Defining and Targeting Mechanisms of Smoke-Mediated Fibrosis Progression (PI: Chen)
The major goal of this project is to characterize the mechanism(s) underlying how cigarette smoke activates the multirole signaling protein, MARCKS, and promotes fibrosis, thereby discovering potential therapeutic targets against smoking-associated lung fibrosis.
Therapeutic Targeting to Inhibit Lung Fibrosis Progression (PI: Chen)
The major goal of this project seeks to identify potential smoke-responsive molecules and investigate their regulatory networks associated with fibroblast differentiation during progressive fibrosis.
Targeting aggressive kidney cancer cells deficient in a metabolic enzyme (PI: Chen)
The major goal of this proposal is focused on the mechanisms underlying how smoking-mediated suppression of a metabolic enzyme contributes to tumor aggressiveness.
Targeting IGF1R signaling in MTAP-deficient kidney cancer (PI: Chen)
The overall objective of this application is to determine if IGF1R signaling drives pathways that contribute to the aggressive nature of renal carcinoma cells lacking MTAP and to evaluate the therapeutic potential of IGF1R inhibition in oncogenic progression.
Tackling Stem-Like Cells in Tobacco Smoke-Mediated Cancer Malignancy (PI: Chen)
The major goal of this project is on how tobacco smoke regulates lung cancer stemness in driving tumor progression.
Evidence-Based Targeted Suppression on Inflammatory Asthma by a Novel Peptide
This application proposes to assess the therapeutic potential of MPS-12042TM peptide on human relevant allergens induced allergic animal models in vivo and ex vivo on bronchial epithelial cells obtained from severe asthma patients due to medical need for bronchial thermoplasty.
MTA-mediated kidney cancer malignancy in response to loss of MTAP (PI: Chen)
The major goal of this project is to characterize the molecular interaction between MTAP dysregulation and its substrate MTA in kidney cancer.
Targeting phospho-MARCKS in smoke-mediated lung cancer (PI: Chen)
The major goal of this project is to study that smoke-activated MARCKS phosphorylation may contribute to malignant changes of bronchial epithelium and lung cancer. The specific aims are to study the functional role of MARCKS phosphorylation in smoke-mediated lung carcinogenesis and cancer metastasis.