Survival Prognosis Of Patients Research Articles

Upregulation of phosphatidylinositol glycan anchor biosynthesis class C is associated with unfavorable survival prognosis in patients with hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common types of malignant tumor, and is the second highest cause of cancer-associated mortality, behind lung carcinoma. It is urgent to identify novel genes that can be used to confirm the diagnosis and prognosis of patients with HCC. The present study aimed to investigate the expression pattern of phosphatidylinositol glycan anchor biosynthesis class C (PIGC) in HCC and assess its clinical prognostic significance. Bioinformatics analyses were used to investigate PIGC mRNA expression levels in HCC and adjacent non-cancerous tissue samples. Furthermore, the present study detected the expression levels of PIGC protein in HCC and matched normal tissue samples via immunohistochemistry, and evaluated the prognostic significance of PIGC protein in HCC. The levels of PIGC mRNA and protein were found to be significantly higher in tissue from patients with HCC compared with non-cancerous liver tissue. The survival analysis showed that the expression levels of PIGC mRNA or protein were associated with the survival of patients with HCC. PIGC protein expression was significantly associated with Tumor-Node-Metastasis stage. A negative correlation between PIGC DNA methylation and mRNA expression was observed (Spearman r=−0.453). PIGC is an oncogene that is negatively regulated by DNA methylation, and high levels of PIGC mRNA or protein may predict an unfavorable prognosis in patients with HCC.

Systemic inflammation scores correlate with survival prognosis in patients with newly diagnosed brain metastases

BackgroundSystemic inflammation measured by the neutrophil-to-lymphocyte ratio (NLR), leucocyte-to-lymphocyte ratio (LLR), platelet-to-lymphocyte ratio (PLR), monocyte-to-lymphocyte ratio (MLR) and CRP/albumin ratio (CRP/Alb) was shown to impact the survival prognosis in patients with extracranial solid cancer.MethodsOne thousand two hundred and fifty patients with newly diagnosed brain metastases (BM) were identified from the Vienna Brain Metastasis Registry.ResultsPLR and CRP/Alb were higher in patients with progressive extracranial disease and lower in patients with no evidence of extracranial disease. Lower NLR (cut-off = 5.07; 9.3 vs. 5.0 months), LLR (cut-off = 5.76; 10.0 vs. 5.3 months), PLR (cut-off = 335; 8.0 vs. 3.8 months), MLR (cut-off = 0.53; 6.0 vs. 3.5 months) and CRP/Alb (cut-off = 2.93; 8.5 vs. 3.7 months; padj < 0.05) were associated with longer overall survival (OS). In multivariate analysis with graded prognostic assessment (hazard ratio (HR) 1.45; 95% confidence interval (CI): 1.32–1.59; padj = 1.62e − 13), NLR (HR 1.55; 95% CI: 1.38–1.75; padj = 1.92e − 11), LLR (HR 1.57; 95% CI: 1.39–1.77; padj = 1.96e − 11), PLR (HR 1.60; 95% CI: 1.39–1.85; padj = 2.87955e − 9), MLR (HR 1.41; 95% CI: 1.14–1.75; padj = 0.027) and CRP/Alb (HR 1.83; 95% CI: 1.54–2.18; padj = 2.73e − 10) remained independent factors associated with OS at BM diagnosis.ConclusionsSystemic inflammation, measured by NLR, LLR, PLR, MLR and CRP/Alb, was associated with OS in patients with BM. Further exploration of immune modulating therapies is warranted in the setting of BM.

The Role of Lysosomes in the Cancer Progression: Focus on the Extracellular Matrix Degradation

Lysosomes are multifunctional cell organelles that not only provide degradation of macromolecules by lumenal acid hydrolases, but also contribute in the regulation of cell metabolism, ion homeostasis maintenance, and programmed cell death induction. The study of this compartment in various pathological conditions, including the oncological diseases by different origins is of particular interest. This article discusses the lysosome involvement in the process of malignant cell transformation, as well as the role of these organelles in the tumor cell metastasis mediated by proteolytic cleavage of the extracellular matrix components. Metabolic and morphological changes of cells during oncogenesis lead to pHdependent redistribution of lysosomes within the cell, accompanied by the secretion of lysosomal proteases cathepsins into the extracellular space. Cysteine, serine, and arginine cathepsins released by both tumor cells and tumor-associated cells catalyze the cleavage of various components of the extracellular matrix and basement membrane, or proteolytically activate other enzymes also involved in this process. In this instance, lysosomal proteases directly affect the ability of cells to invade and the metastatic potential of tumor formation. In addition, it was demonstrated the prognostic importance of some cathepsins (especially cathepsins B, K, and D) the number and activity of which in the tumor tissue and its microenvironment are associated with malignancy of the formation, as well as with a poor prognosis for patient survival and with the possibility of recurrences.

Epigenetic Modulation of SPCA2 Reverses Epithelial to Mesenchymal Transition in Breast Cancer Cells.

Simple SummaryThe triple receptor negative breast cancer subtype, or TNBC, currently has no tailored treatment options. TNBC is highly metastatic, associated with high patient mortality, and disproportionately occurs in Black/African American women where it contributes to racial disparities in health outcomes. Therefore, we focused on new therapeutic approaches to TNBC. We discovered that levels of the Calcium-ATPase SPCA2 are abnormally low in TNBC and that these low levels correlate with poor survival prognosis in patients. Previously, we showed that recombinant SPCA2 prevented TNBC cells from acquiring aggressive “mesenchymal” properties associated with metastasis both in vitro and in vivo. These findings motivated us to search for drugs that turn the SPCA2 gene back on in TNBC cells. In this study, we show that histone deacetylase inhibitors increase SPCA2 levels, activate Ca2+ signaling and convert cancer cells to a less aggressive “epithelial” state. These findings could lead to new treatment options for TNBC.The secretory pathway Ca2+-ATPase SPCA2 is a tumor suppressor in triple receptor negative breast cancer (TNBC), a highly aggressive molecular subtype that lacks tailored treatment options. Low expression of SPCA2 in TNBC confers poor survival prognosis in patients. Previous work has established that re-introducing SPCA2 to TNBC cells restores basal Ca2+ signaling, represses mesenchymal gene expression, mitigates tumor migration in vitro and metastasis in vivo. In this study, we examined the effect of histone deacetylase inhibitors (HDACi) in TNBC cell lines. We show that the pan-HDACi vorinostat and the class I HDACi romidepsin induce dose-dependent upregulation of SPCA2 transcript with concurrent downregulation of mesenchymal markers and tumor cell migration characteristic of epithelial phenotype. Silencing SPCA2 abolished the ability of HDACi to reverse epithelial to mesenchymal transition (EMT). Independent of ATPase activity, SPCA2 elevated resting Ca2+ levels to activate downstream components of non-canonical Wnt/Ca2+ signaling. HDACi treatment led to SPCA2-dependent phosphorylation of CAMKII and β-catenin, turning Wnt signaling off. We conclude that SPCA2 mediates the efficacy of HDACi in reversing EMT in TNBC by a novel mode of non-canonical Wnt/Ca2+ signaling. Our findings provide incentive for screening epigenetic modulators that exploit Ca2+ signaling pathways to reverse EMT in breast tumors.

Identification of hub genes in thyroid carcinoma to predict prognosis by integrated bioinformatics analysis

ABSTRACT The aim of this study was to identify hub genes closely related to the pathogenesis and prognosis of thyroid carcinoma (THCA) by integrated bioinformatics analysis. In this study, through differential gene expression analysis, 1916 and 665 differentially expressed genes (DEGs) were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) database, and 7 and 11 co-expressed modules were identified from the TCGA-THCA and GSE153659 datasets, respectively, by weighted gene co-expression network analysis. We identified 162 overlapping genes between the DEGs and co-expression module genes as candidate hub genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the 162 overlapping DEGs identified significant functions and pathways of THCA, such as thyroid hormone generation and metabolic process. A protein–protein interaction (PPI) analysis detected the top 10 hub genes (QSOX1, WFS1, EVA1A, FSTL3, CHRDL1, FABP4, PRDM16, PPARGC1A, PPARG, COL23A1). Finally, survival analysis, clinical correlation analysis, and protein abundance validation confirmed that 3 of the 10 hub genes were associated with survival prognosis of patients with THCA, and 8 of them were associated with the clinical stages of THCA. In summary, we identified hub genes and key modules that were closely related to THCA, and validated these genes by survival analysis, clinical correlation analysis, and Human Protein Atlas image analysis. Our results provide important information that will help to elucidate the pathogenesis of THCA and identify novel candidate prognostic biomarkers and potential therapeutic targets.

Long non-coding RNA BCAR4 aggravated proliferation and migration in esophageal squamous cell carcinoma by negatively regulating p53/p21 signaling pathway

ABSTRACT Long non-coding RNA breast cancer antiestrogen resistance 4 (lncRNA BCAR4) is an independent factor on the survival prognosis of patients with multiple cancers. However, the role of lncRNA BCAR4 in esophageal squamous cell cancer (ESCC) remains unknown. Here, we unraveled that lncRNA BCAR4 was upregulated in ESCC and predicted poor prognosis. Functionally, lncRNA BCAR4 knockdown induced cell apoptosis and G1/S arrest, while inhibited cell proliferation and migration in vitro; conversely, overexpressing lncRNA BCAR4 promoted proliferation and metastasis. Mechanistically, lncRNA BCAR4 sponged miR-139-3p to upregulate ELAVL1, thereby inhibiting p53/p21 pathway in ESCC cells. In conclusion, lncRNA BCAR4 promotes ESCC tumorigenesis via regulating p53/p21 signaling pathway and develops a brand-new biomarker and medicine target for ESCC.

Prognostic Role of ABO Blood Type in Operable Esophageal Cancer: Analysis of 2179 Southern Chinese Patients.

BackgroundThe prognostic value of ABO blood types is not well clarified for esophageal carcinoma (EC). This study attempted to elucidate the associations between different ABO blood types and disease-free survival (DFS) and overall survival (OS) of EC.MethodsThis study was a retrospective review of the records of 2179 patients with EC who received surgery from December 2000 to December 2008. The prognostic impact of ABO blood group on DFS and OS were estimated using the Kaplan-Meier method and cox proportional hazard models.ResultsUnivariate analyses found significant differences in DFS and OS among the four blood types. Multivariate analyses showed ABO blood type independently predicted DFS (P=0.001) and OS (P=0.002). Furthermore, patients with non-B blood types had a significantly shorter DFS (HR=1.22, 95%CI:1.07–1.38, P=0.002) and OS (HR=1.22, 95%CI:1.07–1.38, P=0.003) than patients with blood type B, and patients with non-O blood types had a significantly better DFS (HR=0.86, 95%CI:0.77–0.96, P=0.006) and OS (HR=0.86, 95%CI:0.77–0.96, P=0.007) than patients with blood type O. Subgroup analyses found that blood type B had a better DFS and OS than non-B in patients who were male, younger, early pathological stages and had squamous-cell carcinomas (ESCC). Blood type O had a worse DFS and OS than non-O in patients who were male, younger, and had ESCC (P<0.05).ConclusionsThe results demonstrate that ABO blood group is an independent prognostic factor of survival, and that type B predicts a favorable prognosis, whereas type O predicts an unfavorable prognosis for survival in patients with EC, especially those with ESCC.

Non-invasive and tracheostomy invasive ventilation in amyotrophic lateral sclerosis: Utilization and survival rates in a cohort study over 12 years in Germany.

The aim of this study was to investigate utilization rates, treatment pathways and survival prognosis in patients with amyotrophic lateral sclerosis (ALS) undergoing non-invasive (NIV) and tracheostomy invasive ventilation (TIV) in a real-world setting. A prospective cohort study using a single-centre register of 2702 ALS patients (2007 to 2019) was conducted. Utilization of NIV/TIV and survival data were analysed in three cohorts: (i) non-NIV; (ii) NIV (NIV without subsequent TIV); and (iii) TIV (including TIV preceded by NIV). A total of 1720 patients with available data were identified, 72.0% of whom (n=1238) did not receive ventilation therapy. NIV was performed in 20.8% of patients (n=358). TIV was performed in 9.5% of patients (n=164), encompassing both primary TIV (7.2%, n=124) and TIV with preceding NIV (2.3%, n=40). TIV was more often utilized without previous NIV (25.7% vs. 8.3% of all ventilated patients), demonstrating that primary TIV was the prevailing pathway for invasive ventilation. The median (range) survival was significantly longer in the NIV cohort (40.8[37.2-44.3] months) and the TIV cohort (82.1[68.7-95.6] months) as compared to the non-NIV cohort (33.6[31.6-35.7] months). Although NIV represents the standard of care, its utilization rate was low. TIV was mainly started without preceding NIV, suggesting that TIV may not be confined to NIV treatment escalation. However, TIV was pursued in a minority of patients who had previously undergone NIV. The survival benefit observed in the patients with NIV was equal to that reported in a controlled pivotal trial, but the prognosis with TIV is highly variable. The determinants of utilization of NIV/TIV and of survival (bulbar syndrome, availability of ventilation-related home nursing, cultural factors) warrant further investigation.

Role of FUT8 expression in clinicopathology and patient survival for various malignant tumor types: a systematic review and meta-analysis.

Dysregulation of α(1,6)-fucosyltransferase (FUT8) plays significant roles in development of a variety of malignant tumor types. We collected as many relevant articles and microarray datasets as possible to assess the prognostic value of FUT8 expression in malignant tumors. For this purpose, we systematically searched PubMed, Embase, Web of Science, Springer, Chinese National Knowledge Infrastructure (CNKI), and Wan Fang, and eventually identified 7 articles and 35 microarray datasets (involving 6124 patients and 10 tumor types) for inclusion in meta-analysis. In each tumor type, FUT8 expression showed significant (p< 0.05) correlation with one or more clinicopathological parameters; these included patient gender, molecular subgroup, histological grade, TNM stage, estrogen receptor, progesterone receptor, and recurrence status. In regard to survival prognosis, FUT8 expression level was associated with overall survival in non-small cell lung cancer (NSCLC), breast cancer, diffuse large B cell lymphoma, gastric cancer, and glioma. FUT8 expression was also correlated with disease-free survival in NSCLC, breast cancer, and colorectal cancer, and with relapse-free survival in pancreatic ductal adenocarcinoma. For most tumor types, survival prognosis of patients with high FUT8 expression was related primarily to clinical features such as gender, tumor stage, age, and pathological category. Our systematic review and meta-analysis confirmed the association of FUT8 with clinicopathological features and patient survival rates for numerous malignant tumor types. Verification of prognostic value of FUT8 in these tumor types will require a large-scale study using standardized methods of detection and analysis.

Lung cancer pathogenesis and poor response to therapy were dependent on driver oncogenic mutations

AimsLung cancer was the most fatal malignancy, dominated the cancer related mortality list for years, and we tried to distinguish the lung adenocarcinoma patients at higher risk from those bearing lower therapy resistance and recurrence risk. MaterialsPatients information from clinical Sequencing Cohorts and from the Regional Medical Center of the Middle-West China were included. The whole-exome sequencing was analyzed for risk evaluation. Key findingsWe found that Smoking stimulated the oncogenic genes mutations, and the most frequently mutated genes of EGFR, KRAS, and TP53 (E/K/P) were identified. Different N stage affected the survival prognosis of patients bearing E/K/P mutations, but the T stage and AJCC stage did not. Radiation failed to prolong survival of phase II/III patients who didn't receive surgery. In those received surgery, radiation also failed to prolong survival of phase II/III patients. Radiation did not improve the prognosis in patients bearing E/K/P mutation burdens, whose differences were identified in gender or smoking-history classified groups. SignificanceSmoking status and history contributed to oncogenic mutation burdens associated therapy resistance, and the aggressive treatment, especially to radiation, may lead to worse therapy response to current and past smoking behavior.

Clinical significance and prognostic value of Porphyromonas gingivalis infection in lung cancer

A variety of pathogenic microorganisms can promote the occurrence and development of malignant tumors by colonizing in the body. It has been shown that Porphyromonas gingivalis (P. gingivalis) can be colonized for a long time in upper gastrointestinal tumors and is closely related to the occurrence and development of esophageal cancer in previous studies of our team. Because the esophagus and trachea are closely adjacent and P. gingivalis can instantly enter and colonize in cells, we speculate that P. gingivalis may be colonized in lung cancer cells through oral or blood, promoting the malignant progression of lung cancer. In this study, we investigated P. gingivalis infection in lung carcinoma tissues and adjacent lung tissues, and found that the colonization rate of P. gingivalis in carcinoma tissues was significantly higher than that in adjacent lung tissues. Therefore, we propose that the microenvironment of cancer cells is more conducive to the survival of P. gingivalis. Then, we analyzed the correlation between P. gingivalis infection and clinicopathological features and survival prognosis of patients with lung cancer. It was found that P. gingivalis infection was closely related to smoking, drinking, lymph node metastasis and clinical stage. Moreover, the survival rate and median survival time of patients with P. gingivalis infection were significantly shortened. Therefore, we put forward the view that long term smoking and drinking will cause a bad oral environment, increasing the risk of P. gingivalis infection, then P. gingivalis infection will promote the malignant progression of lung cancer.

Tracheotomy in comparison with tracheopathia for prolonged intubation of the lungs in surgical patients

A comparative analysis of the MEDLINE, EMBASE, CINAHL and Cochrane Registry databases was carried out to identify the advantages of puncture-dilatation tracheostomy methods over standard tracheotomy in critically ill patients. In addition, bibliographies and selected conference proceedings were reviewed; included randomized clinical trials comparing puncture-dilatation techniques with standard tracheotomy in critically ill adults, which reported clinically significant outcomes. The extracted data are focused on the criteria for the validity of the studies and the results relevant to practice. Puncture methods are less traumatic and can reduce the likelihood of infection of the surgical wound. Compared to the traditional method, a puncture tracheostomy can be applied in just 2 minutes,which can play a significant role in the prognosis of patient survival. The role of the experience of the operators performing the procedures has a significant impact on the results, which cannot be formally and quantitatively assessed in our analysis.

Characteristics and survival prognosis of patients with pure squamous cell carcinoma of the gallbladder.

Pure squamous cell carcinoma (SCC) of the gallbladder is rare and often confused with the adenosquamous carcinoma (ASC) subtype in previous studies. The present study was attempted to differentiate SCC from ASC by resolving their characteristics and prognosis. The Surveillance, Epidemiology, and End Results database was queried for SCC and ASC of gallbladder cases from 1988 to 2015. Patients' clinicopathological characteristics and survival were analysed between the groups. Of the 709 patients with primary gallbladder cancer included in this study, 249 (35.1%) had pure SCC and the remaining 460 (64.9%) had ASC. It was found that pure SCC was associated with a larger median tumour size (58.0 versus 41.0 mm, P < 0.001), while ASC presented with a worse histological grade (47.4% versus 37.8% for grades III-IV, P = 0.019) and more lymph node invasion (27.4% versus 18.9%, P = 0.041). The 3-year overall survival and disease-specific survival rates in pure SCC were lower than those in ASC (7.5% versus 11.5% for overall survival, P < 0.001; 6.2% versus 10.9% for disease-specific survival, P < 0.001). Multivariate analysis showed that early Surveillance, Epidemiology, and End Results historic stage, treatment with surgery and chemotherapy were significant favourable prognostic factors for pure SCC, while tumour size, late study period, treatment with surgery and radiotherapy were significant predictors for ASC. There were significant differences in the clinicopathological characteristics and survival prognosis between pure SCC and ASC. Surgery combined with chemotherapy is the preferred treatment option for pure SCC.

Amplified LncRNA PVT1 promotes lung cancer proliferation and metastasis by facilitating VEGFC expression.

Although the abundance of long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) in lung cancer has been well researched, the underlying mechanisms behind its effects were unknown. Here we investigated the molecular events regulating PVT1 in lung cancer. The pro-proliferative property of PVT1 was examined using a xenograft tumor model. Transwell chambers were used to analyze the impact of PVT1 expression on cell invasiveness and migration. In vivo metastasis was examined by tail-vein-injection in mice. Direct binding of miR-128 to PVT1 was investigated using a probe pulldown assay. The relative expression levels of miR-128 and PVT1 were quantified by real-time polymerase chain reaction and Western blotting. We show here that when PVT1 is amplified, there is a poor survival prognosis for patients with lung cancer. Elevated levels of PVT1 promoted lung cancer cell proliferation and metastasis, both in vitro and in vivo. Mechanistically, we found that PVT1 competes endogenously with miR-128 in the regulation of vascular endothelial growth factor C (VEGFC) expression, which is significantly associated with an unfavorable prognosis in lung cancer. We identified that copy number amplification significantly contributes to the high level of PVT1 transcripts in lung cancer, which promotes cell proliferation and metastatic behavior via modulating VEGFC expression by endogenous competition with miR-128.

A SEMA3 Signaling Pathway-Based Multi-Biomarker for Prediction of Glioma Patient Survival.

Glioma is a lethal central nervous system tumor with poor patient survival prognosis. Because of the molecular heterogeneity, it is a challenge to precisely determine the type of the tumor and to choose the most effective treatment. Therefore, novel biomarkers are essential to improve the diagnosis and prognosis of glioma tumors. Class 3 semaphorin proteins (SEMA3) play an important role in tumor biology. SEMA3 transduce their signals by using neuropilin and plexin receptors, which functionally interact with the vascular endothelial growth factor-mediated signaling pathways. Therefore, the aim of this study was to explore the potential of SEMA3 signaling molecules for prognosis of glioma patient survival. The quantitative real-time PCR method was used to evaluate mRNA expression of SEMA3(A-G), neuropilins (NRP1 and NRP2), plexins (PLXNA2 and PLXND1), cadherins (CDH1 and CDH2), integrins (ITGB1, ITGB3, ITGA5, and ITGAV), VEGFA and KDR genes in 59 II-IV grade glioma tissues. Seven genes significantly associated with patient overall survival were used for multi-biomarker construction, which showed 64%, 75%, and 68% of accuracy of predicting the survival of 1-, 2-, and 3-year glioma patients, respectively. The results suggest that the seven-gene signature could serve as a novel multi-biomarker for more accurate prognosis of a glioma patient’s outcome.

Abstract PR15: CD74 regulated inflammatory pattern is associated with TIL growth and favorable response to adoptive immunotherapy

Abstract We previously reported that in Stage III melanoma patients’ tumors, positive expression of CD74 together with low or absent Macrophage Migration Inhibitory Factor (MIF) associates with favorable prognosis (Ekmekcioglu et al., CCR 2016). As both are known to be regulated by IFN-g, we suggest a differential IFN-g response as well as a novel role for CD74 that may be exploited to improve patient outcome. Our further analyses of The Cancer Genome Atlas (TCGA) datasets confirmed the role of CD74 in prognosis for patient survival, which is likely attributed to regulation of MHC-Class II and antigen presentation in the tumor microenvironment. Immune infiltration of T cells (TIL) into the melanoma microenvironment has been associated with improved survival for some patients, and also has been exploited to grow TIL in vitro for adoptive therapy. However, prognostic significance of immune infiltrating cells in melanoma and other tumors remains a relatively new concept, and markers related to suppressive versus active functional TIL remain unclear. From an ongoing clinical trial using TIL intended for adoptive immunotherapy, we have studied the melanoma patient tumor specimens (FFPE) from 20 patients whose autologous TIL lines grew to sufficient number for possible use clinically. We also examined another 20 sets of melanoma tumor from which the TIL did not grow or did not grow well. We analyzed the differences in the two groups of tumors (40 total FFPE) for CD74 regulated pathway features and inflammatory marker expression. CD74 regulated markers included CD44, MIF, and downstream inflammatory targets including inducible nitric oxide synthase (iNOS), nitrotyrosine (NT) and microsomal prostaglandin E synthase-1 (mPGES1). Our findings confirm our previous report in that tumor CD74 expression significantly associates with favorable OS and PFS (both, p=0.0038) and provides new data that in this set of patients the CD74 also correlates with best irRC of TIL treated patients. New findings include that the NT expression in tumor cells associated with poor TIL growth (p=0.014), as well as lack of clinical response to TIL treatment (p=0.02). We have also found that tumor cell-derived MIF and iNOS expression correlate with unfavorable prognosis for both OS and PFS (p=0.016 and 0.018, respectively). The iNOS and MIF coexpression characteristics and cellular distributions in the tumor are currently under way. In conclusion, we have identified the protein expression of CD74, MIF and of iNOS as providing survival information, and proposed that CD74+/MIF-/iNOS- together be considered to form a “signature” of good prognosis in general melanoma outcomes as well as TIL growth and favorable responses for these patients. Use of this signature for selecting patients for entry into TIL and possibly other immunotherapy trials, as well as research on the differential pathways of IFN-g signaling in melanoma, appear as important areas for future mechanistic research to improve patient outcome. This abstract is also being presented as Poster B14. Citation Format: Dai-Ogata, Caitlin A. Creasy, Sun-Hee Kim, Jason Roszik, Patrick Hwu, Elizabeth A. Grimm, Chantale Bernatchez, Suhendan Ekmekcioglu. CD74 regulated inflammatory pattern is associated with TIL growth and favorable response to adoptive immunotherapy [abstract]. In: Proceedings of the AACR Special Conference on Melanoma: From Biology to Target; 2019 Jan 15-18; Houston, TX. Philadelphia (PA): AACR; Cancer Res 2020;80(19 Suppl):Abstract nr PR15.

Anillin is an emerging regulator of tumorigenesis, acting as a cortical cytoskeletal scaffold and a nuclear modulator of cancer cell differentiation.

Remodeling of the intracellular cytoskeleton plays a key role in accelerating tumor growth and metastasis. Targeting different cytoskeletal elements is important for existing and future anticancer therapies. Anillin is a unique scaffolding protein that interacts with major cytoskeletal structures, e.g., actin filaments, microtubules and septin polymers. A well-studied function of this scaffolding protein is the regulation of cytokinesis at the completion of cell division. Emerging evidence suggest that anillin has other important activities in non-dividing cells, including control of intercellular adhesions and cell motility. Anillin is markedly overexpressed in different solid cancers and its high expression is commonly associated with poor prognosis of patient survival. This review article summarizes rapidly accumulating evidence that implicates anillin in the regulation of tumor growth and metastasis. We focus on molecular and cellular mechanisms of anillin-dependent tumorigenesis that include both canonical control of cytokinesis and novel poorly understood functions as a nuclear regulator of the transcriptional reprogramming and phenotypic plasticity of cancer cells.

Prognostic value of combined preoperative prognostic nutritional index and neutrophil to lymphocyte ratio in esophageal squamous cell carcinoma

BackgroundPreoperative nutritional status and some inflammatory indexes are associated with survival in various malignancies. Prognostic nutritional index (PNI) or neutrophil to lymphocyte ratio (NLR) was demonstrated associated with survival in patients with esophageal squamous cell carcinoma (ESCC). The purpose of the present study was to investigate whether the combination index of PNI and NLR (PNI-NLR) is superior to either alone in survival prognosis of patients with ESCC.MethodsIn total, 271 patients with ESCC who underwent radical esophagectomy from Qianfoshan Hospital from May 2009 to July 2014 were enrolled. Preoperative PNI and other clinical data were collected and analyzed. Using the 5-year survival rate as an end point, a receiver operating characteristic (ROC) analysis was used to find the best cutoff value for PNI and NLR was 49.1 and 3.14, respectively. And all the enrolled patients were classified into three groups: group 1 (score 0, NLR ≤3.14 and PNI >49.1), group 2 (score 1, NLR >3.14 or PNI ≤49.1) and group 3 (score 2, NLR >3.14 and PNI ≤49.1).ResultsThe combined index of PNI-NLR was a sensitive index in survival prognosis, and patients in the group 1, 2 and 3 had median survival times of 64, 47 and 36 months, respectively. Patients in group1 had significantly longer survival time than those of group 2 and group 3. In multivariate analyses, TNM stage, lymph stage, PNI and PNI-NLR affected the overall survival (OS). PNI was significantly correlated with TNM stage.ConclusionsPreoperative PNI-NLR was an independent predictor of survival of patients with ESCC. The index of PNI-NLR can improve the accuracy of prognoses for patients with ESCC than the index of NLR.

1467P The development and verification of nomogram to predict the survival prognosis of patients with esophageal squamous cell carcinoma

1467P The development and verification of nomogram to predict the survival prognosis of patients with esophageal squamous cell carcinoma

Impact of mirna-21 on survival prognosis in patients with pancreatic cancer

Background:Previous studies have reported that microRNA-21 (mRNA-21) has an effect on the prognosis of pancreatic cancer. However, the conclusion is still unclear. Therefore, this study will try to explore the effect of high expression of mRNA-21 on the prognosis of pancreatic cancer.Methods:Retrieved the database, including the China National Knowledge Infrastructure (CNKI), Chinese Biomedical literature Database (CBM), Chinese Scientific and Journal Database (VIP), Wan Fang database, PubMed, and EMBASE. Hazard ratios (HRs) and its 95% confidence intervals (CIs) to assess the prognostic effect of miRNA-21 on overall survival (OS) and disease-free survival (DFS). RevMan 5.3 and STATA 16.0 software were used to perform the meta-analysis.Results:This study will comprehensively review and evaluate the available evidence of high expression of miRNA-21 on the prognosis of patients with pancreatic cancer.Conclusion:Our findings will show the effect of high expression of miRNA-21 on the prognosis of patients with pancreatic cancer. Such studies may find a new prognostic marker for patients with pancreatic cancer and help clinicians and health professionals make clinical decisions.Ethics and dissemination:The private information from individuals will not publish. This systematic review also will not involve endangering participant rights. Ethical approval is not available. The results may be published in a peer- reviewed journal or disseminated in relevant conferences.OSF Registration number:DOI 10.17605/OSF.IO/2A6KJ.