MedComm – Oncology最新文献

{"title":"Tumor–neuron interactions: A novel concept contributor to glioblastoma invasion","authors":"Dongling Pei,&nbsp;Zhenyu Zhang,&nbsp;Long Zhang","doi":"10.1002/mog2.17","DOIUrl":"10.1002/mog2.17","url":null,"abstract":"<p>Recently, a study published in <i>Cell</i> by Venkataramani et al.<span>¹</span> demonstrated that neuronal (NEU), neural progenitor (NPC)-like, and nonmesenchymal (non-MES)-like glioblastoma cells (GBCs) could drive brain tumor cell invasion. Those astrocyte (AS)-unconnected, invasive GBCs (“unconnected^TUM/AC”) transitioned over time and infiltrated into other regions, largely consisting of tumor cell and AS-connected, stable GBCs (“connected^TUM/AC”). This work elegantly indicated that GBCs are not only connected with each other via gap junctions but are also connected with neurons. In addition, NEU activity drives glioma progression via glutamatergic neuron-to-brain tumor synaptic communication and nonsynaptic paracrine stimulation.<span>^{2, 3}</span> However, how these tumors integrate into complex NEU circuits remains unclear.</p><p>Glioblastomas are the most frequently occurring malignant type of primary brain tumor, comprising 12%–15% of all intracranial tumors. However, even with current standard therapies, the majority of patients succumb to the disease within 2 years of diagnosis.<span>⁴</span> Due to the high heterogeneity and invasion of glioblastoma, gross total resection, radiotherapy, and chemotherapy with DNA-alkylaing agent (temozolomide) are largely ineffective.<span>⁵</span> Suvà and co-workers<span>⁶</span> demonstrated that GBCs exist in four cellular states: NPC-like, oligodendrocyte progenitor (OPC)-like, AS-like, and MES-like states. Despite different subtypes, no specific treatment works more effectively. Thus, research into malignant gliomas is complex and challenging.</p><p>Increasing evidence has been found to illustrate the functional and synaptic integration of glioma into the brain network, facilitating brain tumor progression. The NEU activities function through gap junctions, neurotransmitters, ion channels, synapses, tumor microtubes (TMs), and NEU molecules to establish communication with glioma. As reported, there have been several recent discoveries that have described how neurons may form synaptic connections with brain tumor cells. Among cell–cell communication, gap junctions consisted of connexin proteins, which form conductive pores in the plasma membranes among adjacent NEU cells, increasing glioma cell invasiveness and migration.<span>^{7, 8}</span> γ-Aminobutyric acid and glutamate are the predominant neurotransmitters that impair glioma cell growth.<span>^{3, 9}</span> We aimed to provide a simplified explanation of crosstalk on neuron-glioma, found by Venkataramani.</p><p>To understand the rapid spread of malignant glioma, patient-derived human GBC cells were injected into mice via intracranial stereolocalization and the GBCs were separated into two subtypes: unconnected^TUM/AC GBCs and connected^TUM/AC GBCs. Connected^TUM/AC GBCs were found to be anatomically connected with other","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.17","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90223655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Type I collagen homotrimers: A potential cancer-specific interventional target","authors":"Ying Zhou,&nbsp;Linzhu Zhang,&nbsp;Jiang Xie,&nbsp;Junhong Han","doi":"10.1002/mog2.16","DOIUrl":"10.1002/mog2.16","url":null,"abstract":"<p>Pancreatic cancer cell-derived homotrimer type 1 collagen plays an important role in the pathogenesis of pancreatic cancer. Homotrimer type 1 collagen produced by pancreatic cancer cells upregulated proliferation-related pathways through the integrin α3β1 axis. Deletion of homotrimer type 1 collagen in genetically engineered mouse models altered the intratumoral microbiome, increased T-cell infiltration, enhanced anti-PD-1 therapy, and ultimately inhibited tumor growth.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.16","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77168971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The mitochondrial-derived lncRNA MDL1 mediates a mitochondria-to-nucleus retrograde regulation by inhibiting the nuclear translocation of p53","authors":"Jia Li,&nbsp;Ruolin Bai,&nbsp;Weijia Yang,&nbsp;Hui Miao,&nbsp;Yu Li,&nbsp;Hongyuan Dai,&nbsp;Ling Li,&nbsp;Yongyun Zhao,&nbsp;Xu Song","doi":"10.1002/mog2.15","DOIUrl":"10.1002/mog2.15","url":null,"abstract":"<p>It has been clear that mitochondria are not just nucleus-relying entities; instead, they also modulate nuclear events reversely. Long noncoding RNAs (lncRNAs) are classified into nuclear-encoded and mitochondrial-derived lncRNAs (nulncRNAs and mtlncRNAs, respectively). Relative to nulncRNAs, the mtlncRNAs are far from being well characterized. Here we report a mtlncRNA, MDL1, that interacts with both p53 and Tid1 proteins and acts as retrograde signaling. MDL1 can regulate a network of nuclear genes, including p53 targets, and functions in cells in a p53-dependent manner. Mechanistically, MDL1 is necessary for maintenance of the reciprocal interaction between p53 and Tid1, thereby facilitating formation of a ternary MDL1/p53/Tid1 complex that inhibits the nuclear translocation of p53. Since p53 is a canonical transcription factor, the observed inhibition of p53 nuclear translocation would contribute to the MDL1-mediated mitochondrial retrograde regulation on nuclear genes expression. This study advances our understanding of lncRNA biology, and also sheds new light on the role of mtlncRNAs in mitochondrial-nuclear functional network and in diverse biological processes.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.15","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82745395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting human caseinolytic protease P (ClpP) as a novel therapeutic strategy in ovarian cancer","authors":"Baozhu Luo,&nbsp;Jiangnan Zhang,&nbsp;Wenliang Qiao,&nbsp;Yuanzhen Zhou,&nbsp;Jiasheng Huang,&nbsp;Tao Yang,&nbsp;Youfu Luo","doi":"10.1002/mog2.14","DOIUrl":"10.1002/mog2.14","url":null,"abstract":"<p>Ovarian cancer (OC) is currently one of the most life-threatening types of gynecological malignancy with limited treatment options and poor clinical outcomes. Human caseinolytic protease P (HsClpP) is located in the mitochondria and plays an important role in several tumors. Moreover, HsClpP is overexpressed in OC and several other tumor cells. Thus, HsClpP modulation is regarded as a potential approach for OC treatment. In this study, we identified and validated a novel boron peptide Compound <b>43-8F</b> as a potent HsClpP inhibitor. Upon <b>43-8F</b> treatment, mitochondrial damage was observed to be closely correlated with upregulated intracellular reactive oxygen species production, decreasement of membrane potential, and ATP content suppression. Meanwhile, the expression level of SDHB and the ATF4 was increased after <b>43-8F</b> treatment, suggesting that <b>43-8F</b> treatment induces mitochondrial respiratory disorders and activates the integrated stress response pathway to inhibit tumor cell growth. Further, <b>43-8F</b> exhibited a good therapeutic and safety profile in OC xenograft model in nude mice. Together, these results suggest that <b>43-8F</b> exerts an anti-ovarian cancer effect by inhibiting HsClpP pathway.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.14","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75450985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel and potent dihydroorotate dehydrogenase inhibitor suppresses the proliferation of colorectal cancer by inducing mitochondrial dysfunction and DNA damage","authors":"Xiaowei Yang,&nbsp;Chungen Li,&nbsp;Kun Gou,&nbsp;Xiaocong Liu,&nbsp;Yue Zhou,&nbsp;Jiao Zou,&nbsp;Qiang Chen,&nbsp;Youfu Luo,&nbsp;Yinglan Zhao","doi":"10.1002/mog2.6","DOIUrl":"10.1002/mog2.6","url":null,"abstract":"<p>Dihydroorotate dehydrogenase (DHODH) is a quite attractive target in cancer therapy. Nevertheless, the antitumor effects of DHODH inhibitors against colorectal cancer (CRC) and the underlying mechanism have seldom been studied. Here, we explored the anti-CRC efficacy of M62, a novel and potent DHODH inhibitor. In the study, M62 significantly inhibited the proliferation of CRC cells and induced S phase arrest. The antiproliferative effects caused by M62 were rescued by uridine supplementation. Mechanistically, messenger RNA sequencing results showed that M62-triggered gene changes related to mitochondrial dysfunction, DNA damage, and DNA damage repair. Further validation showed that M62 treatment induced the generation of reactive oxygen species and decreased ΔΨm and ATP production. Meanwhile, M62 induced the accumulation of γ-H2AX and longer comet tail moment, which were both markers of DNA damage. The downregulated DNA repair proteins and PI3K/ATK pathway were observed after M62 treatment. Furthermore, M62 significantly inhibited CRC xenograft tumor growth without detectable toxicity. Therefore, we conclude that M62 inhibits CRC growth both in vitro and in vivo by causing mitochondrial dysfunction and DNA damage, suggesting that DHODH inhibitors are potential therapeutic strategies for treating CRC.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82069825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor immunotherapy: Mechanisms and clinical applications","authors":"Cheng Nong,&nbsp;Pengbo Guan,&nbsp;Li Li,&nbsp;Huiyuan Zhang,&nbsp;Hongbo Hu","doi":"10.1002/mog2.8","DOIUrl":"10.1002/mog2.8","url":null,"abstract":"<p>Immunotherapy, which aims to enhance the functions of the host's immune system to eliminate invading pathogens and mutant cells, has been widely used for cancer treatment. Despite the enormous progress in immunotherapy, the efficiency of immunotherapy is urgent to be improved. The tumor microenvironment is composed of multiple types of infiltrating immune cells and stromal cells (such as endothelial cells, fibroblasts, and tumor cells), extracellular matrix, various cytokines, chemokines, growth factors, and metabolites, all of which play crucial roles in tumor progress, metastasis, relapse and the outcome of immunotherapy. Emerging evidence indicates a better understanding of the characteristics of the tumor microenvironment and its associated factors, which could lead to uncovering novel promising immunotherapy approaches. This review will summarize the current knowledge of heterogeneity and function of the immune cells in the tumor microenvironment, the current progress of immunotherapy focusing on immune checkpoint blockade and chimeric antigen T cell therapy, as well as the challenge and limitations of the current immunotherapy strategy. Overall, we aim to provide the conceptions of tumor immune microenvironment and application of immunotherapy, highlighting the potential strategies to improve tumor immunotherapy.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79535817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genomic evolution of cancer metastasis under therapeutic pressure","authors":"Qiu-Luo Liu,&nbsp;Xi Li,&nbsp;Hai-Ning Chen","doi":"10.1002/mog2.5","DOIUrl":"10.1002/mog2.5","url":null,"abstract":"<p>In the era of precision medicine, the selection of cancer treatment relies increasingly on the identification of genomic alterations; however, it is not yet clear how frequently genomic profiling should be performed over the disease course of a patient with metastatic cancer. A large-scale study investigates the genomic evolution of cancer metastases under therapeutic pressure and finds that the actionable genome has remained relatively stable. The findings support the sufficiency of a single biopsy of cancer metastasis for therapeutic decision-making.</p>","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80944216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MedComm - Oncology announcement","authors":"Guido Kroemer,&nbsp;Yong Peng","doi":"10.1002/mog2.13","DOIUrl":"10.1002/mog2.13","url":null,"abstract":"<p>About 400 B.C., the ancient Greek physician Hippocrates used <i>karkinos</i>, Greek for cancer, to denote certain types of malignant tumors that thrust out the invasive “talons” into the surrounding tissues. Cancer has been present throughout the ages. According to the latest World Health Statistics of the World Health Organization, cancer has become the second leading cause of human death, which is responsible for about 16% of deaths globally, affecting people of all ages and from all regions of the world.</p><p>It is the best time for oncology. With the advances in molecular biology and modern medicine, especially the launch of the Human Genome Project, cancer research has entered a new era since the end of the last century. By profiling the genetic fingerprint and molecular makeup, similar hallmarks including sustaining proliferative signaling, activating metastasis, and avoiding immune destruction are defined among distinct cancer subtypes. Moreover, the concepts of cancer heterogeneity, epigenetic regulation, posttranslational modification, and tumor microenvironment, have expanded the scientific scope of oncology. Driven by translational medicine and bioengineering, diverse precise diagnostics and therapeutics have been developed to improve cancer management, such as the artificial intelligence-assisted computed tomography for lung cancer diagnosis, the liquid biopsy for the detection of circulating tumor cell and circulating tumor DNA, human papillomavirus vaccines against cervical cancer, and the immune checkpoint inhibitor PD-1/PD-L1 monoclonal antibodies for the treatment of multiple cancers.</p><p>It is the worst time for oncology. The emergence of the many cutting-edge techniques including multi-omics, high-resolution imaging, single-cell methodologies, and so forth, has characterized many new biomolecules (e.g., noncoding RNAs and small-molecule metabolites) as tumor drivers, making the molecular regulatory network of cancer cells unprecedentedly sophisticated. Cancer is also appreciated as a dynamic disease. The molecular signature, phenotype, and lethality of cancers are variable with disease typing, clinical stage, and therapy. Thus, it is challenging for researchers to clarify the pivotal oncogenic mechanism from massive bioinformatic and experimental evidence, or to develop effective methodologies for diagnosis and treatment. It requires collaboration across multi-disciplines, integration of theory and techniques, and the ambition of patients, clinicians, and scientists to defeat cancer.</p><p>Governments and foundations worldwide are providing increasing financial supports to oncology research. Unquestionably, critical discoveries in this field will be achieved in the near future. Nevertheless, the limited influential journals in oncology cannot guarantee the timely publication of these achievements. To this end, <i>MedComm - Oncology</i> is launched to meet the demand.</p><p><i>MedComm - Oncology</i> is a peer-reviewed and ","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mog2.13","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81980991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PTK2 Promotes Uveal Melanoma Metastasis by Activating Epithelial-to-Mesenchymal Transition","authors":"Zhong-lin Fan, Jingjing Duan, Lei Zhang, Qiong Chen, Wen-hui Xiao, P. Luo, L. Shao, J. Meng, Jianghong An, Gengwei Zhang, Xiaohua Tan","doi":"10.21203/rs.3.rs-885745/v1","DOIUrl":"https://doi.org/10.21203/rs.3.rs-885745/v1","url":null,"abstract":"\u0000 Background: Uveal melanoma (UM) is an aggressive primary intraocular tumor in adults, with high metastatic capacity and high morbidity. However, the mechanisms of UM metastasis have not been clearly elucidated.Methods: The PTK2 expression and activation were performed in the Cancer Genome Atlas (TCGA) database and 25 patients of UM. The role of PTK2 in promoting metastasis was explored in vitro and in vivo. Subsequently, we revealed the correlation between PTK2 expression and epithelial-to-mesenchymal transition (EMT). Finally, we explored the reason for the high expression of PTK2 in UM.Results: Our study found that protein tyrosine kinase 2 (PTK2) was overexpressed in UM specimens, and as a novel independent risk factor, its overexpression predicted the poor survival of UM patients. For the molecular mechanism, PTK2 promoted EMT phenotype, thus leading to tumor metastasis in UM cells. Subsequently, we have demonstrated that PTK2 was a functional gene of chromosome 8q gain accounting for UM metastasis, providing a novel molecular mechanism for the aberrantly expression and activation of PTK2 in UM.Conclusion: Our data reveal the important role and mechanism of PTK2 in the metastatic process of UM, which may clue to a new predictive biomarker for UM metastasis and a new therapeutic target for UM treatment.","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78638251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolomic profiling on plasma reveals potential biomarkers for screening and early diagnosis of gastric cancer and precancerous stages","authors":"L. Du, Shasha Li, Xue Xiao, Jin Li, Yuanfang Sun, Shuai Ji, Huizi Jin, Z. Hua, Juming Ma, Xi Wang, Shikai Yan","doi":"10.21203/rs.3.rs-18127/v1","DOIUrl":"https://doi.org/10.21203/rs.3.rs-18127/v1","url":null,"abstract":"\u0000 Background: Gastric cancer (GC) remains one of the most common cancers all over the world. The greatest challenge for GC is that it is often detected at advanced stages, leading to the loss of optimum time for treatment and giving rise to poor prognosis. Thus, there is a critical need to develop effective and noninvasive strategies for early diagnosis of the disease process. Methods: In total, 82 participants were enrolled in the study, including 50 chronic superficial gastritis (CSG) patients, 7 early gastric cancer (EGC) and 25 advanced gastric cancer (AGC) ones. Metabolites profiling on patient plasma was performed using ultra-high performance liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry ( UPLC-Q-TOF/MS ). Principal components analysis as well as orthogonal partial least squares-discriminant analysis was utilized to evaluate the variation on endogenous metabolites for GC patients and to screen potential biomarkers. Furthermore, the biomarker panels detected above were used to create logistic regression models, which discrimination efficiency and accuracy was ascertained by receiver operating characteristic curve (ROC) analysis. Metabolic pathways were carried out on MetaboAnalyst. Results: Totally 50 metabolites were detected differentially expressed among CSG, EGC and AGC patients. L-carnitine, L-proline, pyruvaldehyde, phosphatidylcholines (PC) (14:0/18:0), lysophosphatidylcholine (14:0) (LysoPC 14:0), lysinoalanine were defined as the potential biomarker panel for the diagnosis among CSG and EGC patients. Compared with EGC patients, 6 significantly changed metabolites, PC(O-18:0/0:0) and LysoPC(20:4(5Z,8Z,11Z,14Z)) were found to be up-regulated, whereas L-proline, L-valine, adrenic acid and pyruvaldehyde to be down-regulated in AGC patients. ROC analysis demonstrated a high diagnostic performance for metabolite panels with area under the curve (AUC) of 0.931 to 1. Moreover, the metabolomic pathway analysis revealed several metabolism pathway disruptions, including amino acid and lipid metabolisms, in GC patients. Conclusions: In this study, a total of six differential metabolites that contributed to GC and precancerous stages were identified, respectively. The biomarker panels further improve diagnostic performance for detecting GC, with AUC values of more than 93.1%. It indicated that the biomarker panels may be sensitive to the early diagnosis of GC disease, which can be used as a promising diagnostic and prognostic tool for disease stratification studies.","PeriodicalId":100902,"journal":{"name":"MedComm – Oncology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90268484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}