Data indicate that genetic errors at the MEN1 locus and distal to it may be involved in the development of sporadic pulmonary carcinoid tumors.

Suppression of lung adenocarcinoma through menin and polycomb gene-mediated repression of growth factor pleiotrophin.

This study confirms the involvement of the MEN1 gene in the development of sporadic pulmonary carcinoids

a previously unknown link between activated K-Ras and menin, an important interplay governing tumor activation and suppression in the development of lung cancer.

Thirteen percent of pulmonary carcinoids harbor MEN1 mutation associated with reduced mRNA expression and poor prognosis

Results revealed that the expression level of menin was lower in lung cancer. Its expression is regulated by miR24 which directly targets menin and significantly inhibit its activity, thereby promoting the growth and metastasis of lung cancer cells.

The loss of menin expression in certain primary lung cancers correlates with elevated neuroendocrine profiles and reduced overall survival.

miR-802 expression levels are increased in lung carcinoma tissues and targets the tumor suppressor menin and downregulates its expression.

Established an ATII-specific Kras(G12D/+)/Men1(-/-) driven genetically engineered model and show that deficiency of menin results in the accumulation of DNA damage and antagonizes oncogenic Kras-induced senescence and the epithelial-to-mesenchymal transition during lung tumorigenesis.