In line with recent evidence, the development of cancer has been described as uncontrolled cell growth that results from gradual accumulation of genetic and epigenetic alterations, involving aberrations in oncogenes, tumor suppressor genes, and defects in genes engaged in DNA repair. As a result, cancer cells acquire a neoplastic phenotype and tumor-associated antigens (TAAs) are presented on their surface. These target structures should be recognized by cells of the immune system. However, a sequence of events at the genetic and epigenetic level disturb immune cells, and in consequence, make them unable to eliminate cancer cells. Both innate and adaptive immunity are mobilized against cancer cells. In response to the appearance of cells with malignant transformation, NK cells release perforin and granzyme, causing direct cytolysis of the target cells. They can also secrete pro-inflammatory cytokines and in that way enhance the anticancer response. The activity of NK cells is regulated by a variety of activating and inhibitory receptors including NKG2D, KIR, CD94 -NKG2 heterodimers and natural cytotoxicity receptors, TNF family ligands, as well as co-stimulatory receptors, which recognize related molecules on target cells. A fundamental trigger of the anticancer immune response is the recognition of TAAs by T cells, via the major histocompatibility complex (MHC), which should be followed by signals from co-stimulatory molecules. Full activation of T lymphocytes requires a third signal provided by the presence of cytokines, and this leads to cell proliferation, differentiation, and secretion of chemokines and cytokines. The effect is to drive the clonal expansion of the T cells directed against TAAs and to recruit other immune effector cells in order to enhance immune defense.

In Epigenetic Regulation of Cancer, a series of volumes from the International Review of Cell and Molecular Biology series, various experts in epigenetics critically cover multiple facets of cancer-associated epigenetic alterations, including the impact of epigenetic deregulation in all steps of oncogenesis as well as promising strategies to therapeutically target cancer-associated epigenetic deregulation. This collection aims at expanding our knowledge on this exciting field of investigation and providing fresh insights as a basis for further investigations that will hopefully translate into an improved clinical management of patients with cancer. - The collection provides accurate and critical review articles from invited experts on the selected topic - Each review provides the newest insights and remarks on multiple subjects of the topic - The volume offers a broad range of perspectives on detailed features

Cancer is a complex and heterogeneous (systematic) disease that exhibits high levels of robustness against various therapeutic interventions. Due to the complex, heterogeneous, and evolving nature of cancer, it is essential for a system-oriented view to be adopted in order to understand the pathogenic mechanism of cancer which will eventually lead to the drug discovery and treatment of patients. This book not only provides new insights from system modeling and large scale experimental data, but also will allow the reader to perceive the systematic characteristics of cancer under some micro-environments. Based on the systems biology method and genome-wide high throughput data, the book presents the PPI network, gene regulatory network and epigenetic network as an integrated genetic and epigenetic cellular network of lung cancer, bladder cancer, thyroid cancer, colorectal cancer, and liver cancer to investigate their core signaling pathways of the carcinogenesis process to identify their corresponding significant carcinogenic biomarkers as drug targets for systems drug discovery and design. Consequently, the book presents the design of a multiple-molecule drug that can target these biomarkers for the therapeutic treatment of cancer with fewer side effects.