Publications by authors named "Shreoshi Sengupta"
Article Synopsis
- Lung cancer remains the leading cause of cancer deaths globally, highlighting the need for better understanding of its early development stages to enable timely interventions.
- An international team of scientists identified knowledge gaps in how premalignant lung lesions progress to lung cancer and developed research questions to fill these gaps and guide future investigations.
- Addressing these gaps is crucial for improving screening and early detection methods, which could lead to innovative strategies that effectively reduce lung cancer incidence and enhance patient outcomes.
Glycine-12 mutations in the GTPase KRAS (KRAS) are an initiating event for development of lung adenocarcinoma (LUAD). KRAS mutations promote cell-intrinsic rewiring of alveolar type-II progenitor (AT2) cells, but to what extent such changes interplay with lung homeostasis and cell fate pathways is unclear. Here, we generated single-cell RNA-seq (scRNA-seq) profiles from AT2-mesenchyme organoid co-cultures, mice, and stage-IA LUAD patients, identifying conserved regulators of AT2 transcriptional dynamics and defining the impact of KRAS mutation with temporal resolution.
View Article and Find Full Text PDFCancer stem cells (CSCs) alone can initiate and maintain tumors, but the function of non-cancer stem cells (non-CSCs) that form the tumor bulk remains poorly understood. Proteomic analysis showed a higher abundance of the extracellular matrix small leucine-rich proteoglycan fibromodulin (FMOD) in the conditioned medium of differentiated glioma cells (DGCs), the equivalent of glioma non-CSCs, compared to that of glioma stem-like cells (GSCs). DGCs silenced for FMOD fail to cooperate with co-implanted GSCs to promote tumor growth.
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