Latest Research
All publications from the Cancer3.AI database, newest first.
Editorial: Research on nanomaterials in tumor diagnosis and therapy, volume II.
Yan Z, et al
This editorial introduces the second volume of a curated research collection focused on the use of nanomaterials in cancer diagnosis and treatment, published in Frontiers in Bioengineering and Biotechnology. Nanomaterials — including nanoparticles, nanocarriers, and nanostructures — have emerged as promising tools for improving the precision and effectiveness of cancer detection and therapy. The collection highlights advances in drug delivery systems, imaging agents, and theranostic platforms that leverage the unique physical and chemical properties of materials at the nanoscale. By enabling targeted delivery of therapeutic agents directly to tumor cells, these technologies aim to reduce side effects and improve outcomes compared to conventional treatments. This editorial serves as an introduction to the contributing research and underscores the growing importance of nanomedicine in the fight against cancer.
Frontiers in bioengineering and biotechnology
Source →Preclinical evaluation of CPL423: a novel potent small-molecule inhibitor of TAM family and FLT3 kinase for cancer therapy.
Mikołajczyk A, et al
Researchers have characterized CPL423, a novel small-molecule drug candidate designed to simultaneously block the TAM family of receptor tyrosine kinases (TYRO3, AXL, MERTK) and FLT3, two groups of proteins that drive cancer growth, spread, and resistance to treatment. In laboratory tests, CPL423 showed exceptionally potent inhibition of these targets at sub-nanomolar concentrations and demonstrated strong antiproliferative effects in acute myeloid leukemia (AML) cell lines carrying the FLT3-ITD mutation, which is associated with poor prognosis. In animal models, the compound achieved up to 98% tumor growth inhibition in AML and showed meaningful activity in melanoma, while appearing well tolerated without observable toxicity. Beyond direct tumor killing, CPL423 also modulated immune cells called dendritic cells, reducing their ability to clear dying cancer cells in a way consistent with TAM pathway inhibition, suggesting an additional immune-related mechanism of action. The compound also displayed favorable drug-like properties including high permeability, metabolic stability, and a low cardiovascular risk profile. These findings position CPL423 as a promising candidate for further clinical development, particularly for AML patients with FLT3-driven disease and solid tumor patients whose cancers overexpress AXL.
Frontiers in pharmacology
Source →Beneficial effect of omega-3 fatty acids supplementation on leaky gut, inflammation and oxidative stress in propionic acid-induced autism in aged rats.
Aloud A, et al
A new study published in Acta Pharmaceutica investigated whether omega-3 fatty acid supplementation could protect the gut-brain axis in aged rats exposed to propionic acid (PPA), a compound used to model autism-related neurotoxicity. Researchers measured inflammation markers, gut barrier proteins, neurotransmitters, and oxidative stress indicators across four groups of aged male rats. Omega-3 supplementation selectively reduced the inflammatory cytokine IL-6 and partially preserved neuronal and intestinal tissue structure, but it failed to reverse elevated TNF-α levels, restore oxidative balance, or fully repair the disrupted gut barrier. Levels of dopamine, serotonin, and beneficial short-chain fatty acids showed positive trends with omega-3 treatment but did not reach statistical significance. The findings suggest that omega-3 fatty acids may be more useful as a preventive strategy rather than a restorative treatment, particularly in older individuals where gut-brain axis integrity is already compromised. These results have important implications for the use of dietary omega-3 supplementation in ageing populations and in conditions involving neuroinflammation and gut permeability.
Acta pharmaceutica (Zagreb, Croatia)
Source →Concurrent moxifloxacin-induced liver injury and toxic epidermal necrolysis after immune checkpoint inhibition: a case report and literature review.
Li Q, et al
Researchers from China report a case of a 58-year-old man with lung adenocarcinoma who developed two simultaneous, life-threatening drug reactions — severe liver injury (DILI) and toxic epidermal necrolysis (TEN) — after receiving the antibiotic moxifloxacin following prior treatment with the immune checkpoint inhibitor (ICI) tislelizumab. Causality assessment tools (RUCAM score 9, ALDEN score 5) identified moxifloxacin as the most likely culprit, with prior immunotherapy believed to have lowered immune tolerance thresholds and amplified T cell-driven reactions to the drug. A companion systematic review of 28 published cases of concurrent DILI and SJS/TEN found that fluoroquinolone antibiotics, the drug class to which moxifloxacin belongs, were disproportionately represented among causative agents. The patient ultimately recovered without tumor recurrence at 23 months post-surgery, but the case highlights a potentially under-recognized danger of prescribing fluoroquinolones to patients who have recently undergone immunotherapy. Clinicians are urged to exercise heightened caution and increase adverse reaction surveillance when combining these drug classes, as prior ICI exposure may persist and intensify immune responses long after treatment ends. This report calls for further research into the immunologic interplay between checkpoint inhibitors and co-administered medications to improve risk prediction and patient safety.
Frontiers in immunology
Source →Dissecting tumor heterogeneity in colorectal cancer: uncovering the role of BCL2L1+ cells through single-cell analysis.
Zhu G, et al
Researchers used single-cell RNA sequencing to investigate tumor diversity in colorectal cancer (CRC), focusing on why some patients with liver metastases respond poorly to treatment. The study identified five distinct tumor cell subtypes within CRC, of which a subtype called C4 BCL2L1+ tumor cells was found to be significantly enriched in liver metastases and characterized by enhanced cell proliferation, altered metabolism, and resistance to programmed cell death. The transcription factor CEBPG was identified as a key regulator that drives the expression of BCL2L1, and silencing CEBPG in laboratory experiments markedly reduced cancer cell growth and invasion. The researchers also developed a prognostic scoring model called BTRS based on this tumor subtype, which successfully stratified patients into risk groups, with high-risk patients showing signs of immune evasion and reduced immune function. These findings suggest that targeting the CEBPG-BCL2L1 pathway could offer new therapeutic strategies for CRC patients with liver metastases, and the BTRS model may help clinicians personalize treatment decisions.
Frontiers in immunology
Source →