Publications by authors named "Marco de Vitis"
Article Synopsis
- The study investigates the impact of low-dose iodine-131 therapy on genetic damage in patients, particularly focusing on DNA damage caused by oxidative stress.
- It compares two groups: one prepared with thyroid hormone withdrawal and the other with recombinant human thyroid-stimulating hormone (rhTSH), assessing genetic alterations before and after therapy.
- The findings reveal increased stable chromosome damage in the hormone withdrawal group, correlated with higher radiation retention and oxidative stress, highlighting the potential risks associated with this preparation method.
Alternative lengthening of telomeres (ALT) is a homology-directed repair (HDR) mechanism of telomere elongation that controls proliferation in aggressive cancers. We show that the disruption of RAD51-associated protein 1 (RAD51AP1) in ALT+ cancer cells leads to generational telomere shortening. This is due to RAD51AP1's involvement in RAD51-dependent homologous recombination (HR) and RAD52-POLD3-dependent break induced DNA synthesis.
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- Cancer cells often need to maintain their telomeres to prevent them from becoming too short, with most using telomerase while a minority relies on an alternative method called ALT.
- This study explored how X-ray radiation affects telomere length and damage over 13 days in normal primary fibroblasts and discovered that radiation causes initial telomere shortening followed by a temporary elongation linked to an HR-based repair mechanism.
- Understanding HR-mediated telomere repair in normal cells could enhance our knowledge of the ALT pathway and help develop new treatment strategies for cancers that utilize this mechanism.
Eukaryotic cells undergo continuous telomere shortening as a consequence of multiple rounds of replications. During tumorigenesis, cells have to acquire telomere DNA maintenance mechanisms (TMMs) in order to counteract telomere shortening, to preserve telomeres from DNA damage repair systems and to avoid telomere-mediated senescence and/or apoptosis. For this reason, telomere maintenance is an essential step in cancer progression.
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