Yingge Li

1 Introduction Cancer therapy-induced thrombocytopenia (CTIT) is a common hematologic toxicity associated with anti-tumor treatments, potentially leading to treatment delays, interruptions, dose reductions, and even bleeding events, which can compromise therapeutic outcomes and long-term survival [1, 2].

Keywords Animals, Kruppel-Like Transcription Factors, Cell Differentiation, Mice, Lung, Pulmonary Fibrosis, Mice, Inbred C57BL, Regeneration, Male, Alveolar Epithelial Cells, Cell Proliferation, Humans, Lung Injury, Disease Models, Animal, CCAAT-Enhancer-Binding Proteins, Hormone receptors, Mechanisms of disease, Target validation, Transcriptional regulatory elements Abstract Aberrant repair underlies the pathogenesis of pulmonary fibrosis while effective strategies to convert fibrosis to...

Abstract Tumor-host interaction plays a critical role in malignant tumor-induced organ wasting across multiple species. Despite known regulation of regional wasting of individual peripheral organs by tumors, whether and how tumors utilize critical host catabolic hormone(s) to simultaneously induce systemic host wasting, however, is largely unknown.