Journal of Carcinogenesis最新文献

{"title":"Programmed death-ligand 1 signaling pathway involves in bladder cancer growth and progression","authors":"E. Samishina, E. Blinova, D. Roshchin, I. Suslova, D. Blinov, P. Zhdanov, O. Deryabina, Olesia V. Kit’ko","doi":"10.4103/JCAR.JCAR_3_19","DOIUrl":"https://doi.org/10.4103/JCAR.JCAR_3_19","url":null,"abstract":"CONTEXT: Exploration of the biological property of programmed death-ligand 1 (PD-L1) signaling that may impact bladder tumor growth in humanized animals and cell culture. AIMS: The aim of this study is to evaluate how PD-L1 signaling involves bladder cancer growth and progression. SETTINGS AND DESIGN: This study design involves experimental in vivo and in vivo study. SUBJECTS AND METHODS: A role of PD-L1 signaling pathway inhibition for bladder cancer growth was assessed in humanized immunodeficient animals carried main molecular subtypes of bladder carcinoma patient-derived xenografts and provided with selective anti-PD-L1 treatment; bladder cancer cells invasiveness was evaluated in mixed RT112/84 cells + CD4+ cells culture incubated with PD-L1 blocker durvalumab. We used two-tailed Student's t-test to explore differences between main and control subgroups. Significance of intergroup comparison was measured with one-way ANOVA followed by the Tukey's or Newman–Keul's criterion. Survival curves were analyzed with Gehan's criterion with the Yate's correction. Differences were considered statistically significant at P < 0.05. RESULTS: Anti-PD-L1 intervention increased survival of the animals carried both primary and relapsed luminal noninvasive, muscular invasive, and relapsed luminal bladder cancer xenografts. There was significant retardation of tumor volume duplication time in aforementioned subgroups correlated with PD-L1 expression. Durvalumab treatment in concentration-dependent manner inhibited tumor cells invasiveness of mixed RT112 + CD4+ culture cells with its maximum at the highest studied concentration (10 μM). CONCLUSIONS: Obtained data constituted the pivotal role of programmed cell death-1/PD-L1 signaling pathway in bladder cancer development and progression. The results will have major implications for further clinical investigations.","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86500178","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":"Immunotherapy in breast cancer.","authors":"Soley Bayraktar,&nbsp;Sameer Batoo,&nbsp;Scott Okuno,&nbsp;Stefan Glück","doi":"10.4103/jcar.JCar_2_19","DOIUrl":"https://doi.org/10.4103/jcar.JCar_2_19","url":null,"abstract":"<p><p>The idea of using the immune system to fight cancer is over 100 years old. A new molecular approach led to a better understanding of the immune system. Checkpoint regulation, understanding the roles of Tregs, Th1, and Th2, development of Chimeric antigen receptor (CAR)-T cells, as well as regulation of dendritic cells and macrophages, are just a few examples of our understating that has also led to the discovery of immune checkpoint inhibitors (ICIs) and modulators. This led the Nobel Prize committee in 2018, to award Dr. James P. Allison the Nobel Prize in medicine for the discovery of Cytotoxic T-lymphocyte-associated antigen-4, and Dr. Tasuku Honjo for the discovery of programmed cell death-1 (PD-1)/PD-1-ligand (PDL-1). Several ICIs are already approved by the regulatory authorities, and many more are currently used in studies of several solid tumors and hematologic malignancies. Positive studies have led to the US Food and Drug Administration (FDA) and European Medicines Agency approval of a number of these compounds, but none to date are approved in breast cancer (BC). Moreover, PD-1/PDL-1, MSI high (and dMMR), and tumor mutational burden are the currently \"best\" predictive markers for benefit from immunotherapy. BCs have some of these markers positive only in subsets but less frequently expressed than most other solid tumors, for example, malignant melanoma or non-small cell lung cancer. To improve the potential efficacy of ICI in BC, the addition of chemotherapy was one of the strategies. Many early and large clinical trials in all phases are underway in BC. We will discuss the role of immune system in BC editing, and the potential impact of immunotherapy in BC outcomes.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"18 ","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2019-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6540776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37301890","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":"Assessment and clinicopathological correlation of matrix metalloproteinase 9 expression in nasopharyngeal carcinoma.","authors":"Ashok Kumar Das, Nizara Baishya, Anupam Sarma, Amal Chandra Kataki, Avdesh Kumar Rai, Chandi Ram Kalita","doi":"10.4103/jcar.JCar_24_18","DOIUrl":"10.4103/jcar.JCar_24_18","url":null,"abstract":"<p><strong>Introduction: </strong>Nasopharyngeal cancer is not a common disease in most parts of the world. In India also, nasopharyngeal carcinoma (NPC) is not a common cancer, except for the Northeastern region of the country. Expression of matrix metalloproteinase 9 (MMP9) in the tumor cells is related to tumor invasion and metastasis. The aim of the present study is to analyze the expression of MMP9 in NPC and evaluate its prognostic implications.</p><p><strong>Materials and methods: </strong>A total of 32 histologically confirmed tissue samples of NPC were examined by immunohistochemical staining to assess the expression of MMP9. Clinicopathological parameters and levels of MMP9 expression in the tumor tissue were analyzed using Chi-square test. Survival analysis was done using the Kaplan-Meier method and was compared using log-rank test. <i>P</i> <0.05 was considered statistically significant.</p><p><strong>Results: </strong>Of the 32 tissue samples of NPC, 23 (71.9%) were male and 9 (28.1%) were female. 7 (21.9%) patients presented in T1 Stage, 8 (25.0%) in T2, 12 (37.5%) in T3, and 5 (15.6%) in T4 Stages, respectively. 29 (90.6%) patients presented with lymph node metastasis. MMP9 expression level was significantly correlated with patient's age (<i>P</i> = 0.033), tumor histology (<i>P</i> = 0.017), tumor stage (<i>P</i> = 0.021), and lymph node metastasis (<i>P</i> = 0.011). The 5-year overall survival is higher for low-level expression as compared to high-level expression of MMP9 (<i>P</i> = 0.046).</p><p><strong>Conclusion: </strong>MMP9 is an important prognostic factor for NPC. High expression of MMP9 is associated with cervical lymph nodes metastasis and poor survival outcome.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"18 ","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2019-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6528440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37301889","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":"Molecular pathways of oral cancer that predict prognosis and survival: A systematic review.","authors":"Surendra Lakshminarayana,&nbsp;Dominic Augustine,&nbsp;Roopa S Rao,&nbsp;Shankargouda Patil,&nbsp;Kamran Habib Awan,&nbsp;Sowmya Samudrala Venkatesiah,&nbsp;Vanishri C Haragannavar,&nbsp;Shwetha Nambiar,&nbsp;Kavitha Prasad","doi":"10.4103/jcar.JCar_17_18","DOIUrl":"https://doi.org/10.4103/jcar.JCar_17_18","url":null,"abstract":"<p><p>Several genes and pathways associated with oral squamous cell carcinoma (OSCC) are significant in terms of early detection and prognosis. The objective of this literature review is to evaluate the current research on molecular pathways and genes involved in oral cancer. Articles on the genes involved in oral cancer pathways were evaluated to identify potential biomarkers that can predict survival. In total, 36 articles were retrieved from internet databases, including EBSCO Host, Google Scholar, PubMed, and Science Direct, using the keywords \"biomarker of oral cancer,\" \"pathways of oral cancer,\" \"genes involved in oral cancer,\" and \"oral cancer pathways.\" A total of 36 studies related to OSCC were chosen. Most of the studies used cell lines, while others used archival tissues, few studies followed up the cases. Three major interlinked pathways found were the nuclear factor kappa B (NF-kB), PI3K-AKT, and Wnt pathways. The commonly mutated genes were cyclin D1 (CCND1), Rb, p53, FLJ10540, and TC21. The NF-kB, PI3K-AKT, and Wnt pathways are most frequently involved in the molecular pathogenesis of oral cancer. However, the CCND1, Rb, p53, FLJ10540, and TC21 genes were found to be more accurate in determining patients' overall survival. Polymerase chain reaction, immunohistochemistry, and immunoblotting were the commonly used detection methods.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"17 ","pages":"7"},"PeriodicalIF":0.0,"publicationDate":"2018-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6334533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36969204","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 cancer syndrome caused by <i>KCNQ1</i>-deficiency in the golden Syrian hamster.","authors":"Rong Li, Jinxin Miao, Alexandru-Flaviu Tabaran, M Gerard O'Sullivan, Kyle J Anderson, Patricia M Scott, Zhongde Wang, Robert T Cormier","doi":"10.4103/jcar.JCar_5_18","DOIUrl":"10.4103/jcar.JCar_5_18","url":null,"abstract":"<p><strong>Background: </strong>The golden Syrian hamster is an emerging model organism. To optimize its use, our group has made the first genetically engineered hamsters. One of the first genes that we investigated is <i>KCNQ1</i> which encodes for the KCNQ1 potassium channel and also has been implicated as a tumor suppressor gene.</p><p><strong>Materials and methods: </strong>We generated <i>KCNQ1</i> knockout (KO) hamsters by CRISPR/Cas9-mediated gene targeting and investigated the effects of KCNQ1-deficiency on tumorigenesis.</p><p><strong>Results: </strong>By 70 days of age seven of the eight homozygous <i>KCNQ1</i> KOs used in this study began showing signs of distress, and on necropsy six of the seven ill hamsters had visible cancers, including T-cell lymphomas, plasma cell tumors, hemangiosarcomas, and suspect myeloid leukemias.</p><p><strong>Conclusions: </strong>None of the hamsters in our colony that were wild-type or heterozygous for <i>KCNQ1</i> mutations developed cancers indicating that the cancer phenotype is linked to <i>KCNQ1</i>-deficiency. This study is also the first evidence linking KCNQ1-deficiency to blood cancers.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"17 ","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2018-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6187935/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36693701","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 case-control study on the association of abdominal obesity and hypercholesterolemia with the risk of colorectal cancer.","authors":"Vaidehi Ulaganathan,&nbsp;Mirnalini Kandiah,&nbsp;Zalilah Mohd Shariff","doi":"10.4103/jcar.JCar_2_18","DOIUrl":"https://doi.org/10.4103/jcar.JCar_2_18","url":null,"abstract":"<p><strong>Background: </strong>Obesity has frequently been associated with the dyslipidemic state and with the risk of various chronic diseases.</p><p><strong>Objective: </strong>The objective of this study was to determine the relationship between obesity and blood lipids with a risk of colorectal cancer (CRC).</p><p><strong>Methodology: </strong>Histologically confirmed CRC patients from five local hospitals were matched with cancer-free controls for age, gender, and ethnicity (<i>n</i> = 140: 280). The study participants underwent physical assessment for the presence of obesity and 10 mL of fasting blood was drawn for blood lipid analysis.</p><p><strong>Results: </strong>In this study, abdominal obesity significantly doubled the risk of CRC (adjusted odds ratio [AOR] =1.69, 95% confidence interval [CI] = 1-2.83). Hypercholesterolemia and low high-density lipoprotein cholesterol (HDL) increased the risk of CRC more than twofolds (AOR = 2.6, 95% CI = 1.7-3.9 and AOR = 3.8, 95% CI = 2.3-6.3, respectively). Abdominal obesity and hypercholesterolemia synergically doubled the risk of CRC (AOR = 2.0, 95% CI = 1-4). Low-HDL has shown no synergic association with other dyslipidemic states with an increased CRC risk.</p><p><strong>Conclusion: </strong>Improving abdominal obesity, hypercholesterolemia, and low HDL may be a clinically relevant strategy to reduce the risk of CRC among Malaysians.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"17 ","pages":"4"},"PeriodicalIF":0.0,"publicationDate":"2018-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6166417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36564664","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":"Role of aberrant glycosylation enzymes in oral cancer progression.","authors":"Bhairavi N Vajaria,&nbsp;Kinjal A Patel,&nbsp;Prabhudas S Patel","doi":"10.4103/jcar.JCar_7_18","DOIUrl":"https://doi.org/10.4103/jcar.JCar_7_18","url":null,"abstract":"<p><strong>Background: </strong>Carcinogenesis, a multistep process involves sequential changes during neoplastic transformation. The various hallmarks of cancer aid in cell survival, proliferation, and dissemination. Aberrant glycosylation, a recently defined hallmark of cancer, is influenced by glycosylation enzymes during carcinogenesis. Therefore, the present study measured α-2,3 and α-2,6 sialyltransferase (ST), sialidase, and α-L-fucosidase activity in patients with oral precancerous conditions (OPC) and oral cancer patients.</p><p><strong>Subjects: </strong>The study enrolled 100 oral cancer patients, 50 patients with OPC, 100 healthy controls, and 46 posttreatment follow-ups of oral cancer patients. Blood and saliva were collected from all the participants.</p><p><strong>Materials and methods: </strong>Sialidase activity was measured by spectrofluorimetric method, α-2,3 and α-2,6 ST by ELISA using biotinylated lectins, and α-L-fucosidase by spectrophotometric method.</p><p><strong>Results: </strong>The results depicted increased levels of sialidase, α-2,3 and α-2,6 ST, α-L-fucosidase in patients with OPC and oral cancer patients. Receiver operating characteristic curve indicated significant discriminatory efficacy in distinguishing controls and oral cancer patients for serum and salivary sialidase and α-L-fucosidase activity, and serum α-2,6 ST. Furthermore, serum and salivary α-L-fucosidase activity and serum sialidase activity significantly distinguished controls and patients with OPC. Serum and salivary sialidase, α-L-fucosidase, and serum α-2,3 ST activity were higher in patients with metastasis as compared to nonmetastatic patients. Higher values of serum α-L-fucosidase activity were significantly associated with low-overall survival.</p><p><strong>Conclusion: </strong>The increased levels of enzymes correlated with tumor initiation, progression, and metastasis in oral cancer patients. The alterations in glycosyltransferases/glycosidases thus support the view of glycosylation as a hallmark of cancer.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"17 ","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2018-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6166416/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36564665","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":"Genetic inhibition of autophagy in a transgenic mouse model of anal cancer.","authors":"Brooks L Rademacher,&nbsp;Louise M Meske,&nbsp;Kristina A Matkowskyj,&nbsp;Bret M Hanlon,&nbsp;Evie H Carchman","doi":"10.4103/jcar.JCar_4_18","DOIUrl":"https://doi.org/10.4103/jcar.JCar_4_18","url":null,"abstract":"<p><strong>Background: </strong>The dynamic role of autophagy in cancer development is a topic of considerable research and debate. Previously published studies have shown that anal cancer development can be promoted or prevented with the pharmacologic inhibition or induction, respectively, of autophagy in a human papillomavirus (HPV) mouse model. However, these results are confounded by the fact that the drugs utilized are known to affect other pathways besides autophagy. It has also been shown that autophagic inhibition occurs in the setting of HPV16 oncoprotein expression (E6 and E7) and correlates with increased susceptibility to anal carcinogenesis.</p><p><strong>Materials and methods: </strong>In this study, we employed a conditional, genetic, autophagic (Atg7) knockout mouse model to determine conclusively that autophagy has a role in anal cancer development, in the absence or presence of E6 and E7.</p><p><strong>Results: </strong>In mice lacking both HPV16 oncogenes, knockout of autophagy followed by exposure to a carcinogen resulted in a tumor incidence of 40%, compared to 0% in mice treated with a carcinogen alone with an intact autophagic pathway (<i>P</i> = 0.007). In mice expressing either one or both HPV16 oncoproteins, the addition of genetic knockout of autophagy to carcinogen treatment did not lead to a significant difference in tumor incidence compared to carcinogen treatment alone, consistent with the ability of HPV oncogenes to inhibit autophagy in themselves.</p><p><strong>Conclusions: </strong>These results provide the first conclusive evidence for the distinct role of autophagy in anal carcinogenesis, and suggest that autophagy is a plausible target for therapies aimed at reducing anal dysplasia and anal cancer development.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"17 ","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2018-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6071480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36408257","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":"Oncogenic and tumor suppressive roles of special AT-rich sequence-binding protein.","authors":"Qiao Yi Chen, Max Costa","doi":"10.4103/jcar.JCar_8_17","DOIUrl":"10.4103/jcar.JCar_8_17","url":null,"abstract":"<p><p>In recent years, research efforts have been centered on the functional roles of special AT-rich sequence-binding protein (SATB2) in cancer development. Existing studies differ in the types of tumor tissues and cell lines used, resulting in mixed results, which hinder the clear understanding of whether SATB2 acts as a tumor suppressor or promoter. Literature search for this review consisted of a basic search on PubMed using keywords \"SATB2\" and \"special AT-rich sequence-binding protein 2.\" Each article was then selected for further examination based on relevance of the title. In consideration to possible missing data from a primary PubMed search, after coding for relevant information, articles listed in the references section were filtered for further review. The current literature suggests that SATB2 can act both as a tumor suppressor and as a promoter since it can be regulated by multiple factors and is able to target different downstream genes in various types of cancer cell lines as well as tissues. Future studies should focus on its contradictory roles in different types of tumors. This paper provides a comprehensive review of currently available research on the role of SATB2 in different cancer cells and tissues and may provide some insight into the contradictory roles of SATB2 in cancer development.</p>","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"17 ","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2018-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6071479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36408256","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":"Evidence-based approaches to reduce cancer health disparities: Discover, develop, deliver, and disseminate.","authors":"Priyanka P Desai,&nbsp;Jana B Lampe,&nbsp;Sulaimon A Bakre,&nbsp;Riyaz M Basha,&nbsp;Harlan P Jones,&nbsp;Jamboor K Vishwanatha","doi":"10.4103/jcar.JCar_13_17","DOIUrl":"https://doi.org/10.4103/jcar.JCar_13_17","url":null,"abstract":"The Texas Center for Health Disparities (TCHD) at the University of North Texas Health Science Center is a National Institute on Minority Health and Health Disparities-funded, specialized center of excellence for health disparities. TCHD organized its 12th annual conference focusing on “Evidence-Based Approaches to Reduce Cancer Health Disparities: Discover, Develop, Deliver, and Disseminate.” At this conference, experts in health care, biomedical sciences, and public health gathered to discuss the current status and strategies for reducing cancer health disparities. The meeting was conducted in three sessions on breast cancer, prostate cancer, and colorectal cancer disparities, in addition to roundtable discussions and a poster session. Each session highlighted differences in the effects of cancer, based on factors such as race/ethnicity, gender, socioeconomic status, and geographical location. In each session, expert speakers presented their findings, and this was followed by a discussion panel made up of experts in that field and cancer survivors, who responded to questions from the audience. This article summarizes the approaches to fundamental, translational, clinical, and public health issues in cancer health disparities discussed at the conference.","PeriodicalId":52464,"journal":{"name":"Journal of Carcinogenesis","volume":"17 ","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2018-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5883827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35999263","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}