{"id":1090,"date":"2026-05-09T04:02:14","date_gmt":"2026-05-09T04:02:14","guid":{"rendered":"https:\/\/cetaitdemain.org\/?p=1090"},"modified":"2026-05-09T04:02:14","modified_gmt":"2026-05-09T04:02:14","slug":"aleman-and-colleagues-observed-a-three-to-five-fold-higher-incidence-of-cvds-in-patients-treated-previously-for-hodgkins-lymphoma-and-followed-for-a-median-of-18years-6","status":"publish","type":"post","link":"https:\/\/cetaitdemain.org\/?p=1090","title":{"rendered":"\ufeffAleman and colleagues observed a three to five-fold higher incidence of CVDs in patients treated previously for Hodgkins lymphoma and followed for a median of 18years [6]"},"content":{"rendered":"

\ufeffAleman and colleagues observed a three to five-fold higher incidence of CVDs in patients treated previously for Hodgkins lymphoma and followed for a median of 18years [6]. in these tissues. Keywords:Radiotherapy, Acute radiation toxicity, Endothelial cell, Microvasculature, Radioprotection, Cell death, Inflammation, Senescence == Introduction == Despite technology-driven improvements in cancer radiotherapy (RT), normal tissue radiation toxicities remain a significant clinical concern [1]. They can influence treatment outcomes, patient quality of life and survivorship. For example, early skin toxicities which develop within the first few weeks of RT commencement tend to be transient. Nonetheless, approximately 30% of breast cancer patients and 60% of head and neck cancer patients treated with RT develop painful, infection-prone severe epithelial barrier breakdown (desquamation) [2,3]. This can complicate tissue reconstruction efforts [4] or necessitate treatment interruptions, which have been found to compromise tumour control or cure [5]. Furthermore, late radiation toxicity occurs months to years following RT, and can result in permanently debilitating organ dysfunction such as cardiovascular diseases (CVDs) [6]. The three categories of radiation protectors include radioprotectants, radiomitigators and therapeutics. These are administered either before radiation exposure, after radiation exposure but before damage manifestation, or after damage manifestation, respectively. In the clinic, acute toxicities such as desquamation are managed non-specifically with mitigative or therapeutic strategies. Medicated ointments and dressings are in use with conflicting or minimal evidence and they do not prevent the manifestation of the problematic damage that impedes patient wellbeing [7]. On the other hand, directly minimizing the biological determinants of the damage is an approach to preventing these impediments. Amifostine is the only targeted radioprotectant with enough clinical evidence to support its use. However, it has practical limitations and a significant toxicity profile [8]. Several biological mechanisms of normal tissue radiation protection are well explored at the preclinical level, but the endothelial cell (EC) compartment is now also emerging as an attractive target for radiation protection. We argue that protecting microvascular endothelial cells from radiation-induced perturbations, or disruptions to the normal homeostatic or angiogenic (Z)-2-decenoic acid state, ultimately protects the normal tissue from radiation damage. These perturbations (Z)-2-decenoic acid include EC death, vascular inflammation (hemodynamic and molecular changes) and loss of functional capacity. == Review == == General mechanisms of radiation protection == General mechanisms of radiation protection include the use of antioxidants, modulation of cell death, inflammation suppression and promotion of wound Rabbit Polyclonal to BL-CAM (phospho-Tyr807)<\/a> healing. These have recently been thoroughly reviewed [9]. Nevertheless, notable examples of (Z)-2-decenoic acid<\/a> targeted agents under preclinical and clinical investigation are discussed while outlining the general process of ionizing radiation (IR)-induced damage. A direct radioprotectant reduces the amount of cellular DNA damage so that a cell can remain healthy and functional. The most well-studied radioprotectant, amifostine, contains a free radical-scavenging sulfhydryl group [10], competes with oxygen to reduce permanent DNA damage fixation and increases expression of an endogenous detoxifying enzyme manganese superoxide dismutase [11], thereby reducing double stranded break accumulation [12,13] and genomic instability [14]. Initially, amifostine was particularly promising for improving the therapeutic ratio of cancer RT due to its preferential accumulation in normal tissue rather than cancerous tissue. Even still, concerns with toxic side-effects and potential cancer recurrence discourage the implementation of this class of radioprotectants during cancer RT [15]. If the IR-induced DNA damage cannot be repaired, the cell (Z)-2-decenoic acid will proceed with clonogenic or reproductive death that can include programmed cell death (apoptosis), mitotic catastrophe or senescence, leading to cellular hypoplasia and the observed symptoms of clinical radiotoxicity. Pifithrin-, an inhibitor of the p53-mediated apoptotic pathway that is activated by DNA damage and genotoxic stress, reduces mortality of mice after total body irradiation (TBI) [16]. (Z)-2-decenoic acid There is concern that preventing normal cells that harbor relevant DNA damage from dying will increase the likelihood of their malignant transformation. After radiation exposure, the master.<\/p>\n","protected":false},"excerpt":{"rendered":"

\ufeffAleman and colleagues observed a three to five-fold higher incidence of CVDs in patients treated previously for Hodgkins lymphoma and followed for a median of 18years [6]. in these tissues. Keywords:Radiotherapy, Acute radiation toxicity, Endothelial cell, Microvasculature, Radioprotection, Cell death, Inflammation, Senescence == Introduction == Despite technology-driven improvements in cancer radiotherapy (RT), normal tissue radiation …<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[38],"tags":[],"class_list":["post-1090","post","type-post","status-publish","format-standard","hentry","category-p60c-src","entry entry-center"],"_links":{"self":[{"href":"https:\/\/cetaitdemain.org\/index.php?rest_route=\/wp\/v2\/posts\/1090","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/cetaitdemain.org\/index.php?rest_route=\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/cetaitdemain.org\/index.php?rest_route=\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/cetaitdemain.org\/index.php?rest_route=\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/cetaitdemain.org\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=1090"}],"version-history":[{"count":1,"href":"https:\/\/cetaitdemain.org\/index.php?rest_route=\/wp\/v2\/posts\/1090\/revisions"}],"predecessor-version":[{"id":1091,"href":"https:\/\/cetaitdemain.org\/index.php?rest_route=\/wp\/v2\/posts\/1090\/revisions\/1091"}],"wp:attachment":[{"href":"https:\/\/cetaitdemain.org\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=1090"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/cetaitdemain.org\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=1090"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/cetaitdemain.org\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=1090"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}