Our findings provide novel insights into the heterogeneity of miRNA expression in the pancreas and the molecular mechanisms underlying pancreatic cancer, offering potential targets for future diagnostic and therapeutic strategies.
Importantly, inactivation of the necroptosis executioner MLKL reverses pre-tumoral inflammation, decreases metastasis as well as neuronal-like reprogramming. Taken together, our findings suggest that pre-tumoral inflammatory cell death contributes to neuronal progenitor mimicry, immunosuppression and increased metastasis in SCLC.
Similar distribution of P/LP potential germline alterations in lung cancer subtypes from distinct populations by smoking status suggests increased next-generation germline sequencing may improve risk assessment.
P1/2, N=63, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2027
1 day ago
Trial completion date • Trial primary completion date • Tumor mutational burden
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PD-L1 IHC 22C3 pharmDx
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Lynparza (olaparib) • carboplatin • Imfinzi (durvalumab) • etoposide IV
CAFs-derived exosomal miR-3126-5p enhanced glycolysis of NSCLC cells via targeting KLF13. KLF13 led to transcriptional inhibition of SH2B1 in NSCLC cells. SH2B1 interplayed with IRS1 to facilitate glycolysis of NSCLC cells. IRS1 promoted glycolysis of NSCLC cells via the activation of PI3K/AKT pathway.
Most data come from SCLC; in the other two diseases, tarlatamab is in early clinical development. Tarlatamab is an effective therapy mainly in relapsed/progressed SCLC, and its assessment in limited SCLC alone or combined with other therapies is supported by the existing data.
It emphasizes the importance of integrating telomere biology and oxidative stress assessment in prognostic modeling. The discussion also considers the modifying effects of lifestyle, treatment regimens, and genetic background, advocating for research that combines clinical, biochemical, and molecular data to enhance prognostication in SCLC.