By David H. Nguyen
This intriguing SpringerBrief offers facts for brand spanking new principles that would problem numerous theories of the way melanoma biology is known. melanoma biology has gone through numerous highbrow revolutions long ago 50 years. A mutation-centric view of melanoma has given solution to the tumor microenvironment view. Reductionistic reports of 1 gene at a time have given option to platforms biology methods that study the total genome (omics) while. even though, this article combines the advanced degrees learning melanoma on the molecular biology point, endocrinology point, and transcriptomics point. What researchers are actually understanding is that there's a have to mix omics with body structure options with the intention to greater comprehend melanoma and this e-book will supply perception to the merging of those fields in an effort to outline how melanoma is studied within the future.
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Additional info for Systems Biology of Tumor Physiology: Rethinking the Past, Defining the Future
During mammalian embryonic development, a process called gastrulation occurs after which the three main germ layers are formed: endoderm, mesoderm, and ectoderm. Cells in these germ layer lineages are called pluripotent, meaning they can become multiple differentiated cell types that are derived from the same germ layer. For example, nerve cells, skins cells, and breast cells are all derived from the ectoderm. A bipotent progenitor cell is one that can only become one of two differentiated cell types within the same germ layer lineage.
Et al. (2013). In vitro expansion of single Lgr5+ liver stem cells induced by Wnt-driven regeneration. Nature, 494, 247–250. , et al. (2014). Sequencing of breast cancer stem cell populations indicates a dynamic conversion between differentiation states in vivo. Breast Cancer Research, 16, R72. , Laberge, G. , et al. (2013). A melanoma brain metastasis with a donor-patient hybrid genome following bone marrow transplantation: First evidence for fusion in human cancer. PLoS One, 8, e66731. Melo, S.
This is not to say that a study that only tested one mouse strain is poorly designed, since testing multiple mouse strains in one publication is often ﬁnancially unfeasible for one laboratory. Furthermore, 38 3 Using Mouse Models and Making Sense of Them without a clear phenotype from a susceptible inbred strain, it would be difﬁcult to identify a cellular or molecular mechanism that is responsible for that phenotype and that might translate to a treatment for the human disease that is being modeled.