MAGEA1 (MAGE Family Member A1)

We established an efferocytosis-related prognostic signature and elucidated its underlying mechanism wherein MAGEA11 promoted immunosuppression via a Gas6-MERTK/AXL-dependent efferocytosis circuit. This integrated study positions efferocytosis as a key driver of the OS microenvironment and a promising target for clinical intervention.

We developed a useful risk model and this study provided new insights for OS therapy.

Serum MAGEA3-IgG levels are significantly elevated in LUAD patients, and this autoantibody is anticipated to serve as a critical biomarker for early diagnosis, treatment monitoring, and prognostic evaluation in LUAD.

105B decreased levels of BET-regulated gene products c-Myc, RUNX2, and KRT14; however, improvements are still necessary to affect selective cytotoxicity. This work reports the first example of a PROTAC recruiting a tissue-specific E3 ligase for cancer-restricted degradation of BET proteins and highlights the need for further development of MAGEA11-recruiting degraders.

To verify this mechanism in GC, we conducted cell function experiments and immunohistochemistry, confirming that MAGEA11 promotes GC development by activating E2F1's transcriptional activity. These findings indicate that MAGEA11 may be a useful molecular marker for predicting GC prognosis.

Additionally, methylation patterns of AR co-regulators located on the X chromosome suggest epigenetic regulation of AR signaling in gliomas. The findings reveal distinct AR pathway activation patterns in adult-type diffuse gliomas, particularly IDH-wildtype GBMs, suggesting that further exploration of antiandrogen therapies is warranted.

Our prognostic model, built with the methylation-related regulators HERPUD1, TECR, MAGEA11, and NSUN6, could effectively predict prognosis in patients with ESCC, enhance diagnostic efficacy, and reflect immune cell infiltration in their microenvironment. Our findings are hypothesis generating and larger confirmatory studies are needed to validate our results.

Furthermore, the scRNA-seq of melanoma cells with MLLT3 knock-out resulted in important changes in cell subsets, activating the TP53 and MAPK pathways and transforming into stem cells. The results indicate that the transcription factor MLLT3 is a suppressor gene that regulates the stemness and progression of melanoma, and is expected to become a target for melanoma therapy.

Our study set cut-off values for seven autoantibodies in identifying GGNs no more than 3cm and constructed a machine learning model for effective diagnosis. This provides a non-invasive and highly discriminative method for the evaluation of ground-glass nodules in high-risk patients.

The sensitivity of different stages and pathological types of NSCLC consistent. Among them, the sensitivity of combined-detection in diagnosing adenocarcinoma and squamous cell carcinoma significantly better than CEA, NSE and CYFRA21-1. The combined detection has better efficacy in assisting the diagnosis of NSCLC and has certain clinical promotion and application value.

This diagnostic model and DCA could provide evidence for upgrading or maintaining the current clinical decision based on malignancy probability stratification. It enables low and moderate risk or ambiguous patients to benefit from more precise clinical decision stratification, more timely detection of malignant nodules, and early treatment.

Our nomogram proved to be a valuable instrument in accurately predicting the overall survival of patients.