Telomeres and telomere dynamics: relevance to cancers of the GI tract

Aberrations in telomere length and telomere maintenance contribute to cancer development. In this article, we review the basic principles of telomere length in normal and tumor tissue and the presence of the two main telomere maintenance pathways as they pertain to gastrointestinal tract cancer. Peripheral blood telomeres are shorter in patients with many types of gastrointestinal tract cancers. Telomere length in tumor DNA also appears to shorten early in cancer development. Tumor telomere shortening is often accompanied by telomerase activation to protect genetically damaged DNA from normal cell senescence or apoptosis, allowing immortalized but damaged DNA to persist. Alternative lengthening of telomeres is another mechanism used by cancer to maintain telomere length in cancer cells. Telomerase and alternative lengthening of telomeres activators and inhibitors may become important chemopreventive or chemotherapeutic agents as our understanding of telomere biology, specific telomere-related phenotypes and its relationship to carcinogenesis increases.     

Recent advances in subtyping tumors of the central nervous system using molecular data

Introduction: Primary brain tumors account for substantial morbidity and mortality. They often infiltrate the brain diffusely, continue growing, and cause adverse events, such as headaches, seizures, and neurological deficits. The classification of primary brain tumors, based for decades on histology, has been fundamentally changed by the World Health Organization in 2016 by incorporation of molecular data.

Areas covered: Literature from glioblastomas, high- and low-grade astrocytic, oligodendroglial, glioneuronal and ependymal tumors from the last five years were reviewed. Results from comprehensive molecular profiling of neoplasms and impact of recent molecular subtyping on neuropathological diagnosis are presented.

Expert commentary: The identification of frequent acquired mutations shows that adult and pediatric glioblastomas have divergent biology with differing prognoses. Astrocytoma and oligodendroglioma are more closely related than previously thought. Molecular profiling now enables the precise classification of most diffuse gliomas into three clinically and therapeutically different subtypes according to the presence or absence of IDH mutation and 1p/19q codeletion. New subgroups with different clinical outcomes and anatomic locations have emerged in ependymomas and pediatric embryonal tumors.