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FOXA2 with mutant KRAS drives invasive mucinous adenocarcinoma of the lung

ABSTRACT: FOXA2 with mutant KRAS drives invasive mucinous adenocarcinoma of the lung

PROVIDER: PRJNA863850 | ENA |

REPOSITORIES: ENA

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Sotorasib Resistance in KRAS G12C-Mutant Invasive Mucinous Adenocarcinoma with Implications for VEGF-A

Project description:Invasive mucinous adenocarcinoma (IMA) is a rare subtype of lung adenocarcinoma with a poor prognosis. Compared to non-small cell lung cancer (NSCLCs), IMA more frequently harbors KRAS mutations in the order KRAS p.G12V, p.G12D, and p.G12C. This report describes a patient with KRAS p.G12C-mutant IMA treated with sotorasib. To date, no studies have investigated the therapeutic efficacy or resistance mechanisms of sotorasib in IMA. The patient was treated with carboplatin and pemetrexed, followed by sotorasib upon disease progression. While the primary lung lesions responded well, metastatic thoracic lymph node lesions continued to increase. A pathological autopsy was performed with the family’s consent to investigate potential resistance mechanisms. RNA sequencing and additional analyses revealed increased VEGF-A expression in metastatic lymph node lesions, suggesting a role in sotorasib resistance. These findings provide insights into the molecular mechanisms underlying treatment resistance in KRAS p.G12C-mutant IMA.

2025-05-02 | GSE295712 | GEO

Sotorasib Resistance in KRAS G12C-Mutant Invasive Mucinous Adenocarcinoma with Implications for VEGF-A

Project description:Sotorasib Resistance in KRAS G12C-Mutant Invasive Mucinous Adenocarcinoma with Implications for VEGF-A

| PRJNA1255652 | ENA

Gene signature driving invasive mucinous adenocarcinoma of the lung

Project description:Gene signature driving invasive mucinous adenocarcinoma of the lung

| PRJNA343081 | ENA

Mucinous colorectal adenocarcinoma

Project description:Mucinous colorectal adenocarcinoma

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FOXA2 Cooperates with Mutant KRAS to Drive Invasive Mucinous Adenocarcinoma of the Lung.

Project description: Not available

| S-EPMC10160002 | biostudies-literature

FoxA1 and FoxA2 are required for gastric differentiation in NKX2-1-negative lung adenocarcinoma [single cell analysis]

Project description:Profound changes in cancer cell identity can alter malignant potential and therapeutic response. Loss of the pulmonary lineage specifier NKX2-1 augments the growth of KRAS-driven lung adenocarcinoma and causes pulmonary to gastric transdifferentiation. Here we show that the transcription factors FoxA1 and FoxA2 are required for initiation of mucinous NKX2-1-negative lung adenocarcinomas in the mouse and for activation of their gastric differentiation program. Foxa1/2 deletion severely impairs tumor initiation and causes a proximal shift in cellular identity, yielding tumors expressing markers of the squamocolumnar junction of the gastrointestinal tract. In contrast, stochastic loss of FoxA1/2 expression in NKX2-1-negative tumors is associated with keratinizing squamous differentiation. Using sequential in vivo recombination, we find that FoxA1/2 loss in established KRAS-driven neoplasia is sufficient for direct induction of keratinizing squamous cell carcinomas in the lung. Thus, NKX2-1, FoxA1 and FoxA2 coordinately regulate the growth and identity of lung adenocarcinoma in a context-specific manner.

2018-12-16 | GSE115900 | GEO

FoxA1 and FoxA2 are required for gastric differentiation in NKX2-1-negative lung adenocarcinoma [total RNA-seq analysis]

2018-12-16 | GSE115899 | GEO

Progression of KRas^G12D;Rosa26-MYC tumours to invasive disease

Project description:The aim of the study was to investigate gene expression tumour progression of KRas*/MYC driven lung tumours from adenocarcinoma in situ to invasive disease.

2018-06-01 | E-MTAB-6432 | biostudies-arrayexpress

FOXA2 with mutant KRAS drives invasive mucinous adenocarcinoma of the lung

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-07-01 | GSE210121 | GEO

High-resolution genome-wide copy number analysis of pre-invasive mucinous ovarian tumours

Project description:Introduction: Mucinous tumors are the second most common form of epithelial ovarian tumor, yet the cell of origin for this histological sub-type remains undetermined. While these tumors are thought to arise through a stepwise progression from benign cystadenoma to borderline tumor to invasive carcinoma, few studies have attempted to comprehensively characterize the genetic changes specific to this subtype or its precursors. Methods: To explore the spectrum of genomic alterations common to mucinous tumors we performed high resolution genome-wide copy number analysis, mutation screening by Sanger sequencing and immunohistochemistry on a series of primary ovarian mucinous cystadenomas (n=20) and borderline tumors (n=22). Results: Integration of copy number data, targeted mutation screening of RAS/RAF pathway members and immunohistochemistry reveals that p16 loss and RAS/RAF pathway alterations are highly recurrent events that occur early during mucinous tumor development. The frequency of concurrence of these events was observed in 40% of benign cystadenomas and 68% of borderline tumors. Conclusions: This study is the largest and highest resolution analysis of mucinous benign and borderline tumors performed to date and provides strong support for these lesions being precursors of primary ovarian mucinous adenocarcinoma. The high level of uniformity in the molecular events underlying the pathogenesis of mucinous ovarian tumors provides an opportunity for treatments targeting specific mutations and pathways. Copy number data was generated for 42 mucinous ovarian tumours (20 benign, 22 borderline). Epithelial and stromal DNA from the tumours and matched-normal lymphocyte DNA were all analysed. Processed/normalized data for the germline DNA samples are not provided because they themselves are normalised to a diploid copy number, making all the probe values 2, which is not informative.

2012-08-26 | E-GEOD-39076 | biostudies-arrayexpress

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