RMST (Rhabdomyosarcoma 2 Associated Transcript)

Utilization of adjuvant immunotherapy among patients with locally advanced residual disease following multimodal treatment has dramatically increased since the Checkmate 577 trial. In this national study, patients who received adjuvant immunotherapy experienced ~5 months of survival benefit. Yet, with such an incremental impact on survival, additional studies are needed to further optimize the multimodal perioperative treatment of patients with EC.

Furthermore, we found that high circRMST expression and low promoter methylation levels are associated with poor prognosis. In conclusion, this study identifies circRMST as a novel oncogene in PF EPN.

These effects were all partially attenuated by silencing of miR-139-5p. RMST can aggravate neuroinflammation and apoptosis in microglia after TBI and thereby affect neurological dysfunction by regulating miR-139-5p.

GH is a common reason for admission in nonagenarians and may indicate broader vulnerability. Geriatric assessment tools could aid in clinical decision-making and discharge planning. Future research should validate frailty-based risk stratification and address functional decline related to hospitalization in this population.

The proposed COMPACT design offers a novel and robust framework for combination cancer therapies with progression-free survival end point.

Sensitivity analysis for patients who received a diagnosis between 2010 and 2013 documented similar 10-year RMST following SH vs MRH or RH, SH vs RH, SH vs MRH, and MRH vs RH. In this cohort study, long-term survival was similar following SH vs MRH or RH, supporting the use of SH in select patients with low-risk early-stage cervical carcinoma.

Our findings indicate that the LncRNA RMST-miR-4295-ITPR1 axis plays a crucial role in regulating autophagy in TNBC cells. The modulation of this axis may represent a novel therapeutic strategy for inhibiting TNBC progression and overcoming chemoresistance.

We investigate the properties of our method using simulations and illustrate its use by an application to data from the SUCCESS-A breast cancer trial. Our numerical experiments demonstrate that PVRF yields accurate estimates of both patient-specific RMST values and RMST-based treatment contrasts.

RMST silencing could attenuate inflammatory response and cardiomyocyte apoptosis and upregulate cardiac function in mice with doxorubicin-induced HF by modulating the miR-10b-5p/TRAF6 axis. The study provides novel therapeutic targets for HF treatment.

The subtle differences observed, particularly in PFS, could inform clinical decision-making, emphasizing the need for personalized treatment strategies. Future research should focus on long-term effects and identifying patient subgroups that may benefit more from one drug over the other.

With MASH becoming a global health issue and its progression to fibrosis associated with hepatocarcinogenesis and poor prognosis, understanding the underlying mechanisms is critical. This research contributes to elucidating lncRNA functions in murine liver diseases and provides a foundation for developing novel therapeutic strategies targeting lncRNAs in MASH and liver fibrosis, offering new avenues for potential therapeutic interventions.

Transcriptomic and epigenetic analyses showed that RMST deletion caused altered expression of key genes involved in neuronal development, ion channels, synaptic signaling and cell adhesion. The in vitro generation of these RMST-deleted GnRH neurons provides an excellent cell-based model to dissect the molecular mechanism of RMST function in Kallmann syndrome and its role in hypothalamic neuronal development.