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Ferroptosis is an iron-dependent form of cell death, which is triggered by disturbed membrane integrity due to an overproduction of lipid peroxides. Induction of ferroptosis comprises several alterations, i.e. altered iron metabolism, response to oxidative stress, or lipid peroxide production. At the physiological level transcription, translation, and microRNAs add to the appearance and/or activity of building blocks that negatively or positively balance ferroptosis. Ferroptosis contributes to tissue damage in the case of, e.g., brain and heart injury but may be desirable to overcome chemotherapy resistance. For a more complete picture, it is crucial to also consider the cellular microenvironment, which during inflammation and in the tumor context is dominated by hypoxia. This graphical review visualizes basic mechanisms of ferroptosis, categorizes general inducers and inhibitors of ferroptosis, and puts a focus on microRNAs, iron homeostasis, and hypoxia as regulatory components.
Clinical outcomes of cancer-associated isolated superficial vein thrombosis in daily practice
(2022)
Highlights
• In acute isolated SVT, the prevalence of cancer is almost 7 %.
• Cancer increases the SVT-associated VTE risk at 3 and 12 months.
• Cancer patients with isolated SVT may benefit from prolonged anticoagulation.
Abstract
Background: Despite significant progress in the understanding of paraneoplastic deep vein thrombosis (DVT) and pulmonary embolism (PE), little is known about the outcomes of cancer-associated superficial vein thrombosis (SVT) in daily practice.
Methods: INSIGHTS-SVT was a prospective observational study on patients with acute isolated SVT. Primary outcome measure was symptomatic venous thromboembolism (VTE), a composite of DVT, PE, and SVT extension/recurrence, at 3 months. Clinically relevant bleeding was also assessed.
Results: Of 1151 patients included, 6.7 % either had active cancer at baseline or were diagnosed with cancer during 12 months of follow-up. At 3 months, symptomatic VTE had occurred in 13.0 % and 5.4 % of cancer and non-cancer patients, respectively (HR 2.6, 95 % CI 1.3–5.0). Regarding secondary outcomes, cancer patients had increased risks of DVT and PE (HR 3.9, 95 % CI 1.3–11.8) and hospitalization due to VTE (HR 11.0, 95 % CI 2.5–49.0). The rate of clinically relevant bleeding was numerically higher in the cancer cohort (3.9 % vs 1.3 %, HR 3.1, 95 % CI 0.9–10.7). At 12 months, the primary composite outcome had occurred in 15.6 % and 11.9 % of cancer and non-cancer patients, respectively (HR 1.9, 95 % CI 1.0–3.5). After adjusting for additional risk factors, including age, history of DVT/PE and cardiovascular risk factors/diseases, the association of cancer with the primary outcome remained statistically significant.
Conclusion: Cancer patients with isolated SVT are at significant risk of symptomatic VTE. While most events occur within 3 months, the VTE risk remains elevated up to one year of follow-up.
ClinicalTrials.gov identifier: NCT02699151.
Radiobiology research in rectal cancer has been limited to cell lines, patient-derived organoids (PDOs), or xenografts. Here, we describe a protocol which recapitulates more efficiently the complex contributions of the tumor microenvironment. This approach establishes a preclinical mouse model of rectal cancer by intrarectal transplantation of genetically modified organoids into immunocompetent mice followed by precise image-guided radiotherapy (IGRT) of organoid-induced tumors. This model represents a useful platform to study the cellular and molecular determinants of therapy resistance in rectal cancer.
The aim of this study was to detect a response difference in primary (PLC) and secondary liver tumors (SLC) with magnetic resonance elastography (MRE) after TACE therapy. Thirty-one patients (25/31 male; mean age 69.6 years [range: 39–85 years]) with repeated TACE therapy of HCC were compared with twenty-seven patients (27/27 female; mean age 61.2 years [range 39–81 years]) with repeated TACE therapy of metastatic liver disease due to breast cancer. Both groups underwent either one (n = 31) or two (n = 27) repetitive magnetic resonance imaging (MRI) and MRE exams in 4- to 6-week intervals using a 1.5-T-scanner. MRE-based liver stiffness and size measurements were evaluated in tumorous lesions and in healthy liver lobe controls. PLC showed a significantly larger tumor size compared to SLC (26.4 cm2 vs. 11 cm2, p = 0.007) and a higher degree of stiffness (5.8 kPa vs. 5.1 kPa, p = 0.04). Both tumors decreased in size during the cycles (PLC: p = 0.8 and SLC: p < 0.0001) and lesions showed an increase in stiffness (PLC: p = 0.002 and SLC: p = 0.006). MRE demonstrates that PLC and SLC have similar responses to TACE therapy. PLC had a greater increase in stiffness and SLC got smaller. An increasing stiffness and decrease in size could show a good response.