Telomere Shortening and Ageing -- Cellular versus Organismal Aging -- Telomere-Induced Senescence of Primary Cells -- Telomeres, Senescence, Oxidative Stress, and Heterogeneity -- Initiation of Genomic Instability, Cellular Senescence, and Organismal Aging by Dysfunctional Telomeres -- Telomerase Mutations and Premature Ageing in Humans -- Telomerase, Telomeres, and Stem Cell Aging -- Mechanisms of Stem Cell Ageing -- Senescence Signatures of Human Hematopoietic Stem Cells -- Telomere Shortening Induces Cell Intrinsic Checkpoints and Environmental Alterations Limiting Adult Stem Cell Function -- p16INK4a and Stem Cell Ageing: A Telomere-Independent Process? -- Telomerase as a Potential Regulator of Tissue Progenitor Cells -- Telomeres, DNA Damage and Cancer -- Telomere Shortening and Telomerase Activation during Cancer Formation -- Telomere Binding Proteins and Disease -- Therapeutic Targets -- Targeting Telomerase: Therapeutic Options for Cancer Treatment -- Werner Syndrome, Telomeres, and Stress Signaling: Implications for Future Therapies?. The understanding of the molecular mechanisms underlying the ageing process is essential to improve quality of life and 'health span' in the growing populations of the elderly. Telomere shortening represents one of the basic aspects of ageing and telomere dysfunction could contribute to the accumulation of DNA damage during ageing. This book summarizes experimental evidence and clinical data indicating that telomere dysfunction influences human ageing, diseases and cancer. In addition, the book describes our current knowledge on checkpoints that limit cellular lifespan (senescence) and survival (apoptosis, crisis) in response to telomere dysfunction. A special focus of the book is on adult stem cells. There is emerging evidence that adult stem cell ageing impairs organismal fitness and survival and contributes to cancer formation (cancer stem cells). The book summarizes basic mechanisms of adult stem cell ageing. Moreover, the authors describe evidence that telomere dysfunction impairs stem cell function by inducing cell intrinsic checkpoints as well as environmental alterations. All of these subjects are of great interest for ageing researchers, physicians and students and should provide a rational basis for beginning to identify molecular targets for novel therapies that aim to improve quality of life during ageing.