Pulmonary nodules may develop following bleomycin therapy, a previously undescribed entity that may simulate metastatic disease. Two asymptomatic patients are reported with nodules that developed following low dose bleomycin treatment for testicular tumors. One patient had previously documented pulmonary metastases that had resolved after chemotherapy. The other patient had nodular-appearing densities on routine chest examination without a history of previous metastatic lung involvement.
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http://dx.doi.org/10.1002/1097-0142(19810901)48:5<1096::aid-cncr2820480508>3.0.co;2-y | DOI Listing |
Respir Res
January 2025
Division of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, School of Medicine and Public Health, University of Wisconsin-Madison, 600 Highland Avenue, Madison, WI, 53792, USA.
Progressive forms of interstitial lung diseases, including idiopathic pulmonary fibrosis (IPF), are deadly disorders lacking non-invasive biomarkers for assessment of early disease activity, which presents a major obstacle in disease management. Excessive extracellular matrix (ECM) deposition is a hallmark of these disorders, with fibronectin being an abundant ECM glycoprotein that is highly upregulated in early fibrosis and serves as a scaffold for the deposition of other matrix proteins. Due to its role in active fibrosis, we are targeting fibronectin as a biomarker of early lung fibrosis disease activity via the PEGylated fibronectin-binding polypeptide (PEG-FUD).
View Article and Find Full Text PDFCommun Biol
January 2025
Department of Respiratory and Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, China.
Invasive lung myofibroblasts are the main cause of tissue remodeling in idiopathic pulmonary fibrosis (IPF). A key mechanism contributing to this important feature is aberrant crosstalk between the abnormal/injured lung epithelium and pulmonary fibroblasts. Here, we demonstrate that lungs from patients with IPF and from mice with bleomycin (BLM)-induced pulmonary fibrosis (PF) are characterized by the induction of human epididymis protein 4 (HE4) overexpression in epithelial cells.
View Article and Find Full Text PDFEur J Med Chem
February 2025
Center for Natural Products Research, Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu, 610041, PR China. Electronic address:
Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease for which few drugs are available in clinical practice. Here, we identified novel capsaicin analogs by combining in-house chemical library screening and further structural optimization. (E)-1-(3,4-dihydroxyphenyl)-7-phenylhept-1-en-3-one (Compound 14) was found to be the most potent in inhibiting TGF-β-induced collagen accumulation, proliferation and migration in fibroblast cells.
View Article and Find Full Text PDFCommun Biol
January 2025
Department of Pulmonary and Critical Care Medicine, Shengjing Hospital of China Medical University, Shenyang, Liaoning, China.
Idiopathic pulmonary fibrosis (IPF) is an irreversible lung condition that progresses over time, which ultimately results in respiratory failure and mortality. In this study, we found that PLAC8 was downregulated in the lungs of IPF patients based on GEO data, in bleomycin (BLM)-induced lungs of mice, and in primary murine alveolar epithelial type II (pmATII) cells and human lung epithelial cell A549 cells. Overexpression of PLAC8 facilitated autophagy and inhibited apoptosis of pmATII cells and A549 cells in vitro.
View Article and Find Full Text PDFRespir Med
January 2025
Princess Máxima Center for Pediatric Oncology, Utrecht, the Netherlands; Wilhelmina Children's Hospital, Utrecht, the Netherlands. Electronic address:
Background: Treatment for childhood cancer may increase the risk of long-term pulmonary complications and dysfunction. Pulmonary surveillance is recommended after established pulmonary toxic exposures, including bleomycin, busulfan, carmustine (BCNU), lomustine (CCNU), radiotherapy to a field exposing the lungs, and pulmonary surgery. However, the role of cyclophosphamide as a pulmonary toxic agent is debated.
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