Genes and CancerPub Date : 2023-01-01DOI: 10.18632/genesandcancer.230
Jerin Thomas, Addison Klebanov, Sahara John, Larry S Miller, Anil Vegesna, Richard L Amdur, Krishanu Bhowmick, Lopa Mishra
{"title":"CEACAMS 1, 5, and 6 in disease and cancer: interactions with pathogens.","authors":"Jerin Thomas, Addison Klebanov, Sahara John, Larry S Miller, Anil Vegesna, Richard L Amdur, Krishanu Bhowmick, Lopa Mishra","doi":"10.18632/genesandcancer.230","DOIUrl":"https://doi.org/10.18632/genesandcancer.230","url":null,"abstract":"<p><p>The CEA family comprises 18 genes and 11 pseudogenes located at chromosome 19q13.2 and is divided into two main groups: cell surface anchored CEA-related cell adhesion molecules (CEACAMs) and the secreted pregnancy-specific glycoproteins (PSGs). CEACAMs are highly glycosylated cell surface anchored, intracellular, and intercellular signaling molecules with diverse functions, from cell differentiation and transformation to modulating immune responses associated with infection, inflammation, and cancer. In this review, we explore current knowledge surrounding CEACAM1, CEACAM5, and CEACAM6, highlight their pathological significance in the areas of cancer biology, immunology, and inflammatory disease, and describe the utility of murine models in exploring questions related to these proteins.</p>","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"14 ","pages":"12-29"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9891707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10662302","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}
Genes and CancerPub Date : 2023-01-01DOI: 10.18632/genesandcancer.232
Kmira Zahra, Wided Cherif, Gereisha Ahmed, Haifa Regaieg, Ben Sayed Nesrine, Monia Zaier, Wided Mootamri, Yosra Ben Youssef, Nejia Brahem, Halima Sennana, Abderrahim Khelif
{"title":"A novel t (5; 17) (q35; q21) associated with t (8; 21) (q22; q22) in a patient with acute myeloid leukemia: case report and review of literature.","authors":"Kmira Zahra, Wided Cherif, Gereisha Ahmed, Haifa Regaieg, Ben Sayed Nesrine, Monia Zaier, Wided Mootamri, Yosra Ben Youssef, Nejia Brahem, Halima Sennana, Abderrahim Khelif","doi":"10.18632/genesandcancer.232","DOIUrl":"https://doi.org/10.18632/genesandcancer.232","url":null,"abstract":"<p><p>The t (8; 21) (q22; q22) with the resulting RUNX1- RUNX1T1 rearrangement is one of the most common cytogenetic abnormalities in acute myeloid leukemia (AML). It is associated with favorable prognosis. The t (5; 17) (q35; q21) is an uncommon translocation, fuses the gene for the nucleophosmin (NPM) to the retinoic acid receptor α(RARA) and was described essentially in acute promyelocytic leukemia (APL) variant. We present the case of a 19-year-old male patient who developed an AML with t (8; 21) (q22; q22) associated to t (5; 17) (q35; 21). Morphology and immunophenotype of the leukemic cells were compatible with AML. The patient received chemotherapy based on cytarabine and anthracycline without all-trans retinoic acid (ATRA) followed by allogenic stem cell transplantation in first remission. To the best of our knowledge, this is the first report of an association between a rare translocation t (5; 17) and t (8; 21) in AML. In this report, we will discuss the prognosis of this association as well as the treatment.</p>","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"14 ","pages":"50-55"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10328316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9809172","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}
Genes and CancerPub Date : 2022-12-02eCollection Date: 2022-01-01DOI: 10.18632/genesandcancer.225
Thatyanne Gradowski Farias da Costa do Nascimento, Mateus Eduardo de Oliveira Thomazini, Nilton de França Junior, Lisiane de Castro Poncio, Aline Simoneti Fonseca, Bonald Cavalcante de Figueiredo, Saulo Henrique Weber, Roberto Hirochi Herai, Lucia de Noronha, Luciane R Cavalli, Bruno César Feltes, Selene Elifio-Esposito
{"title":"Systems biology network reveals the correlation between COX-2 expression and Ch 7q copy number alterations in Ch 11q-deleted pediatric neuroblastoma tumors.","authors":"Thatyanne Gradowski Farias da Costa do Nascimento, Mateus Eduardo de Oliveira Thomazini, Nilton de França Junior, Lisiane de Castro Poncio, Aline Simoneti Fonseca, Bonald Cavalcante de Figueiredo, Saulo Henrique Weber, Roberto Hirochi Herai, Lucia de Noronha, Luciane R Cavalli, Bruno César Feltes, Selene Elifio-Esposito","doi":"10.18632/genesandcancer.225","DOIUrl":"https://doi.org/10.18632/genesandcancer.225","url":null,"abstract":"<p><p>Tumor-associated inflammation and chromosomal aberrations can play crucial roles in cancer development and progression. In neuroblastoma (NB), the enzyme cyclooxygenase-2 (COX-2) is associated with copy number alterations on the long arm of chromosome 11 (Ch 11q), defining an aggressive disease subset. This retrospective study included formalin-fixed paraffin-embedded tumor samples collected from nine patients during diagnosis at the pediatric Pequeno Principe Hospital, Curitiba, PR, Brazil, and post-chemotherapy (CT). COX-2 expression was evaluated using immunohistochemistry and correlated with the genome profile of paired pre- and post-CT samples, determined by array comparative genomic hybridization. A systems biology approach elucidated the <i>PTGS2</i> network interaction. The results showed positive correlations between pre-CT Ch 7q gain and COX-2 expression (ρ = 0.825; <i>p</i>-value = 0.006) and negative correlations between Ch 7q gain and Ch 11q deletion (ρ = -0.919; <i>p</i>-value = 0.0005). Three samples showed Ch 11q deletion and Ch 7q gain. Network analysis identified a direct connection between <i>CAV-1</i> (Ch 7q) and COX-2 in NB tumors and highlighted the connection between amplified genes in Ch 7q and deleted ones in 11q. The identification of hub-bottleneck-switch genes provides new biological insights into this connection between NB, tumorigenesis, and inflammation.</p>","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":" ","pages":"60-71"},"PeriodicalIF":0.0,"publicationDate":"2022-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9718587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35210832","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}
Genes and CancerPub Date : 2022-11-23eCollection Date: 2022-01-01DOI: 10.18632/genesandcancer.224
Mohammad Ghanbari, Aida Aghazadeh, Elaheh Malekabbaslou, Ali Rajabi, Aref Sobhkhizy, Melika Maydanchi, Ali Saber, Reza Safaralizadeh
{"title":"Ectopic expression of lncRNA MVIH as a potential diagnostic biomarker in cervical cancer.","authors":"Mohammad Ghanbari, Aida Aghazadeh, Elaheh Malekabbaslou, Ali Rajabi, Aref Sobhkhizy, Melika Maydanchi, Ali Saber, Reza Safaralizadeh","doi":"10.18632/genesandcancer.224","DOIUrl":"https://doi.org/10.18632/genesandcancer.224","url":null,"abstract":"<p><strong>Aim: </strong>Cervical cancer (CC) is one of the most common cancers in women. Recent advances in screening and vaccination against the papilloma virus (HPV) have increased protection against CC. However, there is no effective diagnostic biomarker and treatment approach during the course of the disease. The current study is thus aimed to evaluate the changes in the expression of lncRNA associated with microvascular invasion in hepatocellular carcinoma (lncRNA MVIH) and its diagnostic value as a biomarker in CC patients.</p><p><strong>Materials and methods: </strong>One-hundred and fifteen (<i>n</i> = 115) pairs of CC primary tumor and marginal non-tumor tissue samples were obtained from Tabriz Valiasr International Hospital (Tabriz, Iran). RNA extraction and cDNA synthesis followed by quantitative reverse transcriptase PCR (qRT-PCR) were considered to investigate alterations in the expression levels of MVIH in patients with CC. The associations between MVIH expression changes and clinicopathological features as well as its potential as a diagnostic biomarker were assessed using SPSS and GraphPad prism software and the receiver operating characteristic (ROC).</p><p><strong>Results: </strong>The expression levels of MVIH were significantly higher in CC tumors as compared to marginal non-tumor samples (<i>p</i> < 0.0001). Overexpression of MVIH was significantly associated with younger age (<i>p</i> = 0.033), lymph node metastasis (<i>p</i> = 0.031), tumor invasion depth (<i>p</i> = 0.035), and squamous cell type of CC (<i>p</i> = 0.019). The ROC analysis for MVIH as a diagnostic biomarker revealed the respective sensitivity and specificity of 67.83 and 80.</p><p><strong>Conclusions: </strong>Overexpression of MVIH in CC tumors suggests its oncogenic role during tumorigenesis. Thus, it may serve as a potential diagnostic biomarker.</p>","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":" ","pages":"52-59"},"PeriodicalIF":0.0,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9718588/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35210830","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}
Genes and CancerPub Date : 2022-08-29eCollection Date: 2022-01-01DOI: 10.18632/genesandcancer.223
Louise Wang, Susan M Domchek, Michael L Kochman, Bryson W Katona
{"title":"Reaching beyond family history as inclusion criteria for pancreatic cancer surveillance in high-risk populations.","authors":"Louise Wang, Susan M Domchek, Michael L Kochman, Bryson W Katona","doi":"10.18632/genesandcancer.223","DOIUrl":"10.18632/genesandcancer.223","url":null,"abstract":"","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"13 ","pages":"49-51"},"PeriodicalIF":0.0,"publicationDate":"2022-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9423661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9962194","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}
Genes and CancerPub Date : 2022-08-26eCollection Date: 2022-01-01DOI: 10.18632/genesandcancer.222
KuanHui E Chen, Ameae M Walker
{"title":"Splice modulating oligomers as cancer therapeutics.","authors":"KuanHui E Chen, Ameae M Walker","doi":"10.18632/genesandcancer.222","DOIUrl":"https://doi.org/10.18632/genesandcancer.222","url":null,"abstract":"Genes are transcribed to produce pre-mRNAs, which are then spliced to create the mature mRNAs translated into protein. In recent years, improved deep sequencing technologies have shown greater than 90% of human pre-mRNAs undergo alternative splicing, thereby amplifying the potential protein products from each gene [1]. Alternatively spliced forms of pre-mRNA may code for proteins with related, distinct, or even opposing functions [1]. Many growth factor and hormone receptors and signaling molecules implicated in cancer have natural splice variants, some of which have been shown to act as dominant negatives. We hypothesized that by altering splicing to decrease growth-promoting and/or increase expression of dominant negative varieties we could eliminate abnormal dependence on growth factors, decrease metastatic potential, and promote cancer cell death. By binding to specific intronic or exonic regions or intron-exon junctions, splice modulating oligomers, which are cDNA sequences, can alter the outcome of splicing [e.g., 2, 3]. To our knowledge, no one had previously tapped the potential of splice modulating oligomers to increase the relative activity of natural dominant negatives in order to combat disease. Where splice modulating oligomers had begun to be explored as therapeutics was for diseases that result from splicing errors and the production of a non-functional protein [4, 5]. Dominant negative receptors may inhibit signaling from the growth-promoting form of the receptor in a variety of ways. In the simplest situation, a dominant negative receptor binds ligand and therefore reduces availability to the growth-promoting receptor. In other instances, the dominant negative receptor may generate an alternate intracellular signal [e.g., 6–9]. Such amplification of the effect of dominant negative receptors through a signaling cascade makes an increase in their relative expression all the more effective. Importantly and additionally, the signals generated can promote differentiation and/or apoptotic cell death [6–8], thereby Editorial","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":" ","pages":"46-48"},"PeriodicalIF":0.0,"publicationDate":"2022-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9423660/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40342837","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}
Genes and CancerPub Date : 2022-06-06eCollection Date: 2022-01-01DOI: 10.18632/genesandcancer.220
Sobia Zaidi, Richard Amdur, Xiyan Xiang, Herbert Yu, Linda L Wong, Shuyun Rao, Aiwu R He, Karan Amin, Daewa Zaheer, Raj K Narayan, Sanjaya K Satapathy, Patricia S Latham, Kirti Shetty, Chandan Guha, Nancy R Gough, Lopa Mishra
{"title":"Using quantitative immunohistochemistry in patients at high risk for hepatocellular cancer.","authors":"Sobia Zaidi, Richard Amdur, Xiyan Xiang, Herbert Yu, Linda L Wong, Shuyun Rao, Aiwu R He, Karan Amin, Daewa Zaheer, Raj K Narayan, Sanjaya K Satapathy, Patricia S Latham, Kirti Shetty, Chandan Guha, Nancy R Gough, Lopa Mishra","doi":"10.18632/genesandcancer.220","DOIUrl":"10.18632/genesandcancer.220","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is the primary form of liver cancer and a major cause of cancer death worldwide. Early detection is key to effective treatment. Yet, early diagnosis is challenging, especially in patients with cirrhosis, who are at high risk of developing HCC. Dysfunction or loss of function of the transforming growth factor β (TGF-β) pathway is associated with HCC. Here, using quantitative immunohistochemistry analysis of samples from a multi-institutional repository, we evaluated if differences in TGF-β receptor abundance were present in tissue from patients with only cirrhosis compared with those with HCC in the context of cirrhosis. We determined that TGFBR2, not TGFBR1, was significantly reduced in HCC tissue compared with cirrhotic tissue. We developed an artificial intelligence (AI)-based process that correctly identified cirrhotic and HCC tissue and confirmed the significant reduction in TGFBR2 in HCC tissue compared with cirrhotic tissue. Thus, we propose that a reduction in TGFBR2 abundance represents a useful biomarker for detecting HCC in the context of cirrhosis and that incorporating this biomarker into an AI-based automated imaging pipeline could reduce variability in diagnosing HCC from biopsy tissue.</p>","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"13 1","pages":"9-20"},"PeriodicalIF":0.0,"publicationDate":"2022-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9170384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43758773","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}
Genes and CancerPub Date : 2022-02-10eCollection Date: 2022-01-01DOI: 10.18632/genesandcancer.219
Farnaz Amini, Mohammad Khalaj-Kondori, Amin Moqadami, Ali Rajabi
{"title":"Expression of HOTAIR and MEG3 are negatively associated with <i>H. pylori</i> positive status in gastric cancer patients.","authors":"Farnaz Amini, Mohammad Khalaj-Kondori, Amin Moqadami, Ali Rajabi","doi":"10.18632/genesandcancer.219","DOIUrl":"https://doi.org/10.18632/genesandcancer.219","url":null,"abstract":"<p><strong>Background: </strong>Chronic infection with <i>Helicobacter pylori</i> is one of the main causes of gastric cancer (GC). Besides, lncRNAs play crucial roles in cancer pathobiology including GC. Here we aimed to investigate the expression of MEG3 and HOTAIR in gastric cancer tissues and evaluate their association with the <i>H. pylori</i> status.</p><p><strong>Materials and methods: </strong>One hundred samples were obtained. Total RNA was extracted, cDNA was synthesized and expression of MEG3 and HOTAIR was assessed using qRT-PCR. Association of their expression with <i>H. pylori</i> status and other clinicopathological characteristics were investigated. Furthermore, sensitivity and specificity of the MEG3 and HOTAIR expression levels for discrimination of the tumor and non-tumor samples were evaluated by Receiver operating characteristic (ROC) curve analysis.</p><p><strong>Results: </strong>We observed upregulation of HOTAIR but downregulation of MEG3 in tumor compared to the non-tumor tissues. We also found a significant negative association between their expression levels and <i>H. pylori</i> positive status. However, only the expression level of HOTAIR was significantly associated with the size and stage of the tumor (<i>P</i> < 0.05). The ROC curve analysis revealed that the expression levels of MEG3 and HOTAIR might discriminate GC tumor and non-tumor tissues.</p><p><strong>Conclusions: </strong>In conclusion, this study revealed a negative association between H. pylori infection and expression of MEG3 and HOTAIR. The results suggested that the expression level of these lncRNAs might be considered as potential biomarkers for GC.</p>","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":" ","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2022-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8849211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39648568","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}
Genes and CancerPub Date : 2022-01-01DOI: 10.18632/genesandcancer.221
Stacey J Baker, Poulikos I Poulikakos, Hanna Y Irie, Samir Parekh, E Premkumar Reddy
{"title":"CDK4: a master regulator of the cell cycle and its role in cancer.","authors":"Stacey J Baker, Poulikos I Poulikakos, Hanna Y Irie, Samir Parekh, E Premkumar Reddy","doi":"10.18632/genesandcancer.221","DOIUrl":"https://doi.org/10.18632/genesandcancer.221","url":null,"abstract":"<p><p>The cell cycle is regulated in part by cyclins and their associated serine/threonine cyclin-dependent kinases, or CDKs. CDK4, in conjunction with the D-type cyclins, mediates progression through the G<sub>1</sub> phase when the cell prepares to initiate DNA synthesis. Although <i>Cdk</i>4-null mutant mice are viable and cell proliferation is not significantly affected <i>in vitro</i> due to compensatory roles played by other CDKs, this gene plays a key role in mammalian development and cancer. This review discusses the role that CDK4 plays in cell cycle control, normal development and tumorigenesis as well as the current status and utility of approved small molecule CDK4/6 inhibitors that are currently being used as cancer therapeutics.</p>","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"13 ","pages":"21-45"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9426627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9448183","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":"Slit2 signaling stimulates Ewing sarcoma growth.","authors":"Kruthi Suvarna, Panneerselvam Jayabal, Xiuye Ma, Yuzuru Shiio","doi":"10.18632/genesandcancer.227","DOIUrl":"https://doi.org/10.18632/genesandcancer.227","url":null,"abstract":"<p><p>Ewing sarcoma is a cancer of bone and soft tissue in children driven by EWS::ETS fusion, most commonly EWS::FLI1. Because current cytotoxic chemotherapies are not improving the survival of those with metastatic or recurrent Ewing sarcoma cases, there is a need for novel and more effective targeted therapies. While EWS::FLI1 is the major driver of Ewing sarcoma, EWS::FLI1 has been difficult to target. A promising alternative approach is to identify and target the molecular vulnerabilities created by EWS::FLI1. Here we report that EWS::FLI1 induces the expression of Slit2, the ligand of Roundabout (Robo) receptors implicated in axon guidance and multiple other developmental processes. EWS::FLI1 binds to the Slit2 gene promoter and stimulates the expression of Slit2. Slit2 inactivates cdc42 and stabilizes the BAF chromatin remodeling complexes, enhancing EWS::FLI1 transcriptional output. Silencing of Slit2 strongly inhibited anchorage-dependent and anchorage-independent growth of Ewing sarcoma cells. Silencing of Slit2 receptors, Robo1 and Robo2, inhibited Ewing sarcoma growth as well. These results uncover a new role for Slit2 signaling in stimulating Ewing sarcoma growth and suggest that this pathway can be targeted therapeutically.</p>","PeriodicalId":38987,"journal":{"name":"Genes and Cancer","volume":"13 ","pages":"88-99"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9753566/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10400077","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}