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Bioinformatics can be loosely defined as the collection, classification, storage, and analysis of biochemical and biological information using computers and mathematical algorithms. Bioinformatics represents a marriage of biology, medicine, computer science, physics, and mathematics, fields of study that have historically existed as mutually exclusive disciplines. Bioinformatics in Cancer and Cancer Therapy, edited by Gavin Gordon, provides an historical and technical perspective on the analytical techniques, methodologies, and platforms used in bioinformatics experiments in order to show how a bioinformatics approach has been used to characterize various cancer-related processes, and to demonstrate how a bioinformatics approach is being used to bridge basic science and the clinical arena to positively impact patient care and management.

Previous work in the anthropology of cancer often examined causes, risks, and medical, familial, and embodied relationships created by the disease. Recent writing has expanded that focus, attending to cancer as a "total social fact" ( Jain 2013 ) and dissecting the landscape of "carcinogenic relationships" ( Livingston 2012 ). Cancer-driven relationships become subjectively real through individual suffering, stigma, and inequality. This article traces concepts developed from a primarily US-centered discourse to a global cancer discourse, including cancer-related issues continuing to raise concern such as stigma, narrative moments of critical reflection on the dominance of biomedicine, and processes by which individuals and communities manage inadequate access to biomedical technologies. Beyond the medical relations and politics of cancer, this article considers the ways in which ethnography addresses local moral worlds and differences that come to matter in attending to the disease, the person, and consequent social and material relations.

Offers insight into the understanding of the management of pancreatic cancer and examines findings in cancer research. This book provides answers to questions of how to know when cancer is resectable, how to proceed when the diagnosis comes too late for a curative approach, and how to assess different study results.

Previous work in the anthropology of cancer often examined causes, risks, and medical, familial, and embodied relationships created by the disease. Recent writing has expanded that focus, attending to cancer as a "total social fact" ( Jain 2013 ) and dissecting the landscape of "carcinogenic relationships" ( Livingston 2012 ). Cancer-driven relationships become subjectively real through individual suffering, stigma, and inequality. This article traces concepts developed from a primarily US-centered discourse to a global cancer discourse, including cancer-related issues continuing to raise concern such as stigma, narrative moments of critical reflection on the dominance of biomedicine, and processes by which individuals and communities manage inadequate access to biomedical technologies. Beyond the medical relations and politics of cancer, this article considers the ways in which ethnography addresses local moral worlds and differences that come to matter in attending to the disease, the person, and consequent social and material relations.

Being a complex disease that affects millions of people world over, cancer research has assumed great significance. Translational cancer research transforms scientific discoveries in the laboratory or population studies into clinical application to reduce incidence of cancer , morbidity and mortality. It is becoming increasingly evident that cancer is a preventable disease. The IVth International Symposium on Translational Cancer Research held in Udaipur, India in December 2011, discussed various aspects of the biological processes in cancer cells and approaches to cancer prevention. A few con

"Cancer research is at a crossroads. Traditionally, cancer has been thought of as a disease of gene mutation, where the stepwise accumulation of cancer gene mutations is the key, and the identification of common gene mutations has been considered to be essential for diagnosis and treatment. Despite extensive research efforts and accumulated knowledge on cancer genes and pathways, the clinical benefits of this traditional approach have been limited. Recently, cancer genome sequencing has revealed an extensive amount of genetic heterogeneity where the long-expected common mutation drivers have been difficult, if not impossible, to identify. These realities ultimately challenge the conceptual framework of current cancer biology. This book introduces a new concept of genome theory of cancer evolution, in an attempt to unify the field. Many important and representative, but often confusing, questions and paradoxes are critically analyzed. By comparing gene- and genome-based theories, the hidden flaws of many popular viewpoints are addressed. This discussion is intended to initiate a much-needed critical re-evaluation of current cancer research."--

Background: Second primary cancers (SPCs) are increasing, which may negatively influence patient survival. Gastric cancer (GC) has poor survival and when it is diagnosed as SPC it is often the cause of death. We wanted to analyze the risk of SPCs after GC and the risk of GC as SPC after any cancer. Such bidirectional analysis is important in relation to fatal cancers because SPCs may be under-reported in the short-term survival period. Methods: Cancers were obtained from the Swedish Cancer Registry from years 1990 through 2015. Standardized incidence ratios (SIRs) were used to estimate bidirectional relative. Results: We identified 23,137 GC patients who developed 1042 SPCs (4.5%); 2158 patients had GC as SPC. While the risk for three SPCs was increased after GC, seven first primary cancers were followed by an increased risk of GC as SPC, including esophageal, colorectal, bladder, squamous cell skin and breast cancers and non-Hodgkin lymphoma. Breast cancer, which was followed by a diagnosis of second GC, showed an excess of lobular histology. Conclusion: Multiple primary cancers in the same individuals may signal genetic predisposition. Accordingly, the association of GC with breast cancer may be related to mutations in the CDH1 gene, and clustering of colorectal, small intestinal and bladder cancers could be related to Lynch syndrome. The third line of findings supports a contribution of immune dysfunction on the increased risk of GC as SPC after skin cancer and non-Hodgkin lymphoma. Early detection of GC in the risk groups could save lives. ; Supported by the European Union's Horizon 2020 research and innovation programme, grant No 856620 (Chaperon), the Swedish Research Council, the Swedish Research Council, Jane and Aatos Erkko Foundation, Sigrid Juselius Foundation, Finnish Cancer Organizations, University of Helsinki, Helsinki University Central Hospital, Novo Nordisk Foundation, Päivikki and Sakari Sohlberg Foundation.

Familial clustering, twin concordance, and identification of high- and low-penetrance cancer predisposition variants support the idea that there are families that are at a high to moderate excess risk of cancer. To what extent there may be families that are protected from cancer is unknown. We wanted to test genetically whether cancer-free families share fewer breast, colorectal, and prostate cancer risk alleles than the population at large. We addressed this question by whole-genome sequencing (WGS) of 51 elderly cancer-free individuals whose numerous (ca. 1000) family members were found to be cancer-free ('cancer-free families', CFFs) based on face-to-face interviews. The average coverage of the 51 samples in the WGS was 42x. We compared cancer risk allele frequencies in cancer-free individuals with those in the general population available in public databases. The CFF members had fewer loss-of-function variants in suggested cancer predisposition genes compared to the ExAC data, and for high-risk cancer predisposition genes, no pathogenic variants were found in CFFs. For common low-penetrance breast, colorectal, and prostate cancer risk alleles, the results were not conclusive. The results suggest that, in line with twin and family studies, random environmental causes are so dominant that a clear demarcation of cancer-free populations using genetic data may not be feasible. ; The study was supported by the European Union's Horizon 2020 research and innovation programme, No 856620. A.H. was supported by Jane and Aatos Erkko Foundation,HUCHResearch Funds (VTR), Sigrid Juselius Foundation, Finnish Cancer Organizations, University of Helsinki, Novo Nordisk Foundation, Päivikki and Sakari Sohlberg Foundation, The Finnish Society of Sciences and Letters. All authors have read and agreed to the published version of the manuscript.

Eleven essays by historians and sociologists examine cancer research and treatment as everyday practice in post-war Europe and North America. These are not stories of inevitable medical progress and obstacles overcome, but of historical contingencies, cultural differences, hope, and often disappointed expectations

Cancer is a complex disease process that spans multiple scales in space and time. Driven by cutting-edge mathematical and computational techniques, in silicobiology provides powerful tools to investigate the mechanistic relationships of genes, cells, and tissues. It enables the creation of experimentally testable hypotheses, the integration of data across scales, and the prediction of tumor progression and treatment outcome (in silicooncology). Drawing on an interdisciplinary group of distinguished international experts, Multiscale Cancer Modelingdiscusses the scientific and technical expertis

Lifestyle factors, including diet, have long been recognised as potentially important determinants of cancer risk. In addition to the significant role diet plays in affecting body fatness, a risk factor for several cancers, experimental studies have indicated that diet may influence the cancer process in several ways. Prospective studies have shown that dietary patterns characterised by higher intakes of fruits, vegetables, and whole-grain foods, and lower intakes of red and processed meats and salt, are related to reduced risks of death and cancer, and that a healthy diet can improve overall survival after diagnosis of breast and colorectal cancers. There is evidence that high intakes of fruit and vegetables may reduce the risk of cancers of the aerodigestive tract, and the evidence that dietary fibre protects against colorectal cancer is convincing. Red and processed meats increase the risk of colorectal cancer. Diets rich in high-calorie foods, such as fatty and sugary foods, may lead to increased calorie intake, thereby promoting obesity and leading to an increased risk of cancer. There is some evidence that sugary drinks are related to an increased risk of pancreatic cancer. Taking this evidence into account, the 4th edition of the European Code against Cancer recommends that people have a healthy diet to reduce their risk of cancer: they should eat plenty of whole grains, pulses, vegetables and fruits; limit high-calorie foods (foods high in sugar or fat); avoid sugary drinks and processed meat; and limit red meat and foods high in salt.

The management of patients with breast cancer has been changing over the last few years and this article highlights some areas of particular interest. The changes have been brought about against a background of an increasing disease incidence coupled with increasing political aspirations from patients and their relatives. This paper focuses on organisational aspects of breast cancer care, screening, induction and high-dose chemotherapy, clinical trials, genetics, training of surgical and nonsurgical oncologists and future prospects.