NSUN2-mediated m5C modification of EPYC contributed to GC cell growth and metastasis, which provided a novel regulatory axis for understanding the pathogenesis of GC.

Notably, the combination of Pi-CARM1-TAT with endocrine therapy drugs or etoposide shows synergistic effects in inhibiting breast tumorigenesis. Furthermore, Pi-CARM1-TAT effectively overcomes endocrine therapy resistance in ER-positive breast cancer cells. In conclusion, we present a novel peptide inhibitor of CARM1, which provides valuable insights and may offer therapeutic potential for the development of CARM1-targeted treatments in breast cancer.

USMB improves the TNBC microenvironment and enhances drug delivery by promoting perfusion and oxygenation, likely via NO signaling. These findings support USMB as a promising strategy for TNBC combination therapy and highlight NO as a potential therapeutic target.

In conclusion, LA treatment protects the cardiac tissue against DOX-induced cardiotoxicity, as evidenced by its antioxidant and anti-inflammatory potential, supporting its possible therapeutic role.

Following completion of weekly paclitaxel(PTX), initiation of epirubicin plus cyclophosphamide(EC)resulted in a marked platelet decrease to 1.3×104/μL on day 7, necessitating repeated platelet transfusions. These findings suggest that in breast cancer patients with ITP, neoadjuvant chemotherapy may not be feasible, and primary surgical intervention should be considered. Furthermore, when administering EC, vigilant hematological monitoring is imperative.

P=N/A, N=90, Not yet recruiting, Tanta University

Myricetin demonstrated protective effects against Dox-induced liver damage through its antioxidant and anti-inflammatory properties. Further research is warranted.

Given the high mutation frequency of PDLIM4 recorded in the TCGA cancer database, our findings reveal a critical regulatory signaling pathway that suppresses LUAD progression and augments chemotherapy efficacy.

Doxorubicin (Dox) is a widely employed chemotherapeutic agent, but its use is clinically limited by dose-accumulative cardiotoxicity...Notably, this cardioprotection is achieved without either compromising Dox's anti-tumor efficacy or producing overall toxicity. These findings establish cmSMRTs 143-122 as a minimally invasive, cardiac-selective mRNA therapy platform with strong potential to prevent chemotherapy-induced cardiotoxicity.

Psychosocial stress significantly worsens DOX-induced cardiotoxicity by promoting cardiac dysfunction, fibrosis, and maladaptive gene expression. This study highlights psychosocial stress as a critical risk factor for adverse cardiovascular outcomes in cancer patients receiving potentially cardiotoxic chemotherapy.

Cell lines with higher ABCG2 expression exhibited lower sensitivity to mitoxantrone, topotecan, and doxorubicin and diminished cytotoxic response. Mechanistically, p38 regulated the expression and membrane localization of oligomeric ABCG2, essential for its efflux activity. This study highlights p38 as a promising target to overcome ABCG2-mediated multidrug resistance and improve treatment outcomes for drug-resistant tumors.

At the tumor site, the nanocomposite disintegrates and releases calcium ion (Ca2+), doxorubicin (DOX), catalase (CAT), and coincidentally produces a large amount of hydrogen peroxide (H2O2) in the acidic tumor microenvironment (TME) containing hyaluronidase. Subsequently, CAT can catalyze the transformation of H2O2 into oxygen (O2) ameliorating the hypoxia...With the combination of relieving hypoxia and suppressing ATP production, the expression of P-gp was remarkable downregulated, thereby overcoming MDR, with confirmed by in vitro and in vivo experiments. This study may provide new avenues for the treatment of multidrug-resistant tumors.