Yuanhong Sun, Joseph D Malaer, Porunelloor A Mathew
{"title":"Lectin-like transcript 1 as a natural killer cell-mediated immunotherapeutic target for triple negative breast cancer and prostate cancer.","authors":"Yuanhong Sun, Joseph D Malaer, Porunelloor A Mathew","doi":"10.20517/2394-4722.2019.29","DOIUrl":"10.20517/2394-4722.2019.29","url":null,"abstract":"<p><p>Breast and prostate cancer are the leading causes of death in females and males, respectively. Triple negative breast cancer (TNBC) does not express the estrogen receptor, progesterone receptor, or human epidermal growth factor receptor 2, resulting in limited treatment options. Androgen deprivation therapy is the standard care for prostate cancer patients; however, metastasis and recurrence are seen in androgen-independent prostate cancer. Both prostate and breast cancer show higher resistance after recurrence and metastasis, which increases the difficulty of treatment. Natural killer (NK) cells play a critical role during innate immunity and tumor recognition and elimination. NK cell function is determined by a delicate balance of inhibitory signals and activation signals received through cell surface receptors. Lectin-like transcript 1 (LLT1, CLEC2D, OCIL) is a ligand of NK cell inhibitory receptor NKRP1A (CD161). Several studies have that reported higher expression of LLT1 is associated with the development of various tumors. Our studies revealed that TNBC and prostate cancer cells express higher levels of LLT1. In the presence of a monoclonal antibody against LLT1, NK cell-mediated killing of TNBC and prostate cancer cells were greatly enhanced. This review highlights the potential that using monoclonal antibodies to block LLT1 - NKRP1A interactions could be an effective immunotherapeutic approach to treat triple negative breast cancer and prostate cancer.</p>","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"2019 5","pages":""},"PeriodicalIF":1.9,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8315106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39255038","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}
Kimberley C Agbo, Jessie Z Huang, Amr M Ghaleb, Jennie L Williams, Kenneth R Shroyer, Agnieszka B Bialkowska, Vincent W Yang
{"title":"Loss of the Krüppel-like factor 4 tumor suppressor is associated with epithelial-mesenchymal transition in colorectal cancer.","authors":"Kimberley C Agbo, Jessie Z Huang, Amr M Ghaleb, Jennie L Williams, Kenneth R Shroyer, Agnieszka B Bialkowska, Vincent W Yang","doi":"10.20517/2394-4722.2019.35","DOIUrl":"https://doi.org/10.20517/2394-4722.2019.35","url":null,"abstract":"<p><strong>Aim: </strong>Colorectal cancer (CRC) is the third leading cancer-related cause of death due to its propensity to metastasize. Epithelial-mesenchymal transition (EMT) is a multistep process important for invasion and metastasis of CRC. Krüppel-like factor 4 (KLF4) is a zinc finger transcription factor highly expressed in differentiated cells of the intestinal epithelium. KLF4 has been shown to play a tumor suppressor role during CRC tumorigenesis - its loss accelerates development and progression of cancer. The present study examined the relationship between KLF4 and markers of EMT in CRC.</p><p><strong>Methods: </strong>Immunofluorescence staining for KLF4 and EMT markers was performed on archived patient samples after colorectal cancer resection and on colonic tissues of mice with colitis-associated cancer.</p><p><strong>Results: </strong>We found that KLF4 expression is lost in tumor sections obtained from CRC patients and in those of mouse colon following azoxymethane and dextran sodium sulfate (AOM/DSS) treatment when compared to their respective normal appearing mucosa. Importantly, in CRC patient tumor sections, we observed a negative correlation between KLF4 levels and mesenchymal markers including TWIST, β-catenin, claudin-1, N-cadherin, and vimentin. Similarly, in tumor tissues from AOM/DSS-treated mice, KLF4 levels were negatively correlated with mesenchymal markers including SNAI2, β-catenin, and vimentin and positively correlated with the epithelial marker E-cadherin.</p><p><strong>Conclusion: </strong>These findings suggest that the loss of KLF4 expression is a potentially significant indicator of EMT in CRC.</p>","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"5 ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7304562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38070845","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}
Matthew Kaufman, Ana Cruz, Janese Thompson, Srinivasa Reddy, Nisha Bansal, Joshua G Cohen, Yanyuan Wu, Jay Vadgama, Robin Farias-Eisner
{"title":"A review of the effects of healthcare disparities on the experience and survival of ovarian cancer patients of different racial and ethnic backgrounds.","authors":"Matthew Kaufman, Ana Cruz, Janese Thompson, Srinivasa Reddy, Nisha Bansal, Joshua G Cohen, Yanyuan Wu, Jay Vadgama, Robin Farias-Eisner","doi":"10.20517/2394-4722.2018.25","DOIUrl":"https://doi.org/10.20517/2394-4722.2018.25","url":null,"abstract":"<p><p>Ovarian cancer (OC) is a serious condition that often presents at advanced stages and has high mortality rates, with the current mode of early-stage screening lacking sensitivity and specificity. OC often presents asymptomatically, which renders early diagnosis difficult. Furthermore, many patients lack significant risk factors or family history of the disease. Five-year survival rates differ between patients with OC among racial, ethnic, and social groups as a result of different social barriers. This review article aims to present the currently existing data regarding health care disparities among OC patients of different ethnic, demographic, and socioeconomic backgrounds, and what next steps should be taken to better understand and eventually eliminate these potentially devastating health care disparities. Increasing data support the notion that a combination of genomic, socioeconomic status, social factors, and cultural differences lead to differential treatments and therefore health care disparities. While genomic and biological factors are important, language barriers, geographic and travel barriers, differences in comorbidity likelihood between populations, and different treatment plans seem to have a greater impact on 5-year survival rates of patients from diverse backgrounds. Language barriers limit a shared-decision model of care. Transportation limitations and geographic differences can lead to limited follow-up and insufficient care in resource and equipment restrictive settings. Patients with these barriers also tend to have a higher incidence of comorbidities that raise the mortality rate of OC. Further research needs to explore effective solutions to bridge health care disparities and understand why they occur.</p>","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"5 ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6590085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37364582","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":"Tumour Microenvironment and Metastasis","authors":"Ke Wang","doi":"10.5772/INTECHOPEN.79319","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.79319","url":null,"abstract":"In recent years, cancer is more and more severe harm to the health of people in the world. Although tumour diagnosis and therapy have made some progresses, there is little improvement in overall. One of the main reasons is that the pathogenesis of cancer metastasis is still enigmatic. Cancer development and metastasis are a complicated process that depends on the antigenic properties of cancer cells and a favoured environment in organs. Cancer cells metastasis causes more than 90% cancer death in the lungs, liver, brain, and bone, and a primary tumour causes less than 10% death. Therefore, understanding the process of cancer metastasis is essential, and it is convenient to deal with the problem of cancer metastasis and reduce cancer-related thrombosis. It has shown that tumour microenvironment plays a significant role in cancer progression. A variety of carcinoma-associated fibroblasts, and tumour-related macrophages play expanding and critical functions in sustaining cell proliferation, evading growth suppressors, promoting survival, activating invasion and metastasis, and reprogramming energy metabolism, but the purpose of each constituent remains unknown. This chapter will focus on discussing the role of the microenvironment on tumour invasion and metastasis to improve molecular diagnostics and therapeutics.","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"58 1","pages":""},"PeriodicalIF":1.9,"publicationDate":"2018-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83139782","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":"Introductory Chapter: Cancer Metastasis","authors":"Gizem Çalıbaşı-Koçal, Y. Başbınar","doi":"10.5772/INTECHOPEN.81914","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.81914","url":null,"abstract":"cascade.","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"40 1","pages":""},"PeriodicalIF":1.9,"publicationDate":"2018-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75490106","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}
H. Adwan, D. Elharouni, D. Habashy, N. Banna, R. Georges, Asim Pervaiz, M. Berger
{"title":"Early Metastasis in Colorectal Cancer Poses an Option for New Diagnostic and Treatment Strategies","authors":"H. Adwan, D. Elharouni, D. Habashy, N. Banna, R. Georges, Asim Pervaiz, M. Berger","doi":"10.5772/INTECHOPEN.79637","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.79637","url":null,"abstract":"Metastasis is the spread of tumor cells from a primary site to a secondary site within the host’s body. It is initiated by the detachment of the tumor cells from the primary tumor followed by invasion into the surrounding tissue. Thereafter the cells migrate across the endothelium and into the blood vessels (intravasation). During the intravasation the cells have to survive the sheer forces and the immune response. Upon arrival to the target organ, the cells leave the circulation and cross the endothelium to reach the host organ. Once there, the tumor cells are greeted with the organ’s local immune cells and with a hostile or inappropriate environment, where they finally have to form proliferating colo -nies. Metastasis is therefore far from being a straight-forward or efficient process with less than 0.1% of disseminating tumor cells (around 1 × 109 cells per day for a 1 cm size tumor) succeeding in colonizing distal organs. The identification of the involved marker during the early metastasis process will be essential for establishment of new diagnostics tools, as well as development of novel treatment strategies.","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"55 1","pages":""},"PeriodicalIF":1.9,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76668034","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":"Genetic Mutations and Ubiquitination in Melanoma Growth and Metastasis","authors":"Anushka Dikshit, Jennifer Y. Zhang","doi":"10.5772/INTECHOPEN.78733","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.78733","url":null,"abstract":"Upon neoplastic transformation, melanoma is intrinsically prone to metastasis, which marks the most dangerous aspect of the disease and dubs it one of the most challenging cancers to treat. BRAF/MEK oncokinase inhibitors and immunotherapies have shown considerable promise in some patients, but the clinical benefits are often short-lived due to rapid development of resistance. Recently, ubiquitination enzymes have emerged as potential therapeutic targets. These enzymes can be targeted to increase expression of tumor suppressors and impede activation of oncogenic signaling pathways mediating cell proliferation and tissue invasion. This chapter describes some of the common genetic mutations in melanoma, ubiquitinating and deubiquitinating enzymes that are linked to melanoma progression, metastasis, and therapeutic resistance.","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"102 1","pages":""},"PeriodicalIF":1.9,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87012508","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":"The Landscape of Histone Modification in Cancer Metastasis","authors":"Zhaoping Qiu, Jianlin Wang, Yadi Wu","doi":"10.5772/INTECHOPEN.78383","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.78383","url":null,"abstract":"Metastasis represents one of the most devastating aspects of cancer. Epithelial to mesen- chymal transition (EMT) has been shown to play a critical role in tumorigenic metastasis. During metastatic progression, both genetic and epigenetic modifications endow cancer cells with properties that modulate the capacity for metastatic success. Histone modifica tion is profoundly altered in cancer cells and contributes to cancer metastasis by con- trolling different metastatic phenotypes. Here, we first review histone modifications and discuss their roles in EMT and metastasis, with a particular focus on histone methylation and acetylation. Second, we review the major histone modification enzymes that control chromatin in cancer metastasis. Third, we discuss the transcriptional regulation concerted by these enzymes with EMT transcription factors at different molecular layers. Finally, we discuss pharmacologic manipulation of histone modification enzymes for metastasis treatment. A comprehensive understanding of histone modification in metastasis will not only provide new insights into our knowledge of cancer progression and metastasis, but also offer a novel approach for the development of innovative therapeutic strategies. gene","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"3 1","pages":""},"PeriodicalIF":1.9,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75985969","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":"Epithelial-Mesenchymal Transition in Tumor Microenvironment Induced by Hypoxia","authors":"G. Eskiizmir, E. Özgür","doi":"10.5772/INTECHOPEN.78717","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.78717","url":null,"abstract":"A tumor microenvironment contains various noncancerous cells including adipocytes, fibroblasts, immune and inflammatory cells, neuroendocrine cells, pericytes, vascular and lymphatic endothelial cells, and the extracellular matrix that surrounds cancerous cells. In the tumor microenvironment, cancer cells interact and cross talk with noncancerous cells and orchestrate different mechanisms of cancer such as tumorigenesis, angiogenesis, and metastasis. Moreover, the expansive nature of cancer cells and chaotic angiogenesis affect microcirculation as well as alter the oxygen concentration progres - sively. Hypoxia, a key player in the multistep process of cancer metastasis, is important in different regions of the tumor microenvironment. Hypoxia may transform cancer cells to become more aggressive and invasive by triggering overexpression of several hypoxia-related factors that activate epithelial-mesenchymal transition (EMT). Herein, the current knowledge of how hypoxia-driven EMT is presented in the tumor microenvironment of solid cancers is discussed. EMT and CSC-like properties including resistance to treatment. Each step of the cancer adap tive process is regulated by HIF, NFĸB, PI3K, and MAPK pathways. Understanding the impact of hypoxia and clarifying the hypoxia-induced responses and signaling modalities may pave the way to achieve important steps against cancer via hypoxia/HIF-targeted treatments.","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"71 1","pages":""},"PeriodicalIF":1.9,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86907757","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":"Ovarian Clear Cell Carcinoma: Metastatic Pathways","authors":"C. Sofoudis","doi":"10.5772/INTECHOPEN.79759","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.79759","url":null,"abstract":"Ovarian carcinoma reflects the biggest challenge among the field of gynecologic oncology. It represents the most common death cause of genital carcinomas throughout years. The major classification consists of epithelial and non-epithelial types. Due to the histologic origin, epithelial types of ovarian carcinoma are endometrioid, serous-mucinous, and clear cell types. Due to intense metastatic infiltration and rapid tumor spread, clear cell ovarian carcinoma constitutes type of lesion with the most poor prognosis, decreased overall survival, decreased free survival, and poor quality of life of the patient. The metastatic infiltration is strongly accompanied with all significant prognostic factors. All biochemical pathways at the time of the infiltration are correlated with tumor size, lymphatic spread, staging of the lesion, histologic type, and grade of differentiation of the lesion.","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"14 1","pages":""},"PeriodicalIF":1.9,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84350905","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}