MUC3A (Mucin 3A, Cell Surface Associated)

This study demonstrates that MUC3A regulates the proliferation and metastasis of cholangiocarcinoma cells through the ERK signaling pathway.

The addition of agonist M05856 restored the inhibitory effect of silencing MUC3A on GC cell proliferation and migration, suggesting that MUC3A regulates GC cells' behavior through the PI3K/Akt/mTOR pathway. MUC3A plays an oncogenic role in GC and may regulate GC cell behavior through the PI3K/Akt/mTOR pathway.

Our study suggests that MUC3A is a potential oncogene that promotes the proliferation, invasion, and chemotherapy resistance of CRC. Moreover, CRC patients with high expression of MUC3A may benefit from rapamycin treatment.

Our studies indicated that MUC3A was a potential oncogene and associated with unfavorable clinical outcomes. NSCLC patients with a high MUC3A level, who should be more frequent follow-up and might benefit less from radiotherapy.

However, the endometrioid-like component not only did not show classic squamous metaplasia, but was also MUC6-positive, while the positivity for ER/PR was only focal. The recognition of gastric/gastrointestinal differentiation in endometrial carcinomas is best accomplished using both morphology and immunohistochemistry rather than either alone.

HPN-DAA is a very rarely occurring cancer that had never been recognized earlier. They belong to the new category of HP-negative cancers, and there seems to be a certain number of such cases.

Conclusions Our results obtained so far highlight a key role for MUC13 in gastric cancer progression and survival. More research is required to understand its exact mechanism.

Also, mucinous BOTs of intestinal-type, exhibiting low nuclear and high cytoplasmic levels of Rb2/p130 might potentially be considered a high-risk category of malignant evolution. Further studies on larger series are needed to clarify how BOTs could be stratified in different prognostic groups according to their Rb proteins immunohistochemical profile.

The neoplastic surfaces were covered by a non-neoplastic epithelium, which caused a gastritis-like appearance. This report suggested the possibility of overlooking this neoplasm.

Our findings suggest that H. pylori infection promotes foveolar hyperplasia as well as metaplasia, while co-infection may promote progressive foveolar and metaplastic lesions as well as dysplasia. Grading of gastric lesions in mice as preneoplastic requires multiple immunostaining markers to assign lineage derivation and behavior.