The processes of tumor metastasis, apoptosis and anti-tumor immune response are among the most complex yet rapidly advancing fields in the area of cancer research. This monograph, with its leading authorship, presents a comprehensive coverage of the recent advances in the various key concepts in these fundamental aspects of human cancer. It contains state-of-the-science reviews on invasion, metastasis, angiogenesis, apoptosis and immunologic aspects related to cancer.

The acknowledgment that viruses are potent biological factors in driving many cancers have seen a dramatic upsurge in recent years in large part to the success of the human papilloma virus vaccine against invasive cervical carcinomas and followed by the awarding of the noble prize in medicine in 2008 to Dr. Harald zurHausen who identified the link between papilloma virus and cervical cancers. Over the last few years there have been some volumes addressing different aspects of viruses and cancers and to some extent focusing on the DNA viruses, more specifically the human DNA viruses. This proposed volume will attempt to review and address the major gaps in current knowledge in DNA viruses as well as RNA viruses bringing a historical perspective of where studies began to a more recent molecular approach and vaccine successes in tumor viruses. We will also cover other known oncogenic viruses associated cancers in other mammals in addition to humans.

Angiogenesis plays rate limiting roles in tumor growth and invasion. Angiogenesis inhibition has been proposed as a general strategy to fight against cancers. This book covers different therapeutic targets for angiogenesis interventions with emphasis on c

Tumor microenvironment (TME) plays an important role in immunosuppressive mechanisms that result in immune editing and treatment resistance. Elucidating the diversity of stromal and immune cell distribution, polarization, and changes in their gene expression signatures will enable a better understanding of key events to improve treatment and prognosis. With the onset of immune checkpoint inhibitors (ICIs) in clinics for patients with solid tumors and hematologic malignancies, immunotherapy has taken a new direction in cancer management, especially as combination therapies. However, limitations encountered with the use of ICIs, including toxicity and immune-related adverse events (irAE) indicate the need to understand multiple regulatory mechanisms at both cellular and molecular levels that alter the immune landscape of the TME. Since predominant changes in the immune landscape occur at the TME, focussed deliberation on these events will provide a comprehensive understanding on this topic for scientists in the fields of basic, translational, and clinical cancer immunology. The heterogeneity of TME and complex immune landscape pose major challenges in the treatment of solid tumors. Thus, integrative approaches, which relate immune mechanisms in the TME to that of peripheral and systemic immune signatures are essential to improve our understanding of the disease complexity and possibly improve immunotherapy outcomes. Such multiparametric studies should combine advances in current understanding of cancer immunobiology with powerful technologies, such as single-cell and spatial transcriptomics, and high dimensional flow cytometry that rapidly expand our ability to explore these interactions. Notably, tumor heterogeneity and inflammatory mediators in the TME vary significantly in neoplasms based on mutational load, lymphocyte infiltration, expression of checkpoint molecules, soluble inhibitors, and tumor cell metabolism. Overall, connecting key events to immune signatures that conform to a consensus will provide a benchmark to delve further into this important topic. Other parameters such as myeloid and lymphoid cell polarization to alter the immune homeostasis at the TME, favoring a tumor-supportive milieu would provide a macroscopic picture that may help guide treatment choices for more refined personalized tumor immunotherapy.

Aug 29-30, 2017 London, UK Key Topics : Women Cancers, Cervical Cancer, Ovarian Cancer, Endometrial Cancer, Vaginal Cancer/Vulvar Cancer, Breast Cancer, Gynecologic Cancers: Signs and Symptoms, Gynecologic Cancers: Treatment and Monitoring, Human papilloma Virus, HPV Vaccines, Women Health, Gynecologic Cancers: Surgical Methods, Gynecologic Cancer: Screening and Diagnosis, Gynecology Oncology, Cancer Pharmacology, Oncology Nursing and Primary care, Gynecologic Cancers: Case Report

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.

A unique book on the interactions and interrelationships between tumor and host that modulate progression and metastasis. Several authors emphasize targeting the host rather than the tumor itself for therapeutic intervention to control cancer.