ROS1 and EGFR are primary oncogenic drivers in non-small cell lung cancer (NSCLC) pathogenesis. However, EGFR mutations and ROS1 fusions are generally mutually exclusive in NSCLC, leading to a negligible probability o...ROS1 and EGFR are primary oncogenic drivers in non-small cell lung cancer (NSCLC) pathogenesis. However, EGFR mutations and ROS1 fusions are generally mutually exclusive in NSCLC, leading to a negligible probability of their co-occurrence. Consequently, clinical data and treatment strategies for their simultaneous presence are remarkably scarce. This report details the first recorded case of a sarcomatoid, poorly differentiated lung adenocarcinoma harboring both a ROS1 fusion and an EGFR mutation, alongside ARID1A and NFKBIA gene mutations. Moreover, this case study encompasses a review of instances featuring concurrent ROS1 and EGFR mutations. The identified genetic alterations in ROS1, EGFR, ARID1A, and NFKBIA are pivotal in the etiology of NSCLC. These mutations significantly influence disease progression and are essential for the development of personalized therapeutic approaches. Recognizing the unique genetic profiles in patients permits healthcare providers to devise customized treatment regimens that target these specific mutations, thereby enhancing patient outcomes in NSCLC.展开更多
Calpains are calcium-activated cysteine proteases. There are two main isoforms of calpain that are ubiquitously expressed in tissues, calpain μ or calpain 1, which requires micromolar Ca<sup>2+</sup> for ...Calpains are calcium-activated cysteine proteases. There are two main isoforms of calpain that are ubiquitously expressed in tissues, calpain μ or calpain 1, which requires micromolar Ca<sup>2+</sup> for activation, and calpain or 2, which requires millimolar Ca<sup>2+</sup> for activation. The presence of other calpains is tissue specific. Atherosclerosis (AS) is an important risk factor for cerebral infarction, coronary heart disease and peripheral vascular disease. It was originally thought that AS was caused by impaired lipid metabolism. This research briefly reviewed Calpain Family, the structure and activation mechanism of calpain1, Calpains in the pathogenesis of atherosclerosis, NLRP3 structural characteristics and activation, ROS/NLRP3 inflammasome activation mechanism and ROS/NLRP3 inflammasome in atherosclerosis. The research showed that the Calpain-1 may play an important role in mitochondrial ROS/NLRP3 inflammasome in atherosclerosis.展开更多
文摘ROS1 and EGFR are primary oncogenic drivers in non-small cell lung cancer (NSCLC) pathogenesis. However, EGFR mutations and ROS1 fusions are generally mutually exclusive in NSCLC, leading to a negligible probability of their co-occurrence. Consequently, clinical data and treatment strategies for their simultaneous presence are remarkably scarce. This report details the first recorded case of a sarcomatoid, poorly differentiated lung adenocarcinoma harboring both a ROS1 fusion and an EGFR mutation, alongside ARID1A and NFKBIA gene mutations. Moreover, this case study encompasses a review of instances featuring concurrent ROS1 and EGFR mutations. The identified genetic alterations in ROS1, EGFR, ARID1A, and NFKBIA are pivotal in the etiology of NSCLC. These mutations significantly influence disease progression and are essential for the development of personalized therapeutic approaches. Recognizing the unique genetic profiles in patients permits healthcare providers to devise customized treatment regimens that target these specific mutations, thereby enhancing patient outcomes in NSCLC.
文摘Calpains are calcium-activated cysteine proteases. There are two main isoforms of calpain that are ubiquitously expressed in tissues, calpain μ or calpain 1, which requires micromolar Ca<sup>2+</sup> for activation, and calpain or 2, which requires millimolar Ca<sup>2+</sup> for activation. The presence of other calpains is tissue specific. Atherosclerosis (AS) is an important risk factor for cerebral infarction, coronary heart disease and peripheral vascular disease. It was originally thought that AS was caused by impaired lipid metabolism. This research briefly reviewed Calpain Family, the structure and activation mechanism of calpain1, Calpains in the pathogenesis of atherosclerosis, NLRP3 structural characteristics and activation, ROS/NLRP3 inflammasome activation mechanism and ROS/NLRP3 inflammasome in atherosclerosis. The research showed that the Calpain-1 may play an important role in mitochondrial ROS/NLRP3 inflammasome in atherosclerosis.
