Mucinous lung adenocarcinoma represents 2-4% of lung adenocarcinomas. This lung carcinoma subtype is genetically less characterized than other more frequent adenocarcinoma variants. We want to elucidate the molecular aberrations in 50 mucinous lung adenocarcinomas by DNA and RNA sequencing with a panel of 300 genes that are frequently altered in human cancers. The aim is to identify recurrently activated signaling pathways that may represent targets for therapy.
PIK3CA is the catalytic subunit of the phosphatidylinositol 3-kinase (PI3K), a central signaling molecule activated by receptor tyrosine kinases and RAS. Mutated PIK3CA can be inhibited by the drug alpelisib. We investigate the frequency and type of PIK3CA mutations together with estrogen receptor mutations and 50 additional cancer genes in three groups of metastasized breast cancer: a) primary estrogen inhibitor resistant b) secondary estrogen receptor resistant and c) hormone inhibitor sensitive.
The identification of gene mutations often cannot predict drug responses. Therefore, we aim to establish in vitro assays with isolated tumor cells kept in short and long term cultures (including organoids) and exposed to various drugs. The results of these cell culture assays shall be combined with the sequencing results to identify drugs with a high likelihood of efficacy for a given tumor.