By Christopher R. Cogle (auth.), Alison L. Allan (eds.)
The “cancer stem mobilephone” speculation postulates that melanoma arises from a subpopulation of tumor-initiating cells or melanoma stem cells (CSCs). whereas the belief of melanoma stem cells has been round for greater than 100 years, facts from the fields of hematology and melanoma biology has now verified the serious function of stem cells in hematological malignancies and recommended that those related mechanisms also are important to the initiation, development, and remedy of reliable cancers. medical and experimental experiences have proven that CSCs convey many classical homes of ordinary stem cells, together with a excessive self-renewal ability and the power to generate heterogeneous lineages; the requirement for a selected “niche”/microenvironment to develop; and an elevated means for self-protection opposed to harsh environments, pollutants, and medicine.
Cancer Stem Cells in sturdy Tumors represents a close evaluate of melanoma stem cells and their position in good cancers. produced from 24 chapters, this quantity will offer readers with a finished knowing of this significant and evolving field.
Topics coated include:
- Introduction of the CSC hypothesis
- Historical views and the contributing classes from leukemia
- Current wisdom in regards to the id and function of CSCs in numerous varieties of reliable melanoma together with breast, mind, colorectal, pancreatic, prostate, cancer, lung, ovarian, hepatocellular, and head and neck melanoma
- Molecular pathways focused on using CSC functionality, with a specific concentrate on the unconventional convergence of embryonic and tumorigenic signaling pathways
- In vitro and in vivo assays, version platforms, and imaging modalities for learning CSCs
- The medical significance of CSCs for melanoma administration and therapy, together with very important implications for diagnosis, prediction, and remedy resistance
- Consideration of the debate surrounding the CSC speculation and demanding unanswered questions during this field
This collective paintings was once written through a gaggle of trendy foreign specialists in melanoma biology, oncology, and/or stem phone biology. it is going to function a invaluable source for verified researchers, professors, overall healthiness care execs, and scholars within the clinical and clinical neighborhood who're investigating stem cells and/or oncology.
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Additional info for Cancer Stem Cells in Solid Tumors
Afify A, Purnell P, Nguyen L (2009) Role of cd44s and cd44v6 on human breast cancer cell adhesion, migration, and invasion. Exp Mol Pathol 86 (2):95–100. 003 53. Jothy S (2003) Cd44 and its partners in metastasis. Clin Exp Metastasis 20 (3):195–201 54. Zen K, Liu DQ, Guo YL, Wang C, Shan J, Fang M, Zhang CY, Liu Y (2008) Cd44v4 is a major e-selectin ligand that mediates breast cancer cell transendothelial migration. PloS one 3 (3):e1826. E. L. Allan 55. Lopez JI, Camenisch TD, Stevens MV, Sands BJ, McDonald J, Schroeder JA (2005) Cd44 attenuates metastatic invasion during breast cancer progression.
Most recently, Meyer et al.  isolated a tumorigenic subset of CD44+ cells from ER-negative breast cancers and found that CD49fhiCD133/2hi cells exhibited 2 Cancer Stem Cells in Breast Cancer 25 xenograft-initiating capability, whereas the CD49fneg/lowCD133/2neg/low population did not. They noted that while this new population enriched for xenograft initiation in mouse mammary fat pads, capability varied between their samples. Additionally, other markers established as CSC markers for other cancers, such as CD133 (a marker for colon and brain cancer initiating cells [76, 77]), may be good candidates for further refining the breast CSC phenotype.
Adding additional variability, the types of glycosylation may vary from isoform to isoform, using side chains such as heparin sulfate and chondroitin sulfate, resulting not only in variations of molecular weight but also in differentially charged environments that affect CD44 function . The human CD44 gene consists of 19 exons, the first 5 of which are constant . The middle 9 exons (v2–v10) are variable regions which may be removed depending on the variant expressed. The next three exons (16–18) are constant, and the last two exons (19 and 20) are variable.