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1.
ATP binding cassette subfamily C member 8 (ABCC8) encodes a protein regulating the ATP-sensitivepotassium channel. Whether the level of ABCC8 mRNA in lower grade glioma (LGG) correlates with immune cellinfiltration and patient outcomes has not been evaluated until now. Comparisons of ABCC8 expression betweendifferent tumors and normal tissues were evaluated by exploring publicly available datasets. The association betweenABCC8 and tumor immune cell infiltration, diverse gene mutation characteristics, tumor mutation burden (TMB),and survival in LGG was also investigated in several independent datasets. Pathway enrichment analysis wasconducted to search for ABCC8-associated signaling pathways. Through an online database, we found that ABCC8expression in LGG was lower than in normal tissues. Then, the association of ABCC8 expression and immune cellinfiltration in LGG was discussed. As we expected, the ABCC8 mRNA levels were negatively associated with non-Timmune cell infiltration levels in all datasets. Consistently, TCGA_LGG RNA-seq data revealed that ABCC8downregulated several non-T immune cell-associated signaling pathways in gene set enrichment analysis. DifferentABCC8 expression groups showed diverse gene mutation characteristics and TMB. The high expression of ABCC8was linked to improved survival of LGG patients. A pathway enrichment analysis of ABCC8-associated genesindicated that the GABAergic synapse signaling pathway might be involved in regulating immunity in LGG. Ourfindings show that ABCC8 reflects LGG tumor immunity and is an ideal prognostic biomarker for LGG. 相似文献
2.
Hepatocellular carcinoma (HCC) is a common immunogenic malignant tumor. Although the new strategies of immunotherapy and targeted therapy have made considerable progress in the treatment of HCC, the 5-year survival rate of patients is still very low. The identification of new prognostic signatures and the exploration of the immune microenvironment are crucial to the optimization and improvement of molecular therapy strategies. We studied the potential clinical benefits of the inflammation regulator miR-93-3p and mined its target genes. Weighted gene co-expression network analysis (WGCNA), univariate and multivariate COX regression and the LASSO COX algorithm are employed to identify prognostic-related genes and construct multi-gene signature-based risk model and nomogram for survival prediction. Support vector machine (SVM) based Cibersort’s deconvolution algorithm and gene set enrichment analysis (GSEA) is used to evaluate the changes in tumor immune microenvironment and pathway differences. The study found the favorable prognostic performance of miR-93-3p and identified 389 prognostic-related target genes. The risk model based on a novel 5-gene signature (cct5, cdk4, cenpa, dtnbp1 and flvcr1) was developed and has prominent prognostic significance in the training cohort (P < 0.0001) and validation cohort (P = 0.0016). The nomogram constructed by combining the gene signature and the AJCC stage further improves the survival prediction ability of the gene signature. The infiltration level of multiple immune cells (especially T cells, B cells and macrophages) were positively correlated with the expression of prognostic signature. In addition, we found that gene markers of T cells and B cells is monitored and regulated by prognostic signature. Meanwhile, several GSEA pathways related to the immune system are enriched in the high-risk group. In general, we integrated the WGCNA, LASSO COX and SVM algorithms to develop and verify 5-gene signatures and nomograms related to immune infiltration to improve the survival prediction of patients. 相似文献
3.
YONGHUI YU SONGHUI XU ERYONG ZHAO YONGSHUN DONG JINBIN CHEN BOQI RAO JIE ZENG LEI YANG JIACHUN LU FUMAN QIU 《Biocell》2022,46(4):999-1011
The outcomes of ovarian cancer are complicated and usually unfavorable due to their diagnoses at a late stage. Identifying the efficient prognostic biomarkers to improve the survival of ovarian cancer is urgently warranted. The survival-related pseudogenes retrieved from the Cancer Genome Atlas database were screened by univariate Cox regression analysis and further assessed by least absolute shrinkage and selection operator (LASSO) method. A risk score model based on the prognostic pseudogenes was also constructed. The pseudogene-mRNA regulatory networks were established using correlation analysis, and their potent roles in the ovarian cancer progression were uncovered by functional enrichment analysis. Lastly, ssGSEA and ESTIMATE algorithms was used to evaluate the levels of immune cell infiltrations in cancer tissues and explore their relationship with risk signature. A prediction model of 10-pseudogenes including RPL10P6, AC026688.1, FAR2P4, AL391840.2, AC068647.2, FAM35BP, GBP1P1, ARL4AP5, RPS3AP2, and AMD1P1 was established. The 10-pseudogenes signature was demonstrated to be an independent prognostic factor in patient with ovarian cancer in the random set (hazard ratio [HR] = 2.512, 95% confidence interval [CI] = 2.03–3.11, P < 0.001) and total set (HR = 1.71, 95% CI = 1.472–1.988, P < 0.001). When models integrating with age, grade, stage, and risk signature, the Area Under Curve (AUC) of the 1-year, 3-year, 5-year and 10-year Receiver Operating Characteristic curve in the random set and total set were 0.854, 0.824, 0.855, 0.805 and 0.679, 0.697, 0.739, 0.790, respectively. The results of functional enrichment analysis indicated that the underlying mechanisms by which these pseudogenes influence cancer prognosis may involve the immune-related biological processes and signaling pathways. Correlation analysis showed that risk signature was significantly correlated with immune cell infiltration and immune score. We identified a novel 10-pseudogenes signature to predict the survival of patients with ovarian cancer, and that may serve as novel possible prognostic biomarkers and therapeutic targets for ovarian cancer. 相似文献
4.
Background: Cytochrome b561 (CYB561) plays a critical role in neuroendocrine function, cardiovascular regulation, and tumor growth; however, the prognostic value of CYB561 in patients with breast cancer and the relationship between CYB561 expression and immune infiltration in breast cancer remain unclear. Methods: The mRNA expression and clinical data of patients with breast cancer were obtained from The Cancer Genome Atlas database. Functional enrichment analysis was used to explore underlying biological functions associated with CYB561. The methylation status of CYB561 was analyzed using the MethSurv database. The enrichment score of immune cell infiltration for CYB561 in breast cancer was calculated using single-sample gene set enrichment analysis. The prognostic value of CYB561 was evaluated using Kaplan-Meier method and Cox regression analysis. Based on the results of the multivariate Cox analysis, a nomogram was constructed to predict the effect of CYB561 expression on overall survival (OS). Results: The results showed that CYB561 was highly expressed in breast cancer tissues. Hypomethylation of CYB561 is associated with an unfavorable prognosis. In multivariate Cox regression analysis, CYB561 was an independent prognostic factor for OS. Functional enrichment analysis indicated that estrogen signaling pathway, inflammatory response, KRAS signaling pathway, epithelial-mesenchymal transition, leukocyte migration, and regulation of lymphocyte activation were strongly enriched in the low CYB561 expression group. Additionally, CYB561 expression was negatively correlated with immune infiltration of B cells, plasmacytoid dendritic cells, dendritic cells, and neutrophils. Conclusion: CYB561 may serve as a potential biomarker for breast cancer diagnosis and prognosis. 相似文献
5.
ZECHAO LU FUCAI TANG HAOBIN ZHOU ZEGUANG LU WANYAN CAI JIAHAO ZHANG ZHICHENG TANG YONGCHANG LAI ZHAOHUI HE 《Biocell》2023,47(2):339-350
Background: Establishing an appropriate prognostic model for PCa is essential for its effective treatment. Glycolysis is a vital energy-harvesting mechanism for tumors. Developing a prognostic model for PCa based on glycolysis-related genes is novel and has great potential. Methods: First, gene expression and clinical data of PCa patients were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), and glycolysis-related genes were obtained from the Molecular Signatures Database (MSigDB). Gene enrichment analysis was performed to verify that glycolysis functions were enriched in the genes we obtained, which were used in non-negative matrix factorization (NMF) to identify clusters. The correlation between clusters and clinical features was discussed, and the differentially expressed genes (DEGs) between the two clusters were investigated. Based on the DEGs, we investigated the biological differences between clusters, including immune cell infiltration, mutation, tumor immune dysfunction and exclusion, immune function, and checkpoint genes. To establish the prognostic model, the genes were filtered based on univariable Cox regression, LASSO, and multivariable Cox regression. Kaplan–Meier analysis and receiver operating characteristic analysis validated the prognostic value of the model. A nomogram of the risk score calculated by the prognostic model and clinical characteristics was constructed to quantitatively estimate the survival probability for PCa patients in the clinical setting. Result: The genes obtained from MSigDB were enriched in glycolysis functions. Two clusters were identified by NMF analysis based on 272 glycolysis-related genes, and a prognostic model based on DEGs between the two clusters was finally established. The prognostic model consisted of LAMPS, SPRN, ATOH1, TANC1, ETV1, TDRD1, KLK14, MESP2, POSTN, CRIP2, NAT1, AKR7A3, PODXL, CARTPT, and PCDHGB2. All sample, training, and test cohorts from The Cancer Genome Atlas (TCGA) and the external validation cohort from GEO showed significant differences between the high-risk and low-risk groups. The area under the ROC curve showed great performance of this prognostic model. Conclusion: A prognostic model based on glycolysis-related genes was established, with great performance and potential significance to the clinical application. 相似文献
6.
YI WANG SHANGQI CHEN PENGCHENG YU ZHEHAN BAO CAN HU YUHANG XIA RUOLAN ZHANG LI YUAN HUA RUAN JIANCHENG SUN 《Biocell》2023,47(5):991-1002
Aim: Scavenger receptor class B, type I (SR-BI) is an integral plasma membrane protein that has been reported to be overexpressed in various malignancies, such as renal cancer, breast cancer, and prostate cancer, and is an independent prognostic factor. However, the clinical value and expression of SR-BI in GC are unknown. Our research aimed to explore the role of SR-BI in combination with immune markers as a diagnostic and prognostic marker for gastric cancer (GC). Methods: GC tissues, paracancerous tissues, and clinicopathological data of 149 patients were collected. The expression level of SR-BI, Tumor-infiltrating lymphocytes (TILs), and PD-L1 were evaluated by immunohistochemistry (IHC). The associations of the SR-BI staining intensity with clinicopathological features and immune markers were determined by the chi-square test. Univariate and multivariate COX regression analyses were used to evaluate independent prognostic factors. Kaplan–Meier analyses were performed to plot the survival curve. Results: Our results indicated that SR-BI was expressed at higher levels in tumor tissues than in adjacent paracancerous tissues (p < 0.001), and patients with high levels of SR-BI expression had a worse prognosis. Univariate and multivariate analyses revealed that high SR-BI expression was an independent factor for poor prognosis. The chi-square test determined that the expression of SR-BI was negatively correlated with CD4+ T cells and CD8+ T cells (CD4+ T cells, p = 0.013; CD8+ T cells, p = 0.021), and positively correlated with PD-L1 (p = 0.022). Finally, survival analysis revealed that CD4+ T cells were associated with the prognosis of GC patients (p = 0.019), and the combined survival analysis of SR-BI and CD4+ T cells was also statistically significant (p = 0.030). Conclusion: SR-BI is highly expressed in GC tissue and associated with poor prognosis. Moreover, SR-BI can also regulate the GC tumor immune microenvironment. 相似文献
7.
Esophageal cancer (EC) was an aggressive malignant neoplasm characterized by high morbidity and poor prognosis. Identifying the changes in DNA damage repair genes helps to better understand the mechanisms of carcinoma progression. In this study, by comparing EC samples and normal samples, we found a total of 132 DDR expression with a significant difference. Moreover, we revealed higher expression of POLN, PALB2, ATM, PER1, TOP3B and lower expression of HMGB1, UBE2B were correlated to longer OS in EC. In addition, a prognostic risk score based on 7 DDR gene expression (POLN, HMGB1, TOP3B, PER1, UBE2B, ATM, PALB2) was constructed for the prognosis of EC. Meanwhile, EC cancer samples were divided into 3 subtypes based on 132 DDR genes expressions. Clinical profile analysis showed cluster C1 and C2 showed a similar frequency of T2, which was remarked higher than that in cluster 3. Moreover, we found the immune cell inflation levels were significantly changed in different subtypes of EC. The infiltration levels of T cell CD8+, B cell and NK cells were greatly higher in cluster 2 than that in cluster 1 and cluster 3. The results showed T cell CD4+ infiltration levels were dramatically higher in cluster 1 than that in cluster 2 and cluster 3. Finally, we perform bioinformatics analysis of DEGs among 3 subtypes of EC and found DDR genes may be related to multiple signaling, such as Base excision repair, Cell cycle, Hedgehog signaling pathway, and Glycolysis/Gluconeogenesis. These results showed DDR genes may serve as new target for the prognosis of EC and prediction of the potential response of immune therapy in EC. 相似文献
8.
GIUSEPPE STEFANO NETTI FEDERICA SPADACCINO VALERIA CATALANO GIUSEPPE CASTELLANO GIOVANNI STALLONE ELENA RANIERI 《Biocell》2022,46(10):2235-2239
Pentraxin-3 (PTX3), the prototype of long pentraxins, seems to influence complement system (CS) modulation.PTX3 and CS sustain carcinogenesis, enriching tumor microenvironment (TME) with pro-inflammatory moleculespromoting angiogenesis in prostate cancer (PC) and renal cell carcinoma (RCC). Furthermore, cancer cellsoverexpress complement regulatory proteins, such as CD46, CD55 and CD59, which negatively affect complementpathways for support cancer cells survival. This viewpoint aims to elucidate the ambivalent role of PTX3 and the CSin the context of tumor microenvironment (TME). 相似文献
9.
Metabolic reprogramming and immunologic suppression are two critical characteristics promoting the progression of head and neck squamous cell carcinoma (HNSCC). The integrative analysis of all the metabolism-related genes (MRGs) in HNSCC is lacking and the interaction between the metabolism and the immune characteristics also requires more exploration to uncover the potential mechanisms. Therefore, this study was designed to establish a prognostic signature based on all the MRGs in HNSCC. Genes of HNSCC samples were available from the TCGA and GEO databases while the MRGs were retrieved from a previous study. Ultimately 4 prognostic MRGs were selected to construct a model possessing robust prognostic value and accuracy in TCGA cohorts. The favorable reproducibility of this model was confirmed in validation cohorts from GEO databases. The risk score calculated by this model was an independent prognostic factor that further classified these HNSCC patients into high-/low-risk groups. GSEA analyses and somatic mutations indicated the low-risk group could activate several anti-tumor pathways and possessed lower TP53 mutation. The results of ESTIMATE, single-sample GSEA, CIBERSORT, and some immune-related molecules analyses suggested the low-risk group exhibited lower metabolic activities and higher immune characteristics. The Spearman correlation test implied most metabolic pathways with tumor-promoting function were negatively correlated with the immune activity, indicating a plausible approach of combining the anti-metabolism and the immunotherapy drugs in the high-risk group to enhance therapeutic effects than applied separately. In conclusion, this prognostic signature linking MRGs with the immune landscape could promote the individualized treatment for HNSCC patients. 相似文献
10.
ANGELES C. TECALCO-CRUZ 《Biocell》2022,46(5):1209-1213
Cytoskeletal remodeling affects the shape, adhesion, and motility of cells. Cytoskeletal dynamics are modulated by matrix proteins, integrins, and several cytokines in the tumor microenvironment. In this scenario, signaling is activated by integrins and interferons, which can induce ISG15 gene expression. This gene encodes a ubiquitin-like protein that functions as a protein modifier via the ISGylation system. Furthermore, non-conjugated ISG15 acts as a cytokine-like protein. In this viewpoint, the interplay between free ISG15, protein ISGylation, and cytoskeletal dynamics in the tumor microenvironment is discussed. 相似文献
11.
WEI LIANG QIANG LUO ZONGWEI ZHANG KEJU YANG ANKANG YANG QINGJIA CHI HUAN HU 《Biocell》2022,46(8):1989-2002
Diabetic nephropathy (DN) is a common microvascular complication that easily leads to end-stage renal disease. Itis important to explore the key biomarkers and molecular mechanisms relevant to diabetic nephropathy (DN). We used highthroughput RNA sequencing to obtain the genes related to DN glomerular tissues and healthy glomerular tissues of mice.Then we used LIMMA to analyze differentially expressed genes (DEGs) between DN and non-diabetic glomerularsamples. And we performed KEGG, gene ontology functional (GO) enrichment, and gene set enrichment analysis toreveal the signaling pathway of the disease. The CIBERSORT algorithm based on support vector machine was used todetermine the immune infiltration score. Random forest algorithm and Cytoscape obtained hub genes. Finally, we appliedco-staining, immunohistochemical staining, RT-qPCR and western blotting to validate the protein and mRNA expressionof both hub genes. We obtained 913 DEGs mainly related to inflammatory factors and immunity. GSEA results showedthat differential genes were mainly enriched in IL-17 signaling pathway, lipid and atherosclerosis, rheumatoid arthritis,TNF signaling pathway, neutrophil extracellular trap formation, Staphylococcus aureus infection and other pathways. Theintersection of the random forest algorithm and Cytoscape revealed both hub genes of CD300A and CXCL1. Experimentshave shown that the both key genes of CD300A and CXCL1 shown increased expression in glomerular podocytes, andare related to the inflammation of diabetic nephropathy. And immunohistochemical staining and RT-qPCR furtherconfirmed that the protein and mRNA expression level of CD300A or CXCL1 in glomeruli tissue in DN mice wereincreased. The expression levels of CD300A and CXCL1 increased significantly under HG (high glucose) stimulation,further confirming that diabetes can lead to increased levels of CD300A and CXCL1 at the cellular level. Throughbioinformatics analysis, machine learning algorithms, and experimental research, CD300A and CXCL1 are confirmed asboth potential biomarkers in diabetic nephropathy. And we further revealed the main pathways of differential genes andthe differentially distributed immune infiltrating cells in diabetic nephropathy. 相似文献
12.
Background: Tanshinone IIA, one of the main ingredients of Danshen, is used to treat hepatocellular carcinoma (HCC). However, potential targets of the molecule in the therapy of HCC are unknown. Methods: In this study, we collected the tanshinone IIA targets from public databases for investigation. We screened differentially expressed genes (DEGs) across HCC and normal tissues using mRNA expression profiles from The Cancer Genome Atlas (TCGA). Univariate Cox regression analysis and least absolute shrinkage and selection operator (LASSO) Cox regression models were used to identify and construct the prognostic gene signature. Results: Finally, we discovered common genes across tanshinone IIA targets and HCC DEGs. We reported Fatty acid binding protein-6 (FABP6), Polo-like Kinase 1 (PLK1), deoxythymidylate kinase (DTYMK), Uridine Cytidine Kinase 2 (UCK2), Enhancer of Zeste Homolog 2 (EZH2), and Cytochrome P450 2C9 (CYP2C9) as components of a gene signature. The six-gene signature’s prognostic ability was evaluated using the Kaplan-Meier curve, time-dependent receiver operating characteristic (ROC), multivariate Cox regression analysis, and the nomogram. The mRNA level and protein expression of UCK2 were experimentally validated after treatment with different concentrations of tanshinone IIA in HEPG2 cells. CIBERSORTx, TIMER2.0, and GEPIA2 tools were employed to explore the relationship between the prognostic signature and immune cell infiltration. Conclusion: We established a six-gene signature as a reliable model with significant therapeutic possibility for prognosis and overall survival estimation in HCC patients, which might also benefit medical decision-making for appropriate treatment. 相似文献
13.
FRANCESCO MAININI 《Biocell》2021,45(5):1171-1173
Adoptive cell therapy and Immune Checkpoint Blockade Inhibitors have recently revolutionized the field of oncology. However, these types of immunotherapeutic approaches have limited success in treating solid tumors. In particular, chimeric antigen receptor (CAR)-T cells efficacy is hampered by immunosuppressive signals in the tumor microenvironment (TME) and by a limited infiltration of re-infused T cells to the tumor site. The field of nanobiotechnology applied to oncology is also rapidly expanding. Nanoparticles-based delivery systems can be employed to modulate the activity of immune cells present in the TME enhancing the efficacy of CAR-T cells. Interestingly, nano-backpacks can be attached to CAR-T cells prior to re-infusion to support their homing to the tumor site and to slowly release immunopotentiators directly in the TME. Furthermore, nanovaccines can also be employed to support the in vivo expansion of CAR-T cells with consequent enhancement of their therapeutic potential. In this viewpoint, recent advancement in the field of nanobiotechnology to support CAR-T cell therapy will be discussed. The development of novel therapeutic CAR-T cells protocols together with nanotherapies is warranted in order to take full advantage of the high therapeutic potential of CAR-T cell therapy. 相似文献
14.
SHA LI YAQIONG LIU CHAOLING YAO ANJI XU XIAOLING ZENG YUXIN GE XIAOWU SHENG HAILIN ZHANG XIAO ZHOU YING LONG 《Biocell》2023,47(5):1003-1019
Background: Nuclear receptor binding SET domain protein-3 (NSD3) is a histone lysine methyltransferase and a crucial regulator of carcinogenesis in several cancers. We aimed to investigate the prognostic value and potential function of NSD3 in 33 types of human cancer. Methods: The data were obtained from The Cancer Genome Atlas. Kaplan-Meier analysis, CIBERSORT, gene set enrichment analysis, and gene set variation analysis were performed. The expression of NSD3 was measured using quantitative real-time polymerase chain reaction and western blot. Results: The expression of NSD3 was altered in pan-cancer samples. Patients with higher levels of NDS3 generally had shorter overall survival and disease-specific survival. Levels of NSD3 were positively correlated with DNA copy number variation (CNV) in pan-cancer. NSD3 expression was also associated with tumor mutation burden and microsatellite instability. The levels of immune-cell infiltration differed significantly between high and low NSD3 expression. NSD3 negatively correlated with levels of CD8+ T cells. Functional enrichment analysis showed that while NSD3 expression was positively associated with several immune cell-related and histone methylation-related pathways, it was negatively correlated with cell metabolism-related, drug transport-related, and drug metabolism-related pathways. NSD3 levels in the cell lines tested were significantly different. In U251 and NCI-H23 cells, silencing NSD3 inhibited cell proliferation and promoted apoptosis. Conclusions: NSD3 expression was changed in pan-cancer samples that was also verified in cell lines. NSD3 was associated with CNV and immune-cell infiltration. A poor prognosis was predicted in patients with high expression of NSD3. NSD3 might hence be a potential marker for predicting tumor prognosis. 相似文献
15.
Breast cancer is one of the most common cancers in the world and seriously threatens the health of women worldwide. Prognostic models based on immune-related genes help to improve the prognosis prediction and clinical treatment of breast cancer patients. In the study, we used weighted gene co-expression network analysis to construct a co-expression network to screen out highly prognostic immune-related genes. Subsequently, the prognostic immune-related gene signature was successfully constructed from highly immune-related genes through COX regression and LASSO COX analysis. Survival analysis and time receiver operating characteristic curves indicate that the prognostic signature has strong predictive performance. And we developed a nomogram by combing the risk score with multiple clinical characteristics. CIBERSORT and TIMER algorithms confirmed that there are significant differences in tumor-infiltrating immune cells in different risk groups. In addition, gene set enrichment analysis shows 6 pathways that differ between high- and low-risk group. The immune-related gene signature effectively predicts the survival and immune infiltration of breast cancer patients and is expected to provide more effective immunotherapy targets for the prognosis prediction of breast cancer. 相似文献
16.
WENXI GAO QIANQIAN MA CHENYU TANG YUELI ZHAN YINONG DUAN HUIHUA NI YUNZHAO XU 《Biocell》2020,44(4):597-605
Cervical cancer (CESC) is one of the most common cancers and affects the female genital tract. Consistent HPVinfection status has been determined to be a vital cause of tumorigenesis. HPV infection may induce changes to theimmune system and limit the host’s immune response. Immunotherapy is therefore essential to improving the overallsurvival of both locally advanced and recurrent CESC patients. Using 304 relevant samples from TCGA, we assessedimmune cell function in CESC patients to better understand the status of both tumor micro-environment cells andimmune cells in CESC. Functional enrichment analysis, pathway enrichment analysis, and PPI network constructionwere performed to explore the differentially expressed genes (DEGs). The analysis identified 425 DEGs, whichincluded 295 up-regulated genes and 130 down-regulated genes. We established that upregulation of CCL5 wascorrelated with significantly better survival, meaning that CCL5 expression could serve as a novel prognosticbiomarker for CESC patients. We further focused on CCL5 as a hub gene in CESC, as it had significant correlationswith increased numbers of several types of immune cells. Cell-type fractions of M1 macrophages were significantlyhigher in the high-immune-scores group, which was associated with better overall survival. Finally, we concluded thatCCL5 is a promising prognostic biomarker for CESC, as well as a novel chemotherapeutic target. 相似文献
17.
Immunotherapy targets the dysfunctional immune system to induce cancer cell killing by CD8-positive T cells. Immune checkpoint inhibitors (ICIs), specifically anti-PD-1 antibodies, anti-PD-L1 antibodies, and anti-CTLA4 antibodies, have revolutionized the management of many malignancies due to their significant role in generating a durable clinical response. However, clinical data suggest that response rates to ICI monotherapy are low due to the immunologically silent characteristics of breast cancer (BC). Chemotherapy, surgery, radiotherapy, and targeted therapy were recently reported to alter the tumor microenvironment and enhance the ICI response. Some clinical studies supported that ICIs, in combination with other treatment strategies, show superior efficacy in BC control, especially triple-negative breast cancer. Therefore, seeking a reasonable combination therapy is a promising way to improve ICI response. The present review highlights the clinical efficacy of ICIs treatment options in combination with standard-of-care therapies, such as chemotherapy and targeted therapy. 相似文献
18.
Using three methods to measure cell proliferation, namely DNA cell cycle; anti-proliferating cell monoclonal antibody (MAb) (Ki67, P145) analysis by flow cytometry; and the histological silver (argyrophilic) staining technique to visualize nuclear-organizing regions (AgNOR), twenty-two paired samples of primary breast tumour and axillary lymph node were analysed. The results showed variable levels of correlation between the methods used for the tumour group (r = 0.915, P <0.001 for Ki677 versus P145; r = 0.42, P <0.005 for percentage S/G2/M-phase versus P145; r = 0.16, P <0.5 for percentage S/G2/M-phase versus AgNOR; r = 0.400, P < 0.1 for Ki67 versus AgNOR). The lymph-node group showed slightly poorer correlations, yet involved nodes showed a consistently higher level of proliferation than non-involved nodes by all methods used. Overall, MAb binding of Ki67 or P145 was seen to be a good indicator of cycling cells, detecting G1-phase cells in addition to S/G2/M-phase cells indentified by the other methods used. However, no advantage was found over the usual DNA flow cytometric analysis of cells, which had clear prognostic value. AgNOR scores were found to be able to discriminate between diploid and aneuploid; and dividing and non-dividing cells, but areas of score overlap limited the application of this technique to that of a positive discriminator only. 相似文献
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乳腺癌前哨淋巴结不同检测方法效果研究 总被引：1，自引：0，他引：1
目的 :研究染色法、同位素法、联合法3种不同检测方法对乳腺癌前哨淋巴结检测的影响。方法:选取2007年9月2013年11月在我院就诊的早期女性乳腺癌患者为研究对象,将患者随机分为3组,蓝染料组、核素组、联合组。比较各组乳腺癌前哨淋巴结活检的成功率、准确率及假阴性率。结果 :与单纯使用染料的方法相比,联合法的假阴性率显著性降低,差异有统计学意义。与单用染料组及核素组相比,联合法发现的SLN数较多,但无统计学差异。结论:联合应用染料及同位素示踪较单一方法更能提高前哨淋巴结检测的成功率,降低假阴性率。 相似文献