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Changqing Ma

Publications and source records attributed to Changqing Ma.

2 recordsLinked to original sources

Comprehensive Profiling of Claudin 18.2 Immunohistochemical Expression in 564 Surgically Resected Gastric and Gastroesophageal Junction Adenocarcinomas.

Claudin 18 isoform 2 (CLDN18.2) is a novel therapeutic target for advanced, HER2-negative gastric/gastroesophageal junction (GEJ) adenocarcinoma positive for CLDN18.2 immunohistochemical (IHC) expression, defined as &#x2265;75% tumor cells with moderate-to-strong membranous staining. Clinical studies for emerging CLDN18.2-targeted therapeutics have used less stringent enrollment criteria to test the efficacy of such therapies in patients with moderate-to-low CLDN18.2 IHC expression. Anticipating the advent of such treatments, this study aimed to provide a comprehensive survey of CLDN18.2 expression using a clinical trial-validated CLDN18.2 monoclonal antibody in surgically resected gastric/GEJ adenocarcinomas and characterize CLDN18.2-positive carcinomas using both high- and low-expression thresholds. Crisp membranous CLDN18.2 staining was detected in 59% (335/564) carcinomas, including 57% (164/286) of gastric and 62% (171/278) of GEJ adenocarcinomas. Most gastric (147/164, 90%) and GEJ (166/171, 97%) adenocarcinomas with staining demonstrated moderate or strong staining intensity. Using the high-expression threshold (&#x2265;75% tumor cells with moderate-to-strong staining), positive CLDN18.2 expression was observed in 20% (57/286) of gastric and 27% (75/278) of GEJ adenocarcinomas and was associated with Epstein-Barr virus status (P < .001) and stage I gastric adenocarcinomas (P = .02) but stage IV GEJ adenocarcinomas (P = .03). Using a low-expression threshold (&#x2265;10% tumor cells with membranous staining), positive CLDN18.2 remained significantly associated with stage I (P = .004) and showed an unadjusted association with improved disease-specific survival in gastric adenocarcinomas (P = .045), which was not retained in multivariable analysis. Whole transcriptomic analysis showed concordance between IHC and CLDN18 messenger RNA expression. Transcriptomic alterations in CLDN18.2 IHC-positive gastric adenocarcinomas included pathways in drug resistance and tumor invasion. In summary, our study presents a detailed characterization of the prevalence and distribution of CLDN18.2 IHC expression patterns. Our results showed that 59% surgically resected gastric/GEJ adenocarcinomas exhibited CLDN18.2 staining. CLDN18.2 IHC positivity defined by both high- and low-expression thresholds may be associated with early-stage gastric adenocarcinoma. These findings expand our recognition of patients who may benefit from CLDN18.2-targeted therapy.

CLDN18.2

Macrophage LRRK2 hyperactivity impairs autophagy and induces Paneth cell dysfunction.

LRRK2 polymorphisms (G2019S/N2081D) that increase susceptibility to Parkinson's disease and Crohn's disease (CD) lead to LRRK2 kinase hyperactivity and suppress autophagy. This connection suggests that LRRK2 kinase inhibition, a therapeutic strategy being explored for Parkinson's disease, may also benefit patients with CD. Paneth cell homeostasis is tightly regulated by autophagy, and their dysfunction is a precursor to gut inflammation in CD. Here, we found that patients with CD and mice carrying hyperactive LRRK2 polymorphisms developed Paneth cell dysfunction. We also found that LRRK2 kinase can be activated in the context of interactions between genes (genetic autophagy deficiency) and the environment (cigarette smoking). Unexpectedly, lamina propria immune cells were the main intestinal cell types that express LRRK2, instead of Paneth cells as previously suggested. We showed that LRRK2-mediated pro-inflammatory cytokine release from phagocytes impaired Paneth cell function, which was rescued by LRRK2 kinase inhibition through activation of autophagy. Together, these data suggest that LRRK2 kinase inhibitors maintain Paneth cell homeostasis by restoring autophagy and may represent a therapeutic strategy for CD.

Leucine-Rich Repeat Serine-Threonine Protein Kinas