ITGA4 (Integrin, alpha 4)

As the ECM is pivotal in regulating tumor invasion, immune evasion, and drug resistance, we propose that hypermethylation-associated disruption of ECM function may contribute to CRC progression. Our findings highlight potential biomarkers for early detection and novel therapeutic targets for epigenetic intervention.

Inhibitors such as STM2457, METTL3-directed PROTACs, and rational drug combinations with agents including venetoclax, anthracyclines, and ATRA, have reversed resistance phenotypes and impaired leukemic cell fitness...By integrating molecular, cellular, and microenvironmental evidence, this review underscores METTL3 as a central driver of drug resistance and a promising therapeutic target in relapsed or refractory AML. Unlike previous summaries, it highlights the convergence of METTL3-mediated m6A modifications with noncoding RNA regulation, autophagy, and niche adaptation, and critically evaluates emerging therapeutic approaches, including catalytic inhibitors, PROTACs, and natural compounds.

Among 33 inflammatory polyps, 24 scored negative, as well as 64/70 normal contralateral mucosa and one fungus ball. Therefore, excluding benign/borderline tumours, the detected sensitivity was 85.7% and specificity 85.6% (AUC: 0.878).

Furthermore, risk models incorporating specific protein signatures effectively stratified patients by platinum sensitivity/resistance (9-protein panel: ILK, CDCP1, CD86, CLDN4, CLEC1B, CDHR5, CLDN11, JAM2, FOLH1), lymph node metastasis status (7-protein panel: APOE, CD28, CLDN4, FOLH1, ITGAL, JAML, ULBP3), and post-surgical residual disease burden (4-protein panel: CD44, CLMP, ITGA4, AMIGO1), with Cluster 13 (ITGB1-high) also significantly associated with residual disease. This work demonstrates the power of single-EV proteomics combined with machine learning for non-invasive diagnosis and clinical outcome assessment in advanced ovarian cancer, though the absence of early-stage patients limits its applicability for early detection.

Results showed that the newly established mAb, named mAb ANAP, induced immediate cell death against NK lymphoma cells in a cytoskeleton-dependent manner, which was also complement-, antibody-dependent cell-mediated cytotoxicity-, and caspase-independent, forming large pores on target cell surface within 20 min; mAb ANAP did not injure normal cells and could bind to the ITGA4 (CD49d). Contrary to existing anti-ITGA4 antibodies, which did not exhibit any destructive activity against NK lymphoma, ANAP antibody has promising potential as a therapeutic agent for NK lymphoma.

It is highly suggestive that CD49d is able to distinguish patients with a higher risk of death, progression, or need for treatment without its dependence on other clinical factors, making it highly reliable in a clinical setting. It is necessary to assess its utility in the context of novel treatment options and determine the importance of bimodal expression of CD49d regarding prognostic value.

The large number of women with HPV infections in China each year has led to excessive cytological screenings and colposcopy referrals. A feasible triage tool for women who are hrHPV-positive significantly reduces unnecessary medical resource utilization and offers substantial health and economic benefits.

The effects of IMiDs (pomalidomide, lenalidomide) on CD38 expression and isatuximab-induced apoptosis, either alone or in combination with IMiDs, were also examined. Additionally, both antibodies effectively inhibited MM cell migration and significantly reduced cell adhesion. Their non-competitive binding and shared impact on cell dynamics suggest opportunities for optimizing treatment strategies through combinatorial or sequential approaches in MM therapy.

Serial samples obtained from one leukemia cutis case throughout consecutive immune checkpoint blockade with ipilimumab followed by nivolumab showed a consistently high degree of overlap between local and circulating T cell receptor (TCR) sequences, suggesting that only a minority of eAML-associated T cells are leukemia-specific. Our analysis reveals eAML to associate with complex changes in leukemia and T cell gene expression profiles that suggest multiple potential avenues for therapeutic targeting.

In vivo experiments demonstrated that EbSe@LNP regulates immune cell ratios in tumor and spleen, effectively combating cancer progression. Collectively, this study not only offers a nano-delivery strategy to overcome the poor aqueous solubility of EbSe, but also elucidates its underlying antitumor mechanisms, offering a strong scientific foundation for its clinical translation.

Targeting the STAT1/ETS1 axis, in combination with EGFR-TKIs or immune checkpoint inhibitors, may provide a novel strategy to overcome resistance and improve patient outcomes. Further validation in larger patient cohorts and functional studies is warranted to confirm these observations and support clinical translation.

In mouse TNBC models, this temporally optimized two-phase MPTT approach achieves superior tumor reduction compared to conventional single-treatment (+87%) or non-optimized protocols (+43%). The findings establish a novel time modulated framework for enhancing nanomedicine efficacy by aligning treatment scheduling with underlying molecular kinetics-a strategy with potential applications across various siRNA-based cancer therapies where timing of intervention may significantly impact therapeutic outcomes.