
Hui Wang ◽  
Jiayu Fang ◽  
Dongnian Du ◽  
Ze Tian ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Carcinoma ◽  
Carcinoma Cell ◽  
Underlying Mechanism ◽  
Protein Levels ◽  
Proliferation And Metastasis ◽  
Gain Loss ◽  
Thyroid Carcinoma Cell ◽  
Cell Proliferation And Metastasis

Abstract COP9 signalosome subunit 5 (CSN5) plays a key role in carcinogenesis of multiple cancers, and contributes to stabilization of target proteins through deubiquitylation. However, the underlying role of CSN5 in thyroid carcinoma has not been reported. In this research, our data showed that CSN5 was overexpressed in thyroid carcinoma tissues compared with para-cancerous tissues. Furthermore, a series of gain/loss functional assays were performed to demonstrate the role of CSN5 in facilitating thyroid carcinoma cell proliferation and metastasis. Additionally, we found that there was a positive correlation between CSN5 and angiopoietin-like protein 2 (ANGPTL2) protein levels in thyroid carcinoma tissues and that CSN5 promoted thyroid carcinoma cell proliferation and metastasis through ANGPTL2. We also identified the underlying mechanism that CSN5 elevated ANGPTL2 protein level through directly binding it, and decreasing its ubiquitination and degradation. Overall, our results highlight the significance of CSN5 in promoting thyroid carcinoma carcinogenesis and implicate CSN5 as a promising candidate for thyroid carcinoma treatment.

Hodgkin’s Disease in the Elderly: Improved Treatment Outcome With a Doxorubicin-Containing Regimen

2002 ◽  
Vol 20 (4) ◽  
pp. 1087-1093 ◽  
Author(s):  
Colin D. Weekes ◽  
Julie M. Vose ◽  
Jim C. Lynch ◽  
Dennis D. Weisenburger ◽  
Philip J. Bierman ◽  
...  
Keyword(s):  
Hodgkin's Disease ◽  
Hodgkin’S Disease ◽  
Age Distribution ◽  
Lactic Dehydrogenase ◽  
The Elderly ◽  
Karnofsky Performance Score ◽  
Event Free Survival ◽  
Performance Score ◽  
Histologic Subtype ◽  
Free Survival

PURPOSE: Hodgkin’s disease (HD) is a malignancy that displays a bimodal age distribution. Previous reports of treatment in patients ≥ 60 years have found a poor outcome, particularly in patients with advanced disease. Because of an improved side-effect profile, the regimen of chlorambucil, vinblastine, procarbazine, and prednisone (ChlVPP) has been proposed for use in elderly patients. PATIENTS AND METHODS: From September 1982 to May 1998, 262 patients with previously untreated HD received either ChlVPP (n = 176) or ChlVPP plus doxorubicin/bleomycin/vincristine (ChlVPP/ABV hybrid; n = 86). Fifty-six patients were ≥ 60 years old, and 206 were younger than 60 years. RESULTS: The 5-year overall survival (OS; 87% v 39%) and the 5-year event-free survival (EFS; 75% v 31%) favored patients younger than 60 years of age. Prognostic factors analyzed in patients ≥ 60 years of age, other than type of therapy, included sex, stage, Karnofsky performance score, lactic dehydrogenase, number of extranodal sites, B symptoms, size of largest mass, and histologic subtype. In patients older than 60 years, none of the clinical features was a statistically significant predictor of EFS; however, ChlVPP/ABV hybrid was associated with a decreased risk of an event (relative risk, 0.40; 95% confidence interval, 0.19 to 0.83; P = .014) compared with ChlVPP. The 5-year OS for patients ≥ 60 years who received ChlVPP was 30%, compared with 67% for those patients receiving the ChlVPP/ABV regimen (P = .0086) CONCLUSION: Patients ≥ 60 years with HD who require chemotherapy are better treated with ChlVPP/ABV hybrid than with ChlVPP alone.

scholarly journals Clinicopathological Significance of Up-Regulated Pir-1366 in NSCLC and its Effect on Tumor Migration and Metastasis

2021 ◽  
Author(s):  
Jun Zhou ◽  
Hong Guo ◽  
Wen Lu ◽  
Hongchan Shi ◽  
Chenghai Wang
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Tumor Grade ◽  
Tumor Location ◽  
Lung Cancer Cells ◽  
Luciferase Reporter ◽  
Normal Tissues ◽  
Positive Expression ◽  
Nsclc Patients

Abstract Background: piRNAs are a kind of noncoding RNAs that involve in tumorigenesis and development, but the role of piRNAs in NSCLC remain unclear. In this study, we explored the role of piR-1366 in NSCLC .Methods:The identification of piRNAs was performed using Human Arraystar piRNA Array in NSCLC tissues and adjacent normal tissues. up-regulated piR-1366 were validated in the NSCLC and selected for further study of migration and metastasis. In addition, the expression of piR-1366 in 87 cases of NSCLC was detected by in situ hybridization and the correlation between piR-1366 expression and pathological parameters of NSCLC patients was analyzed. meanwhile, bioinformatics, qRT-PCR and West blotting were used to examine the signal pathway of piR-1366 in migration. Results: piR-1366 was up-regulated and positive expression in NSCLC ,The positive expression of piR-1366 was closely related to lymph node metastasis of NSCLC, but not with age, gender, tumor location, tumor size, tumor grade and TNM stage. piR-1366 is transfected into lung cancer cells to promote its migration and metastasis. Mechanistically,WT1-3'UTR was complementary combination with piR-1366 by bioinformatic prediction and identified as a direct target of piR-1366 through dual-luciferase reporter assay. Over-expression and knockdown of WT1 could respectively rescue and simulate the effects induced by piR-1366. Finally, piR-1366 promoted migration and metastasis by the WT1 /CDH1 pathway in lung cancer cells. Conclusions:Thus,our article suggested that piR-1366 was a novel pro-metastasis oncogene and may represent a novel marker of diagnosis and treatment for Metastatic NSCLC.

scholarly journals Human DECR1 is an androgen-repressed survival factor that regulates PUFA oxidation to protect prostate tumor cells from ferroptosis

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Zeyad D Nassar ◽  
Chui Yan Mah ◽  
Jonas Dehairs ◽  
Ingrid JG Burvenich ◽  
Swati Irani ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Mitochondrial Oxidative Stress ◽  
Free Survival ◽  
Resistant Lines ◽  
Proliferation And Metastasis ◽  
Xenograft Models ◽  
And Migration ◽  
Prostate Tumor Cells ◽  
Rate Limiting ◽  
Cell Proliferation And Metastasis

Fatty acid β-oxidation (FAO) is the main bioenergetic pathway in human prostate cancer (PCa) and a promising novel therapeutic vulnerability. Here we demonstrate therapeutic efficacy of targeting FAO in clinical prostate tumors cultured ex vivo, and identify DECR1, encoding the rate-limiting enzyme for oxidation of polyunsaturated fatty acids (PUFAs), as robustly overexpressed in PCa tissues and associated with shorter relapse-free survival. DECR1 is a negatively-regulated androgen receptor (AR) target gene and, therefore, may promote PCa cell survival and resistance to AR targeting therapeutics. DECR1 knockdown selectively inhibited β-oxidation of PUFAs, inhibited proliferation and migration of PCa cells, including treatment resistant lines, and suppressed tumor cell proliferation and metastasis in mouse xenograft models. Mechanistically, targeting of DECR1 caused cellular accumulation of PUFAs, enhanced mitochondrial oxidative stress and lipid peroxidation, and induced ferroptosis. These findings implicate PUFA oxidation via DECR1 as an unexplored facet of FAO that promotes survival of PCa cells.

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