doxorubicin hydrochloride

Initial studies were done by molecular docking of five analogs of quinazoline- quinazolinone hybrids, erlotinib, and doxorubicin against the epidermal growth factor receptor. The insertion of a nitro group at the 7 position of quinazolinone enhanced the cytotoxic efficacy against MCF-7 cells, likely attributable to electronic influences. Consequently, this compound could serve as a lead compound in the search for new classes of effective anticancer agents.

Tumor tissue and serial plasma samples were collected from 15 patients with aUC treated with dose-dense methotrexate, vinblastine, doxorubicin, and cisplatin (ddMVAC). While the NOIR-SS-based assay proved sensitive and informative, limitations include the cost and time required for sequencing, potential temporal discordance between tissue and plasma sampling, and the absence of correction for clonal hematopoiesis of indeterminate potential. Overall, ctDNA profiling using this targeted panel and NOIR-SS suggested the feasibility of sensitive, non-invasive molecular monitoring in aUC, and may have future clinical applicability if validated prospectively in larger cohorts.

Collectively, our findings uncover a novel mechanism by which doxorubicin enhances NB tumor susceptibility to γδT-cell-mediated killing through ULBP1 up-regulation. This study provides a strong rationale for combining chemotherapy with γδT-cell-based immunotherapy to improve outcomes in high-risk NB patients.

Further investigation revealed that the potassium channel auxiliary subunit KCNE2 is a critical target of fMet; KCNE2 knockdown abrogated the anti-ferroptotic effects of fMet in cardiomyocytes. Collectively, this study delineates a FRD-fMet-KCNE2 axis that suppresses cardiomyocyte ferroptosis and mitigates DIC, providing a mechanistic rationale for nutritional interventions to alleviate chemotherapy-associated cardiotoxicity.

mRNA sequencing reveals an FASTIS-associated transcriptomic profile that overlaps between ACC and FASN inhibitors yet differs significantly from that of other mechanistically diverse TIS inducers, including bleomycin, alisertib, doxorubicin, and palbociclib. The FASTIS phenomenon is a therapeutic outcome through which cancer cells adapt to survive clinical-grade lipogenesis inhibitors. The cholesterol-addicted FASTIS fate can be rationally exploited as a collateral sensitivity in "one-two punch" senogenic-(immuno)senolytic strategies.

P2, N=132, Recruiting, National Cancer Institute (NCI) | Trial completion date: Mar 2030 --> Mar 2031 | Trial primary completion date: May 2026 --> May 2027

P1, N=15, Not yet recruiting, National Cancer Institute (NCI)

P2/3, N=140, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed | Trial completion date: Dec 2026 --> Mar 2026

Importantly, in vivo studies using a xenograft mouse model demonstrate significant tumor growth inhibition, with the nanoformulation + NIR irradiated group showing the most effective anti-tumor outcome with negligible hepatic, renal, and cardiac toxicities. Taken together, it may be stated that the doxorubicin/JQ1 co-loaded PBNCs might be a potential next-generation anti-TNBC theranostic agent, which combines dual-mode MRI capability and combination therapy with reduced side effects.

These cell lines harbor wild-type p53, which, in response to treatment with doxorubicin or Nutlin-3, promoted the expression of well-known p53 target genes (CDKN1A, MDM2). Treatment with adenoviral vectors encoding canine p14ARF and interferon-β (IFNβ) resulted in cell death with liberation of immunogenic cell death markers in vitro and reduction of tumor progression when subcutaneous tumors in nude mice were treated with in situ gene therapy. These results indicate that adenovirus-mediated delivery of p14ARF and IFNβ is effective in a canine model of oral melanoma, supporting the feasibility of applying comparative oncology approaches to the development of this gene therapy strategy.

We present engineered exosomes as next-generation Trojan horses for TNBC: NIR-activatable photothermal agents (polydopamine, BPQDs, or ICG) are integrated into the membrane and chemotherapeutics or nucleic acids (doxorubicin, paclitaxel, siKRAS, siPD-L1, miR-145) encapsulated in the lumen. Future directions include AI/CRISPR-optimized design, NIR-II platforms, checkpoint inhibitor synergy, with early-stage clinical translation of photothermal and immunomodulatory exosome-based therapeutics currently underway, highlighting their potential to advance precision oncology. "However, challenges including scalability, batch variability, and regulatory standardization remain significant barriers to clinical translation."

The patient was started on rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) with a good clinical response. Diagnosis was delayed due to the significant procedural barriers as a result of her small stature and microcephaly associated with her Angelman syndrome. Prompt multidisciplinary evaluation and alternative tissue acquisition were essential for diagnosis and treatment.