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CANCER:

Retinoblastoma

Related cancers:
19d
Philippine Clinical Practice Guidelines for Periodic Health Examination: Screening for Neoplastic Diseases. (PubMed, Acta Med Philipp)
Through a comprehensive and systematic search of the best available evidence, the Neoplastic Diseases Task Force developed 20 recommendations on screening and risk factor assessment for 10 specific questions on neoplastic diseases. These recommendations serve as guidance on screening neoplastic diseases at the primary care level.
Clinical guideline • Journal
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AFP (Alpha-fetoprotein)
19d
Early Check: Expanded Screening in Newborns (clinicaltrials.gov)
P=N/A, N=30000, Active, not recruiting, RTI International | Enrolling by invitation --> Active, not recruiting | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Nov 2025 --> Nov 2026
Enrollment closed • Trial completion date • Trial primary completion date
20d
A CDK4/6 inhibitor-armed oncolytic adenovirus reverses T cell exhaustion through the Rb-p65-CCL5 pathway and potentiates the antitumor activity of anti-PD-1 or CAR-T therapy in colorectal cancer. (PubMed, Front Immunol)
Correspondingly, ADV-PTD4-D3 treatment improved the antitumor response to both PD-1 blockade and CAR-T cell therapy in combination studies. These findings suggest that engineering oncolytic viruses to locally modulate pathways involved in T cell exhaustion represents a viable and translatable strategy for enhancing antitumor immunity.
Journal • PD(L)-1 Biomarker • IO biomarker
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CD8 (cluster of differentiation 8)
21d
Protocol for the Study and Treatment of Participants With Intraocular Retinoblastoma (clinicaltrials.gov)
P2, N=174, Active, not recruiting, St. Jude Children's Research Hospital | Trial completion date: Jan 2028 --> Feb 2027
Trial completion date
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carboplatin • doxorubicin hydrochloride • cyclophosphamide • etoposide IV • vincristine • topotecan • mesna • Neulasta (pegfilgrastim) • Neupogen (filgrastim)
23d
PRMT5 as a Key Driver of Stemness and Metastatic Potential in Triple-Negative Breast Cancer. (PubMed, Biomolecules)
Notably, PRMT5 inhibitors demonstrate synergistic anticancer activity when combined with inhibitors of key oncogenic signaling pathways, including EGFR, PARP, and AKT. While several PRMT5 inhibitors are currently being evaluated in clinical trials for other malignancies, no clinical trials have yet been initiated specifically for TNBC.
Review • Journal • PARP Biomarker • IO biomarker
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EGFR (Epidermal growth factor receptor) • PTEN (Phosphatase and tensin homolog) • RB1 (RB Transcriptional Corepressor 1) • CDH1 (Cadherin 1) • KLF4 (Kruppel-like factor 4) • PRMT5 (Protein Arginine Methyltransferase 5) • TP53BP1 (Tumor Protein P53 Binding Protein 1)
27d
Selective CDK2 Degradation via Noncanonical Recruitment. (PubMed, J Med Chem)
B12 further exhibits improved pharmacokinetics, measurable oral bioavailability, and in vivo target engagement, achieving intratumoral CDK2 degradation following intraperitoneal administration. Collectively, this study provides a structural blueprint for designing selective kinase degraders and establishes B12 as a chemically tractable probe for targeting CDK2-driven malignancies.
Journal
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CCNE1 (Cyclin E1) • CRBN (Cereblon) • CDK2 (Cyclin-dependent kinase 2)
1m
Research Advances in Claudin-1 in the Eye. (PubMed, Exp Eye Res)
We critically evaluate recent mechanistic and translational advances implicating claudin-1 dysregulation in a spectrum of ocular pathologies: anterior segment disorders (dry eye disease, pterygium, infectious keratitis, and gelatinous drop-like corneal dystrophy), retinal diseases (diabetic retinopathy, age-related macular degeneration, central serous chorioretinopathy, and retinoblastoma), and other conditions (uveitis, glaucoma, post-cataract macular edema, and cataract). Finally, we assess the emerging therapeutic potential of claudin-1-both as a molecular target for barrier modulation and as a facilitator of paracellular drug delivery in ophthalmology.
Review • Journal
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CLDN1 (Claudin 1)
1m
Mechanism of matrine inhibiting retinoblastoma cell growth by downregulating NR1D2 to regulate phosphorylation of the PI3K/AKT signaling pathway. (PubMed, Sci Rep)
Total PI3K and AKT levels were unchanged, but their phosphorylated forms were altered; matrine-induced apoptosis correlated with Bax, Cleaved Caspase-3 upregulation and Bcl-2 downregulation. Thus, matrine inhibits RB Y79 cell growth by downregulating NR1D2, inhibiting PI3K/AKT phosphorylation and inducing RB cell apoptosis.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • CASP3 (Caspase 3)
1m
Amentoflavone Suppresses Stemness of Retinoblastoma Cell via Targeting Smoothened (SMO) Protein. (PubMed, Stem Cells Int)
These analyses revealed that AMF directly targets smoothened (SMO) to disrupt the SHh signaling pathway, thereby suppressing RB stem cell (RBSC) self-renewal and tumor progression. This work uncovers a previously unreported mechanism by which AMF hinders RB development and highlights its potential as a promising therapeutic candidate for this aggressive pediatric cancer.
Journal
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CD44 (CD44 Molecule) • POU5F1 (POU Class 5 Homeobox 1) • NANOG (Nanog Homeobox)
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POU5F1 expression
1m
Clinicogenomic analysis of EGFR-mutant lung tumors identifies Rb pathway inactivation as a hallmark of squamous transformation. (PubMed, Sci Transl Med)
Patients with EGFR-mutant LUSC or LUAS had shorter overall survival on first-line osimertinib compared with those with EGFR-mutant LUAD...Combined EGFR and MET inhibition suppressed tumor growth in patient-derived xenograft models of LUSC transformation. Together, these findings highlight Rb pathway inactivation as a promoter of LUSC transformation in EGFR-mutant lung cancer and identify MET signaling as a therapeutic vulnerability that may suppress plasticity in this setting and extend response to targeted therapy.
Journal
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EGFR (Epidermal growth factor receptor) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B)
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EGFR mutation • EGFR wild-type • CDKN2A deletion • MET mutation
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Tagrisso (osimertinib)
1m
Orientin inhibits cyclin E/cyclin A-CDK2 to induce growth arrest at senescence in human gastric cancer cells. (PubMed, Food Chem Toxicol)
In vivo, Orientin also suppressed tumor progression, promoted p16 and p21 expression, and inhibited CCNE/CCNA-CDK2 signaling. Orientin exerts anti-cancer effects in GC through triggering cellular senescence and cell cycle arrest, likely via activating p16/p21-Rb signaling axis and inhibiting the CCNE/CCNA-CDK2 pathway.
Journal
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CCNE1 (Cyclin E1) • CCNA2 (Cyclin A2) • CDK2 (Cyclin-dependent kinase 2) • CCNE2 (Cyclin E2)