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Over the past few decades, lymphoma patient outcomes have improved as a result of multidrug chemotherapy and radiation therapy, intensification of treatment, improvement in supportive care, and better imaging and staging systems. Even more recently, there has been tremendous progress in the understanding of cancer cell biology and its microenvironment which has resulted in the development of biologic agents, also called "target" therapies. These therapies are more specific in targeting cancer cells either directly or via enhancement of the immune system. Many clinical studies have focused on biological agents in combination with traditional chemotherapy with the goal of improved outcomes, or reduced acute long term complications that are associated with lymphoma therapy. This volume will review different classes of "target" drugs that have been developed, approved, or are under investigation in the field of lymphoma therapy. The discussion will not only be on the understanding of the mechanisms of action or clinical response of those agents, but will also help the reader to understand the nature of lymphoma biology in patients who relapse or are refractor after exposure to those drugs. Contributors will discuss what is currently known about mechanisms of tumor-related or host-related resistance, and how to overcome this resistance. This understanding is crucial given the dismal outcomes of patients with relapsed or refractory lymphomas. The book provides a unique opportunity to review and reflect on the recent successes and pitfalls of the modern lymphoma therapy era.
In the last decade, the literature on molecular mechanisms and activated pathways in the different lymphoma categories increased exponentially, which was followed by a more diffuse and successful use of targeted therapies. In this book, expert authors revisit the most relevant aspects of these therapies, with special emphasis on molecular mechanisms and clinical effects of resistance. The knowledge of the underlying mechanisms involved in tumor resistance to target therapies is of paramount importance because they will result in a better selection of patients with sensitive disease and the establishment of suitable combinations of drugs that target different molecules and could overcome the established resistance.
This volume details our current understanding of the architecture and signaling capabilities of the B cell antigen receptor (BCR) in health and disease. The first chapters review new insights into the assembly of BCR components and their organization on the cell surface. Subsequent contributions focus on the molecular interactions that connect the BCR with major intracellular signaling pathways such as Ca2+ mobilization, membrane phospholipid metabolism, nuclear translocation of NF-kB or the activation of Bruton’s Tyrosine Kinase and MAP kinases. These elements orchestrate cytoplasmic and nuclear responses as well as cytoskeleton dynamics for antigen internalization. Furthermore, a key mechanism of how B cells remember their cognate antigen is discussed in detail. Altogether, the discoveries presented provide a better understanding of B cell biology and help to explain some B cell-mediated pathogenicities, like autoimmune phenomena or the formation of B cell tumors, while also paving the way for eventually combating these diseases.
Genetic alterations in cancer, in addition to being the fundamental drivers of tumorigenesis, can give rise to a variety of metabolic adaptations that allow cancer cells to survive and proliferate in diverse tumor microenvironments. This metabolic flexibility is different from normal cellular metabolic processes and leads to heterogeneity in cancer metabolism within the same cancer type or even within the same tumor. In this book, we delve into the complexity and diversity of cancer metabolism, and highlight how understanding the heterogeneity of cancer metabolism is fundamental to the development of effective metabolism-based therapeutic strategies. Deciphering how cancer cells utilize various nutrient resources will enable clinicians and researchers to pair specific chemotherapeutic agents with patients who are most likely to respond with positive outcomes, allowing for more cost-effective and personalized cancer therapeutic strategies.
This book summarizes current knowledge of the biology and molecular pathogenesis of aggressive lymphomas and reviews the state of the art in diagnostic and therapeutic strategies. The aim is both to provide the reader with a sound understanding of the very significant progress that has been achieved in the understanding and management of these malignancies over recent years and to facilitate appropriate choice of the therapeutic strategy in individual cases. The assessment of different prognostic parameters are clearly presented in order to permits effective risk stratification that impacts on treatment choice. Recent insights into lymphomagenesis are exemplified and may assist in identifying emerging therapeutic targets. The comprehensive and up-to-date nature of the book will make it an ideal reference for all physicians and researchers interested in lymphoma, including clinicians from various medical specialties, biologists, pathologists, radiologists and nuclear medicine specialist, as well as students.
In this book the reader will find a collection of chapters written by different research teams describing different aspects of peripheral T-cell lymphoma pathobiology, classification, and treatment. This work is mainly addressed to researchers already working in this area, but it is also accessible to anyone with a scientific background who desires to have an updated overview of the recent progress in this domain. It will also be valuable to scientists and physicians who have become newly involved in this field. Each chapter is self-contained and can be read independently of the others. This book intends to provide highlights of the current research as well as the current gold standards for diagnosis and treatment of these diseases, showing the recent advances in the personalized approach to T-cell derived lymphomas.
This text provides a state-of-the-art overview on Non-Hodgkin's lymphoma (NHL) in children and adolescents. The volume is divided into seven sections, each of which focuses on a critical component of pediatric NHL, including history and epidemiology, pathology and molecular biology, disease evaluation and response, common and rare sub-types of NHL, and current and novel treatment strategies. The text also comprehensively reviews the late effects of treatment, quality of patient life, and NHL treatment in countries with limited resources. Written by experts in the field, Non-Hodgkin's Lymphoma in Childhood and Adolescence is a valuable resource for clinicians and practitioners who treat children and adolescents with NHL.
More than 40 years ago, the observation that doxorubicin-resistant tumor cells were cross-resistant to several structurally different anticancer agents was the first step in the discovery of P-glycoprotein (P-gp). P-gp belongs to the superfamily of ATP-binding cassette (ABC) transporters;its overexpression has become a therapeutic target for overcoming multidrug resistance in tumors. However, P-gp is also expressed in cells of normal tissues where it plays a physiological role, by protecting them from the toxic effects of xenobiotics. Also, ABCB1 gene polymorphisms may influence the response to anticancer drugs substrate of P-gp. Several strategies to overcome P-gp tumor drug resistance have been suggested. P-gp 'circumvention’ is the most explored and is based on the coadministration of anticancer agents and pump inhibitors (P-gp modulators). Despite the positive findings obtained in preclinical studies, results of clinical trials are not yet successful and clinical research is still ongoing. Other investigational approaches have been studied (e.g. P-gp targeting antibodies, use of antisense strategies or transcriptional regulators targeting ABCB1 gene expression) but their use is still circumscribed to the preclinical setting. A further approach is represented by the encapsulation of P-gp substrate anticancer drugs into liposomes or nanoparticles. This strategy has shown higher efficacy in tumor previously treated with the free drug. The reasons explaining the increased efficacy of liposomal/nanoparticle-based drugs in Pgp-overexpressing tumors include the coating with specific surfactants, the composition changes in the plasma membrane microdomains where P-gp is embedded, the direct impairment of P-gp catalytic mechanisms exerted by specific component of the liposomal shell, but are not yet fully understood. A second strategy to overcome P-gp tumor drug resistance is represented by exploiting the P-gp presence. Actually, P-gp-overexpressing cells show increased sensitivity (collateral sensitivity) to some drugs (e.g. verapamil, narcotic analgesics) and to some investigational compounds (e.g. NSC73306). P-gp-overexpressing cell are hypersensitive to reactive oxygen species, to agents perturbing the energetic metabolic pathways, changing the membrane compositions, reducing the efflux of endogenous toxic catabolites. However, the mechanisms explaining collateral sensitivity have not been fully elucidated. Another approach to exploit P-gp is represented by ABCB1 gene transfer to transform bone marrow progenitor cells into a drug resistant state which may allow conventional or higher doses of anticancer drug substrates of P-gp to be administered safely after transplantation. More recently the development and introduction in the clinics of anticancer drugs which are not substrates of P-gp (e.g. new microtubule modulators, topoisomerase inhibitors) has provided a new and promising strategy to overcome P-gp tumor drug resistance (P-gp 'evasion'). This ‘research topic’ issue aims at exploding the above mentioned matters, in particular by: -retracing the history of the first researches on P-gp - describing the physiological role of P-gp - describing the molecular basis, structural features and mechanism of action of P-gp - describing diagnostic laboratory methods useful to determine the expression of P-gp and its transporter function - describing strategies to overcome tumor drug resistance due to P-gp and other ABC transporters - indicating novel approaches to overcome P-gp multidrug resistance, ranging from basic research studies to pre-clinical/clinical studies.
Cutaneous T-cell lymphoma (CTCL) is a general term for many lymphomas of the skin including mycosis Fungoides and Sezary syndrome. This book presents the state of the art in CTCL epidemiology, clinical features, pathology, immunochemistry, diagnostic molecular techniques, staging and prognosis, and treatment. Edited by one of the leading experts in
This is a comprehensive textbook of Hodgkin's and non-Hodgkin's lymphomas written by leaders in the field of childhood lymphomas. It includes clinical, pathologic and molecular biology of each subtype of lymphoma. The pathology chapters are comprehensive and include excellent photographs. The book is at the level of subspecialists in pediatric hematology and oncology, radiation oncology, pediatric surgery and hematopathology.