Over two decades from the first publication of the Hallmarks of Cancer, proposed in the millennium by Douglas Hanahan and Robert Weinberg, the landscape of cancer research has changed significantly. In 2010, a total of ten hallmarks (six established and four emerging) were solidified to provide a set of criteria to describe how normal, healthy cells can eventually transform to malignant tumors through a successive number of emerging characteristics.
Over time, the field has accepted that tumors are comprised of a plethora of heterogenic cell types, interacting and communicating to build resistance against therapies, innate defense mechanisms and drive proliferation. Furthermore, it is more thoroughly understood how exactly the tumor microenvironment influences disease progression and clinical outcomes, something the more recent hallmarks contribute significantly to. By understanding such processes and integrating the interactions they form with novel therapeutics, we can develop a deeper understanding of how mutagenic cells form and survive.
At Frontiers, we would like to commemorate the incredible research and advancements made surrounding these principles over the last decade by introducing this special series hosted by Frontiers in Oncology. By collecting pioneering research focusing on these principles, we hope to allow for Open Access platforms to drive the next decade of change and technological growth within the oncology field.
With this initiative, we aim to focus on the many aspects involved in cancer diagnosis and treatment and build on our understanding of how they all fit together in the context of the Hallmarks of Cancer. Furthermore, we wish to explore recent research in the emerging hallmarks, while simultaneously horizon scanning and looking to the future of where this might take us.
Hallmark of Cancer: Replicative Immortality
Under normal conditions, healthy cells are limited in their replicative ability by a concept know as the Hayflick Limit. This is the mechanism behind cellular aging that allows cells to replicate and divide roughly forty to sixty times before cell senescence or programmed cell death. This is to prevent older cells who are at an increased risk of mutagenesis from continuing to divide. However, in cancer, malignant cells develop the capacity to bypass this limit and continue replicating indefinitely. Central to this process are the protective caps on chromosomes known as telomeres and the enzyme telomerase. In tumors, telomeres are constantly extended by telomerase to increase cellular lifespan, prevent senescence and drive proliferation.
This Research Topic welcomes high-quality Original Research, Review, and Perspective articles focusing on the role replicative immortality plays in cancer. From causes and roles to present and future targeted therapeutics. We aim to celebrate the advances made within the last ten years and the many to come.
See below for other collections in the Hallmarks series:
Hallmark of Cancer: Avoiding Immune SuppressionHallmark of Cancer: Genomic Instability and MutationsHallmark of Cancer: Resisting Cell DeathHallmark of Cancer: Sustained ProliferativeHallmark of Cancer: Inducing Angiogenesis Hallmark of Cancer: Replicative ImmortalityHallmark of Cancer: Evasion of Growth SuppressorsHallmark of Cancer: Reprogramming of Cellular MetabolismHallmark of Cancer: Activating Invasion and MetastasisHallmark of Cancer: Tumor Promoting InflammationPlease note: manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) will not be accepted in any of the sections of Frontiers in Oncology.
