Abstract: In terrestrial vertebrates, bone tissue constitutes the ‘osteoimmune’ system, which functions as a locomotor organ and a mineral reservoir as well as a primary lymphoid organ where haematopoietic stem cells are maintained. Bone and mineral metabolism is maintained by the balanced action of bone cells such as osteoclasts, osteoblasts and osteocytes, yet subverted by aberrant and/or prolonged immune responses under pathological conditions. However, osteoimmune interactions are not restricted to the unidirectional effect of the immune system on bone metabolism. In recent years, we have witnessed the discovery of effects of bone cells on immune regulation, including the function of osteoprogenitor cells in haematopoietic stem cell regulation and osteoblast-mediated suppression of haematopoietic malignancies. Moreover, the dynamic reciprocal interactions between bone and malignancies in remote organs have attracted attention, extending the horizon of osteoimmunology. Here, we discuss emerging concepts in the osteoimmune dialogue in health and disease.
A major new open access paper in today’s Nature describes the evolutionary history of somatic mutations that result in cancer. It confirms the primary role of driver mutations and that these often occur early in development, just as Steve Frank predicted in his 2007 book Dynamics of Cancer. Later mutations are much more likely to be divergent.
Abstract: Cancer develops through a process of somatic evolution1,2. Sequencing data from a single biopsy represent a snapshot of this process that can reveal the timing of specific genomic aberrations and the changing influence of mutational processes3. Here, by whole-genome sequencing analysis of 2,658 cancers as part of the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA)4, we reconstruct the life history and evolution of mutational processes and driver mutation sequences of 38 types of cancer. Early oncogenesis is characterized by mutations in a constrained set of driver genes, and specific copy number gains, such as trisomy 7 in glioblastoma and isochromosome 17q in medulloblastoma. The mutational spectrum changes significantly throughout tumour evolution in 40% of samples. A nearly fourfold diversification of driver genes and increased genomic instability are features of later stages. Copy number alterations often occur in mitotic crises, and lead to simultaneous gains of chromosomal segments. Timing analyses suggest that driver mutations often precede diagnosis by many years, if not decades. Together, these results determine the evolutionary trajectories of cancer, and highlight opportunities for early cancer detection.
June 1: Last day to cancel registration and get a refund
June 30: Late registration begins, final program posted.
July 15, 2020: Welcome reception in the evening, pre-meeting activities during that day will include a pre-conference workshop on “The Evolution of Emerging Viruses”
July 15-18: The 6th Annual Meeting of the International Society for Evolution, Medicine, and Public Health
About the 2020 Annual Meeting
The Sixth Annual Meeting of the International Society for Evolution, Medicine, and Public Health will be in Athens, Georgia, from July 15-18, 2020. ISEMPH 2020 will gather delegates from around the world. It follows in the footsteps of successful previous meetings in Tempe, Arizona; Durham, North Carolina; Groningen, The Netherlands; Park City, Utah; and Zurich, Switzerland. ISEMPH 2020 is profoundly interdisciplinary and emphasizes the multiple interfaces between evolutionary biology and human health in the complementary fields of medicine, evolutionary biology, anthropology, evolutionary psychology, behavioral ecology and epidemiology. The meetings welcome students and clinicians at all stages of professional development.
The 2020 program will include plenary sessions led by some of the world’s leading evolutionary medicine experts including:
Kevin Keel, DVM, PhD, Associate Professor of Pathology, Microbiology & Immunology at the UC Davis School of Veterinary Medicine.
Sudhir Kumar, PhD, the Laurel H. Carnell Professor and Director of the Institute of Genomics and Evolutionary Medicine at Temple University, who will speak on how “Evolution Informs Genomic Medicine.”
Paul Turner, PhD, the Rachel Carson Professor of Ecology and Evolutionary Biology at Yale University School of Medicine, who will speak about “Leveraging Evolutionary Trade-Offs and Phage Selection Pressure to Reduce Bacterial Pathogenicity.”
Abstract: Global exposures to air pollution and cigarette smoke are novel in human evolutionary history and are associated with at least 12 million premature deaths per year. We investigate the history of the human exposome for relationships between novel environmental toxins and genetic changes during human evolution in six phases. Phase I: With increased walking on savannas, early human ancestors inhaled crustal dust, fecal aerosols, and spores; carrion scavenging introduced new infectious pathogens. Phase II: Domestic fire exposed early Homo to novel toxins from smoke and cooking. Phases III and IV: Neolithic to preindustrial Homo sapiens incurred infectious pathogens from domestic animals and dense communities with limited sanitation. Phase V: Industrialization introduced novel toxins from fossil fuels, industrial chemicals, and tobacco at the same time infectious pathogens were diminishing. Thereby, pathogen-driven causes of mortality were replaced by chronic diseases driven by sterile inflammogens, exogenous and endogenous. Phase VI: Considers future health during global warming with increased air pollution and infections. We hypothesize that adaptation to some ancient toxins persists in genetic variations associated with inflammation and longevity.