{"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}
{"title":"Prognostic Biomarkers for Breast Cancer Metastasis","authors":"Kwok Kin Lee, W. Chng, S. Jha","doi":"10.5772/INTECHOPEN.80576","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.80576","url":null,"abstract":"Breast cancer treatment has improved rapidly through the years, starting from surgery, to hormonal therapy, to targeted therapy. Despite this, tumor metastasis remains the highest cause of breast cancer–related death. The current regime to deter metastasis is through adjuvant therapy, but such therapy frequently yields undesirable side effects. As such, prognostic markers for metastasis are important to stratify patients for adju- vant therapy so as to ameliorate the standard of living of patients with low metastatic potential. So far, only a few well-characterized prognostic biomarkers for metastasis are used in clinics. This chapter will cover both established and novel prognostic biomarkers for breast cancer metastasis and metastatic breast cancer prognosis. The potential of using these biomarkers as predictive biomarkers or new targeted therapy will also be discussed.","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"42 1","pages":""},"PeriodicalIF":1.9,"publicationDate":"2018-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77966268","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":"Recent trend in gastric cancer treatment in the USA.","authors":"Kazuto Harada, Hideo Baba, Jaffer A Ajani","doi":"10.20517/2394-4722.2017.74","DOIUrl":"https://doi.org/10.20517/2394-4722.2017.74","url":null,"abstract":"<p><p>Gastric adenocarcinoma (GAC) is estimated as the fifteenth most common cancer in the USA. Incidence rate has been gradually decreasing, but prognosis remains dismal. For patients with locally advanced GAC (stage > T1B and < T4B), multimodality therapies, such as surgery, chemotherapy, and radiation therapy, are needed. Perioperative chemotherapy or postoperative chemoradiation/chemotherapy is recommended. For metastatic GAC patients, combination of two cytotoxics (platinum compound and fluoropyrimidine) has become a common place in the USA, and when HER2 is positive, trastuzumab is added. When GAC progresses after the first line therapy, additional biomarkers (microsatellite instability and programmed death ligand 1) should be tested so that checkpoint inhibitors can be used. Overall, the options for advanced GAC patients are limited and more research is needed.</p>","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"4 ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2018-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8188734/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39083775","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}
Shirley Jusino, Fabiola M Fernández-Padín, Harold I Saavedra
{"title":"Centrosome aberrations and chromosome instability contribute to tumorigenesis and intra-tumor heterogeneity.","authors":"Shirley Jusino, Fabiola M Fernández-Padín, Harold I Saavedra","doi":"10.20517/2394-4722.2018.24","DOIUrl":"https://doi.org/10.20517/2394-4722.2018.24","url":null,"abstract":"<p><p>Centrosomes serve as the major microtubule organizing centers in cells and thereby contribute to cell shape, polarity, and motility. Also, centrosomes ensure equal chromosome segregation during mitosis. Centrosome aberrations arise when the centrosome cycle is deregulated, or as a result of cytokinesis failure. A long-standing postulate is that centrosome aberrations are involved in the initiation and progression of cancer. However, this notion has been a subject of controversy because until recently the relationship has been correlative. Recently, it was shown that numerical or structural centrosome aberrations can initiate tumors in certain tissues in mice, as well as invasion. Particularly, we will focus on centrosome amplification and chromosome instability as drivers of intra-tumor heterogeneity and their consequences in cancer. We will also discuss briefly the controversies surrounding this theory to highlight the fact that the role of both centrosome amplification and chromosome instability in cancer is highly context-dependent. Further, we will discuss single-cell sequencing as a novel technique to understand intra-tumor heterogeneity and some therapeutic approaches to target chromosome instability.</p>","PeriodicalId":15167,"journal":{"name":"Journal of Cancer Metastasis and Treatment","volume":"4 ","pages":""},"PeriodicalIF":1.9,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6205736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36624674","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}