33 research outputs found

    Absolute co-supplement and absolute co-coclosed modules

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    A module M is called an absolute co-coclosed (absolute co-supplement) module if whenever M ≅ T/X the submodule X of T is a coclosed (supplement) submodule of T. Rings for which all modules are absolute co-coclosed (absolute co-supplement) are precisely determined. We also investigate the rings whose (finitely generated) absolute co-supplement modules are projective. We show that a commutative domain R is a Dedekind domain if and only if every submodule of an absolute co-supplement R-module is absolute co-supplement. We also prove that the class Coclosed of all short exact sequences 0→A→B→C→0 such that A is a coclosed submodule of B is a proper class and every extension of an absolute co-coclosed module by an absolute co-coclosed module is absolute co-coclosed.Scientific and Technical Research Council of Turke

    Low Prognostic Nutritional Index (PNI) Predicts Unfavorable Distant Metastasis-Free Survival in Nasopharyngeal Carcinoma: A Propensity Score-Matched Analysis

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    <div><p>Background</p><p>Poor nutritional status is associated with progression and advanced disease in patients with cancer. The prognostic nutritional index (PNI) may represent a simple method of assessing host immunonutritional status. This study was designed to investigate the prognostic value of the PNI for distant metastasis-free survival (DMFS) in patients with nasopharyngeal carcinoma (NPC).</p><p>Methods</p><p>A training cohort of 1,168 patients with non-metastatic NPC from two institutions was retrospectively analyzed. The optimal PNI cutoff value for DMFS was identified using the online tool “Cutoff Finder”. DMFS was analyzed using stratified and adjusted analysis. Propensity score-matched analysis was performed to balance baseline characteristics between the high and low PNI groups. Subsequently, the prognostic value of the PNI for DMFS was validated in an external validation cohort of 756 patients with NPC. The area under the receiver operating characteristics curve (AUC) was calculated to compare the discriminatory ability of different prognostic scores.</p><p>Results</p><p>The optimal PNI cutoff value was determined to be 51. Low PNI was significantly associated with poorer DMFS than high PNI in univariate analysis (P<0.001) as well as multivariate analysis (P<0.001) before propensity score matching. In subgroup analyses, PNI could also stratify different risks of distant metastases. Propensity score-matched analyses confirmed the prognostic value of PNI, excluding other interpretations and selection bias. In the external validation cohort, patients with high PNI also had significantly lower risk of distant metastases than those with low PNI (Hazards Ratios, 0.487; P<0.001). The PNI consistently showed a higher AUC value at 1-year (0.780), 3-year (0.793) and 5-year (0.812) in comparison with other prognostic scores.</p><p>Conclusion</p><p>PNI, an inexpensive and easily assessable inflammatory index, could aid clinicians in developing individualized treatment and follow-up strategies for patients with non-metastatic NPC.</p></div

    DataSheet_2_LRRC3B and its promoter hypomethylation status predicts response to anti-PD-1 based immunotherapy.xlsx

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    BackgroundThe leucine rich repeat containing 3B (LRRC3B) gene is a tumor suppressor gene involved in the anti-tumor immune microenvironment. Expression of LRRC3B and DNA methylation at the LRRC3B promoter region may serve as a useful marker to predict response to anti-PD-1 therapy. However, no studies have yet systematically explored the protective role of LRRC3B methylation in tumor progression and immunity.MethodsExpression of LRRC3B of 33 cancer types in The Cancer Genome Atlas (TCGA) was downloaded from UCSC Xena (http://xena.ucsc.edu/). And, we evaluated the differential expression of LRRC3B according to tumor stage, overall survival, and characteristics of the tumor microenvironment. The immunotherapeutic cohorts included IMvigor21, GSE119144, and GSE72308 which were obtained from the Gene Expression Omnibus database. We conducted pearson correlation analysis of LRRC3B and tumor microenvironment (TME) in pan-cancer. Also, six immune cell types (B cells, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells) and tumor purity were analyzed using the Tumor IMmune Estimation Resource (TIMER1.0) (Tumor IMmune Estimation Resource (TIMER2.0). And, a “silencing score” model base on LRRC3B promoter methylation to predict overall survival (OS) by multivariate Cox regression analysis was constructed. Finally, the model was applied to predict anti-PD-1 therapy in non-small cell lung cancer (NSCLC) and breast cancer (BRCA).ResultsLRRC3B expression associated with less tumor invasion, less severe tumor stage, and decreased metastasis. The inactivation of LRRC3B promoted the enrichment of immuneosuppressive cells, including myeloid-derived suppressor cells (MDSCs), cancer-associated fibroblasts (CAFs), M2 subtype of tumor-associated macrophages (M2-TAMs), M1 subtype of tumor-associated macrophages (M1-TAMs), and regulatory T (Treg) cells. A high silencing score was significantly associated with immune inhibition, low expression of LRRC3B, poor patient survival, and activation of cancer-related pathways.ConclusionOur comprehensive analysis demonstrated the potential role of LRRC3B in the anti-tumor microenvironment, clinicopathological features of cancer, and disease prognosis. It suggested that LRRC3B methylation could be used as a powerful biomarker to predict immunotherapy responses in NSCLC and BRCA.</p

    DataSheet_1_LRRC3B and its promoter hypomethylation status predicts response to anti-PD-1 based immunotherapy.docx

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    BackgroundThe leucine rich repeat containing 3B (LRRC3B) gene is a tumor suppressor gene involved in the anti-tumor immune microenvironment. Expression of LRRC3B and DNA methylation at the LRRC3B promoter region may serve as a useful marker to predict response to anti-PD-1 therapy. However, no studies have yet systematically explored the protective role of LRRC3B methylation in tumor progression and immunity.MethodsExpression of LRRC3B of 33 cancer types in The Cancer Genome Atlas (TCGA) was downloaded from UCSC Xena (http://xena.ucsc.edu/). And, we evaluated the differential expression of LRRC3B according to tumor stage, overall survival, and characteristics of the tumor microenvironment. The immunotherapeutic cohorts included IMvigor21, GSE119144, and GSE72308 which were obtained from the Gene Expression Omnibus database. We conducted pearson correlation analysis of LRRC3B and tumor microenvironment (TME) in pan-cancer. Also, six immune cell types (B cells, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells) and tumor purity were analyzed using the Tumor IMmune Estimation Resource (TIMER1.0) (Tumor IMmune Estimation Resource (TIMER2.0). And, a “silencing score” model base on LRRC3B promoter methylation to predict overall survival (OS) by multivariate Cox regression analysis was constructed. Finally, the model was applied to predict anti-PD-1 therapy in non-small cell lung cancer (NSCLC) and breast cancer (BRCA).ResultsLRRC3B expression associated with less tumor invasion, less severe tumor stage, and decreased metastasis. The inactivation of LRRC3B promoted the enrichment of immuneosuppressive cells, including myeloid-derived suppressor cells (MDSCs), cancer-associated fibroblasts (CAFs), M2 subtype of tumor-associated macrophages (M2-TAMs), M1 subtype of tumor-associated macrophages (M1-TAMs), and regulatory T (Treg) cells. A high silencing score was significantly associated with immune inhibition, low expression of LRRC3B, poor patient survival, and activation of cancer-related pathways.ConclusionOur comprehensive analysis demonstrated the potential role of LRRC3B in the anti-tumor microenvironment, clinicopathological features of cancer, and disease prognosis. It suggested that LRRC3B methylation could be used as a powerful biomarker to predict immunotherapy responses in NSCLC and BRCA.</p

    Comparisons of the area under the receiver operating curve (AUC) for predicting distant metastasis free survival (DMFS) by PNI, mGPS, PLR and NLR.

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    <p>(A) At 1-year (AUC = 0.780, 0.705, 0.673 and 0.572, respectively), (B) 3-year (AUC = 0.793, 0.711, 0.653 and 0.542, respectively) and (C) 5-year (AUC = 0.812, 0.715, 0.642 and 0.530, respectively).NLR, neutrophil to lymphocyte ratio; PLR, the platelet to lymphocyte ratio; mGPS, the modified Glasgow Prognostic Score; PNI, prognostic nutritional index.</p

    Forest plot of subgroup effects for distant metastasis-free survival (DMFS) in 1,168 patients with nasopharyngeal carcinoma who underwent definitive radiotherapy.

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    <p>Subgroups are defined by factors showing significant associations between the PNI and DMFS. Univariate hazard ratios and 95% CI (bars) are presented. WBC, white blood cell count; HGB, hemoglobin; ALT, <a href="http://dict.cnki.net/dict_result.aspx?searchword=%e8%b0%b7%e4%b8%99%e8%bd%ac%e6%b0%a8%e9%85%b6(alt)&tjType=sentence&style=&t=alanine+transaminase+(alt)" target="_blank">alanine transaminase; AST, aspartate transaminase; ALP, alkaline phosphatase; LDH, lactate dehydrogenase; CRP, C-reactive protein; ALB, albumin; EBV, Epstein-Barr virus DNA;</a> CRT, conventional radiotherapy: IMRT, intensity-modulated radiation therapy; 3D-CRT, three-dimensional conformal radiation therapy; RT, radiotherapy; chemo-radiotherapy, chemotherapy plus radiotherapy.</p

    Prognostic value of the prognostic nutritional index (PNI) for distant metastasis-free survival (DMFS).

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    <p>(A) In the training cohort before matching, (B) the validation cohort and (C) the training cohort after 2:1 ratio matching.</p
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