Solid malignancies continue represent the leading malignancies and causes of tumor-related deaths worldwide. Both impaired DNA repair mechanisms and disrupted telomere length homeostasis are key culprits in cancer initiation, progression and prognosis. Altered DNA repair predisposes the accumulation of mutations in the genome and genomic instability. DNA repair also determines the response to the majority of chemotherapeutics in cancer treatment and its utilization opens an individual approach to patients. Telomere attrition resulting in replicative senescence, simultaneously by-passing cell cycle checkpoints, is a hallmark of malignant transformation of the cell. Telomerase is almost ubiquitous in advanced solid cancers and its expression is fundamental to cell immortalization. Therefore, there is a persistent effort to develop therapeutics, which are telomerase-specific and gentle to non-malignant tissues. We would like to address the crosstalk between DNA repair system and telomere length homeostasis in relation to solid cancers and the mechanisms underlying above biological traits.
This Research Topic would like to address the crosstalk between DNA repair system and telomere length homeostasis in relation to solid cancers. The issue should emphasize the insight into the mechanisms underlying above biological traits. Further, an excursion into the possibility to determine DNA damage/DNA repair in telomeric DNA regions will be undertaken.
The role of DNA damage/DNA repair and altered telomere homeostasis in the solid cancer onset.
DNA damage, DNA repair and telomere homeostasis as a possible determinant of tumor heterogeneity.
The crosstalk between DNA repair system and telomere length homeostasis in relation to solid cancers and the mechanisms underlying above biological traits.
DNA damage, DNA repair and telomere homeostasis in the context of tumor microenvironment.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Solid malignancies continue represent the leading malignancies and causes of tumor-related deaths worldwide. Both impaired DNA repair mechanisms and disrupted telomere length homeostasis are key culprits in cancer initiation, progression and prognosis. Altered DNA repair predisposes the accumulation of mutations in the genome and genomic instability. DNA repair also determines the response to the majority of chemotherapeutics in cancer treatment and its utilization opens an individual approach to patients. Telomere attrition resulting in replicative senescence, simultaneously by-passing cell cycle checkpoints, is a hallmark of malignant transformation of the cell. Telomerase is almost ubiquitous in advanced solid cancers and its expression is fundamental to cell immortalization. Therefore, there is a persistent effort to develop therapeutics, which are telomerase-specific and gentle to non-malignant tissues. We would like to address the crosstalk between DNA repair system and telomere length homeostasis in relation to solid cancers and the mechanisms underlying above biological traits.
This Research Topic would like to address the crosstalk between DNA repair system and telomere length homeostasis in relation to solid cancers. The issue should emphasize the insight into the mechanisms underlying above biological traits. Further, an excursion into the possibility to determine DNA damage/DNA repair in telomeric DNA regions will be undertaken.
The role of DNA damage/DNA repair and altered telomere homeostasis in the solid cancer onset.
DNA damage, DNA repair and telomere homeostasis as a possible determinant of tumor heterogeneity.
The crosstalk between DNA repair system and telomere length homeostasis in relation to solid cancers and the mechanisms underlying above biological traits.
DNA damage, DNA repair and telomere homeostasis in the context of tumor microenvironment.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
