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What is the relationship between invasive mucinous adenocarcinoma and genetic mutations? 


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Invasive mucinous adenocarcinoma (IMA) of the lung is associated with specific genetic mutations. Research has shown that IMAs are characterized by frequent KRAS mutations and gene fusions, particularly involving NRG1. Comprehensive molecular analysis of IMAs revealed that nearly all cases exhibit major oncogenic drivers, with KRAS mutations being the most common, followed by NRG1 fusions and ERBB2 alterations. Notably, NRG1-rearranged IMAs display more aggressive characteristics compared to KRAS-mutant IMAs, leading to worse recurrence-free survival outcomes. Additionally, targetable gene fusions were identified in a significant portion of KRAS wild-type IMAs, highlighting the importance of comprehensive molecular testing that includes fusion analysis for effective targeted therapy.

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Mutant KRAS and FOXA2 cooperation drives invasive mucinous adenocarcinoma of the lung, with specific gene expression changes observed in comparison to normal lung tissue.
Mutant KRAS cooperates with FOXA2 to drive invasive mucinous adenocarcinoma of the lung, as shown by differential gene expression in IMA compared to normal lung tissue.
FOXA2 cooperates with mutant KRAS to drive invasive mucinous adenocarcinoma of the lung, indicating a relationship between genetic mutations and this specific type of cancer progression.
Invasive mucinous adenocarcinoma (IMA) is associated with genetic mutations like KRAS, NRG1 fusions, and ERBB2 alterations, with distinct aggressive characteristics observed in NRG1-rearranged tumors.
Invasive mucinous adenocarcinoma (IMA) is associated with genetic mutations like KRAS, NRG1 fusions, and ERBB2 alterations, with distinct aggressive characteristics observed in NRG1-rearranged tumors.

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