We reported the dual function of LINC00525 in fine-tuning p21 production at both the transcriptional and post-transcriptional levels. We suggest that LINC00525 may represent a potential therapeutic target for clinical intervention in lung adenocarcinoma.

In this study, a novel cell cycle regulator named meiotic nuclear divisions 1 (MND1) was firstly screened out as a potential oncogene in LUAD using different bioinformatic and statistical analyses. In mechanism, MND1 could directly bind to tumor suppressor kruppel-like factor 6 (KLF6) to protect E2F1 from the transcriptional repression of KLF6. Interestingly, in return, E2F1 could activate MND1 transcription by binding to a specific site in the promoter region of MND1.

Our results define the signaling pathways deregulated in HER2⁺ breast cancer under diabetic condition, which can be intervened by anti-insulin resistance therapy.

LncRNAs play complex and diverse roles in EC by mediating proliferation, cell cycle, apoptosis, invasion, migration, EMT, drug resistance, etc., and are closely related to EC clinicopathology and prognosis.

BAT8001 demonstrated favorable safety and tolerability profiles, with promising anti-tumour activity in patients with HER2-positive advanced or recurrent solid tumours. BAT8001 has the potential to provide a new therapeutic option in heavily pretreated patients with metastatic Her2-positive breast cancer.

These findings provide a potential combinational drug target for promoting the therapeutic effects of MLN8237 and reveal a relationship between centromere-related functions and the sensitivity of Aurora-A inhibitor.

Tepotinib have high retention in the tumor and sustained inhibition of MET and its downstream pathways. Tepotinib is a key drug for cancer patients with MET exon 14 skipping mutation. However, its bioavailability in the CSF in humans has not been elucidated. The blood brain barrier protects the CNS from toxicity, but also prevents therapeutic drugs from accessing the brain. We report a case of leptomeningeal metastasis successfully treated with tepotinib in a patient with poor PS and on the bioavailability of tepotinib in the CSF in humans.