The term capillary leak syndrome (CLS) describes the manifestations associated with an increased capillary permeability to proteins leading to an escape of plasma from the blood circulatory system to surrounding tissues, muscle, organs, or body cavities. This results clinically in the typical triad of hypotension, edema, and elevated hematocrit. The more severe cases of CLS may present with cardiovascular collapse, shock, and death. The most classic form of this pathology is represented by the idiopathic systemic CLS (SCLS) also called Clarkson's disease, but capillary leaks are also described as adverse drug reactions foremost among which are anticancer drugs. This review will focus on oncologic drugs such as gemcitabine, therapeutic growth factors or cytokines, and monoclonal antibodies (mAbs) that appear now as the strongest candidates for anticancer drug-induced CLS.
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http://dx.doi.org/10.1016/j.ekir.2022.02.014 | DOI Listing |
NPJ Precis Oncol
January 2025
Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital, 100006, Beijing, China.
Despite advances in various chemotherapy regimens, current therapeutic options are limited for ovarian cancer patients. Oxidative stress-induced growth inhibitor 1 (OSGIN1), which is a tumor suppressor gene known to regulate the cellular stress response and apoptosis, is associated with ovarian cancer development. However, the underlying mechanisms involved in ferroptosis regulation have not been elucidated.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Pharmacology, Kasturba Medical College Mangalore, Manipal Academy of Higher Education, Manipal, Karnataka, India.
Drug-induced eosinophilic pneumonia (EP) is an uncommon adverse drug reaction. Many drugs have been reported to cause EP, the evidence mainly being in the form of case reports/case series. This study aims to conduct an exploratory analysis of the United States Food and Drug Administration adverse event reporting system (FAERS) database to identify previously unknown drugs that can cause EP and supplement the available evidence for known culprit drugs.
View Article and Find Full Text PDFDrug Resist Updat
December 2024
Department of Oncology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200123, China. Electronic address:
PP2C serine-threonine phosphatase Wip1 plays an important role in normal tissue homeostasis, stress signaling and pathogenesis of various human diseases. It is an attractive drug target for cancer treatment and inhibition of its expression or activity constitute a novel therapeutic intervention strategy to prevent the development of various cancers. However, previous strategies for Wip1 suppression may be ineffective in cancers lacking p53.
View Article and Find Full Text PDFPharmaceuticals (Basel)
November 2024
School of Pharmacy, Hangzhou Normal University, Hangzhou 311121, China.
Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) play critical roles in tumorigenesis, cancer progression, and drug resistance. Persistent activation of the ER stress system enhances the survival capacities of malignant tumor cells, including increased proliferation, invasion, and resistance to treatment. Dysregulation of ER function and the resultant stress is a common cellular response to cancer therapies and may lead to cancer cell death.
View Article and Find Full Text PDFAnal Chem
January 2025
School of Chemistry and Chemical Engineering University of Jinan, Jinan 250022, People's Republic of China.
Mitochondrial DNA (mtDNA) damage is a prevalent phenomenon that has been proven to be implicated in a wide spectrum of diseases. However, the progressive attenuation of probe signals in response to mtDNA damage within living cells inherently limits the sensitivity and precision of current probes for detecting mtDNA damage. Herein, we employ an innovative organelle signal ratio imaging approach, utilizing the mitochondria-nucleus migration probe MCQ, to achieve unparalleled sensitivity in detecting mtDNA damage in living cells.
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