Spheroids in Cancer Research


Book Description

Malignant growth of cells is often characterized by disorganization of tissue structure, abnormal blood vessel development, and insuffi cient vascular supply. As a consequence, the cancer cells grow in a three-dimensional pattern in atypical microenvironments which include physical, chemical, and nutritional stresses. Necrosis often develops some distance away from the blood vessels. In association with an inherent instability in malignant cell populations, and also because of the changing micromilieu, significant cellular heteroge neity emerges with regard to various phenotypic characteristics. Both biological behavior and responses to therapeutic agents can be affected. A variety of in vitro and in vivo experimental models exist for research on properties of cancer cells during growth. The multicell spheroid model was developed as a system of intermediate complexity in which three dimensional growth of cells enhances cell-cell interactions and creates micro environments that simulate the conditions in intervascular microregions of tumors or microme tastatic foci. Spheroids may change their cellular characteristics with changing environments during growth. These can be studied under controlled conditions in vitro. Interest in details of experimental methods for this model system stimulated the organization of the First International Conference in Rochester, NY in 1980, the Proceedings of which were summarized in Cancer Research in 1981. Since then there has been a rapid increase in the use of this model system, and increased research on the significance of cell-cell and cell-microenvironment interactions in biology in general.




Cancer Clinical Trials


Book Description

A readable guide for anyone who is considering therapeutic options in addition to standard cancer therapy. The book seeks to share knowledge about cancer clinical trials with people living with cancer, their families and loved ones.




The Heterogeneity of Cancer Metabolism


Book Description

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.




Sourcebook of Models for Biomedical Research


Book Description

The collection of systems represented in Sourcebook of genomic programs, although this work is certainly well Models for Biomedical Research is an effort to re?ect the represented and indexed. diversity and utility of models that are used in biomedicine. Some models have been omitted due to page limitations That utility is based on the consideration that observations and we have encouraged the authors to use tables and made in particular organisms will provide insight into the ? gures to make comparisons of models so that observations workings of other, more complex, systems. Even the cell not available in primary publications can become useful to cycle in the simple yeast cell has similarities to that in the reader. humans and regulation with similar proteins occurs. We thank Richard Lansing and the staff at Humana for Some models have the advantage that the reproductive, guidance through the publication process. mitotic, development or aging cycles are rapid compared As this book was entering production, we learned of the with those in humans; others are utilized because individual loss of Tom Lanigan, Sr. Tom was a leader and innovator proteins may be studied in an advantageous way and that in scienti?c publishing and a good friend and colleague to have human homologs. Other organisms are facile to grow all in the exploratory enterprise. We dedicate this book to in laboratory settings or lend themselves to convenient analy- his memory. We will miss him greatly.




Topics in Anti-Cancer Research: Volume 10


Book Description

Topics in Anti-Cancer Research covers new developments in the field of cancer diagnosis and drug therapy. Novel drugs as anticancer agents include natural and synthetic phenazirines and other anti-cancer compounds. The series also covers information on the current understanding of the pathology and molecular biology of specific neoplasms. The diversity of research topics published in this book series give broad and valuable perspectives for cancer researchers, clinicians, cancer professionals aiming to develop novel anti-cancer targets and patents for the treatment of various cancers. The topics covered in this volume are: - Peptides can play a major role in combating cancer diseases - Studying of the CLL after treatment using fractal parameter of neoplastic lymphocytes detection (ΛNLD) - Mechanistic insight of rhenium-based compounds as anti- cancer agents - Targeting cancer-specific inflammatory components in cancer therapeutics - Marine natural products as a source of novel anticancer agents: a treasure from the ocean - PDX clinical trial design in anti-cancer research




Lung Cancer and Personalized Medicine


Book Description

This, the first of two volumes on personalized medicine in lung cancer, touches on the core issues related to the understanding of lung cancer—statistics and epidemiology of lung cancer—along with the incidence of lung cancer in non-smokers. A major focus of this volume is the state of current therapies against lung cancer—immune, targeted therapies against EGFR TKIs, KRAS, ALK, angiogenesis; the associated challenges, especially resistance mechanisms; and recent progress in targeted drug development based on metal chemistry. Chapters are written by some of the leading experts in the field, who provide a better understanding of lung cancer, the factors that make it lethal, and current research focused on developing personalized treatment plans. With a unique mix of topics, this volume summarizes the current state-of-knowledge on lung cancer and the available therapies.







Experimental Leukemia and Mammary Cancer


Book Description

Charles Brenton Huggins won the Nobel prize in 1966 for his extensive work in cancer research. He has spent fifty years at the laboratory bench exploring the nature of this disease in an attempt to understand and control it. In this volume, based almost exclusively on experiments conducted over the past twenty years at the University of Chicago, is both the record of Huggins's own research and, in Huggins's words, "a do-it-yourself guide for cancer research workers." Written simply and clearly so that the experiments can be easily reproduced, the book presents Huggins's experiments in the induction of breast cancer and leukemia in rodents. It also describes the methods he discovered to prevent cancer and to cure many of the cancers he has been able to induce. Although most of the material concerns breast cancer and leukemia, research on other kinds of tumors is also described.




How Tobacco Smoke Causes Disease


Book Description

This report considers the biological and behavioral mechanisms that may underlie the pathogenicity of tobacco smoke. Many Surgeon General's reports have considered research findings on mechanisms in assessing the biological plausibility of associations observed in epidemiologic studies. Mechanisms of disease are important because they may provide plausibility, which is one of the guideline criteria for assessing evidence on causation. This report specifically reviews the evidence on the potential mechanisms by which smoking causes diseases and considers whether a mechanism is likely to be operative in the production of human disease by tobacco smoke. This evidence is relevant to understanding how smoking causes disease, to identifying those who may be particularly susceptible, and to assessing the potential risks of tobacco products.




RUNX Proteins in Development and Cancer


Book Description

This volume provides the reader with an overview of the diverse functions of the RUNX family of genes. As highlighted in the introduction and several of the 29 chapters, humans and other mammals have three RUNX genes that are known to play specific roles in blood, bone and neuronal development. However, their evolutionary history has recently been traced back to unicellular organisms and their involvement in many well-known signaling pathways (Wnt, TGFb, Notch, Hippo) is indicative of a more general function in cell biology. Their documented roles in cell fate decisions include control of proliferation, differentiation, survival, senescence and autophagy. The pleiotropic effects of RUNX in development are mirrored in cancer, where RUNX genes can function as oncogenes that collaborate strongly with Myc family oncogenes or as tumour suppressor genes. In the latter role, they display hallmarks of both ‘gatekeepers’ that modulate p53 responses and ‘caretakers’ that protect the genome from DNA damage. Several chapters focus on the importance of these genes in leukemia research, where RUNX1 and CBFB are frequently affected by chromosomal translocations that generate fusion oncoproteins, while recent studies suggest wider roles for RUNX modulation in solid cancers. Moreover, RUNX genes are intimately involved in the development and regulation of the immune system, while emerging evidence suggests a role in innate immunity to infectious agents, including HIV. At the biochemical level, the RUNX family can serve as activators or repressors of transcription and as stable mediators of epigenetic memory through mitosis. Not surprisingly, RUNX activity is controlled at multiple levels, this includes miRNAs and a plethora of post-translational modifications. Several chapters highlight the interplay between the three mammalian RUNX genes, where cross-talk and partial functional redundancies are evident. Finally, structural analysis of the RUNX/CBFB interaction has led to the development of small molecule inhibitors that provide exciting new tools to decipher the roles of RUNX in development and as targets for therapy. This volume provides a compendium and reference source that will be of broad interest to cancer researchers, developmental biologists and immunologists.