BLMH (Bleomycin Hydrolase)

Measuring BLMH levels may help stratify patients and personalize ECT application; however, it is not the sole factor for response prediction. Future studies in clinical tumor samples are warranted to evaluate its predictive value and to develop integrated biomarker models.

A 19-year-old woman with a history of stage IIIB left ovarian dysgerminoma was undergoing combined chemotherapy (bleomycin, etoposide, and cisplatin). The bleomycin-induced FE must be identified early for appropriate management that allows the continuation of antineoplastic treatment. Discontinuation of the drug should be considered when the patient's quality of life is compromised and balanced with oncological control, which optimizes antineoplastic therapy.

Overall, ME exhibited genotoxicity at high concentrations but demonstrated a significant chemopreventive effect at lower, nontoxic doses. These findings provide insights into the dual biological activity of ME and support its potential use as a protective agent against genotoxic damage.

Glod4 depletion in N2a-APPswe cells upregulated AβPP, and downregulated autophagy-related Atg5, p62, and Lc3 genes. These findings suggest that GLOD4 interacts with AβPP and the autophagy pathway, and that disruption of these interactions leads to Aβ accumulation and cognitive/neurosensory deficits.

We developed a stemness-based gene signature for prognosis prediction with accuracy and reliability. This signature also helps clinical decision-making of immunotherapy for GC patients.

Our findings show that Blmh interacts with AβPP and the Phf8/H4K20me1/mTOR/autophagy pathway, and that disruption of those interactions causes Aβ accumulation and cognitive/neuromotor deficits.

BLM also mediates downregulation of bleomycin hydrolase (Blmh), which is responsible for cellular degradation of BLM, as well as several factors known to be involved in fibrotic responses. PCI-mediated delivery might thus allow reduced dosage of BLM and alleviate unwanted side effects from treatment, including pulmonary fibrosis.

Blmh deficiency and HHcy dysregulated mTOR signaling/autophagy via increased mTOR promoter occupancy by Phf8-dependent H4K20me1, which caused Aβ accumulation and ultimately impaired cognition and neuro-motor activities. Supported by NCN grants 2016/21/D/NZ4/00478, 2016/23/N/NZ3/01216, 2018/29/B/NZ4/00771, 2019/33/B/NZ4/01760.