CCND1 (Cyclin D1)

P2, N=20, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Feb 2026 --> Feb 2028 | Trial primary completion date: Feb 2026 --> Feb 2028

Risk modeling further predicted higher PM2.5-attributed lung cancer mortality in UR populations. Collectively, these findings indicated that elevated PM2.5 exposure was associated with early genotoxic and JAK2/STAT3-associated pro-carcinogenic alterations in airway cells and leukocytes of asymptomatic individuals, reflecting heightened biological sensitivity in urban populations.

Although the FDA-approved combination of encorafenib and cetuximab provides clinical benefit in this population, only 22% of patients respond and most eventually develop resistance...Importantly, we demonstrate that addition of TVB3664 to the PLX8394 or encorafenib regimen significantly postpones development of resistance to BRAF-targeted therapy by inhibiting the cell cycle progression via a decrease in pRb (Ser780) and downregulation of E2F transcription factor and Cyclin D1 expression. Consistently, clinical data show that patients with BRAFV600E CRC who have high FASN expression in tumor tissues have higher expression of cell cycle-associated genes, including CDKs, E2F, CCDN1 (Cyclin D1), survivin, and MKI67. Collectively, these findings identify FASN-driven lipid metabolism as a critical mediator of resistance to BRAF-targeted therapy and suggest that incorporation of FASN inhibitors may enhance therapeutic efficacy and delay acquired resistance in BRAFV600E CRC.

This study provides a comprehensive genomic overview of AM, highlighting recurrent alterations in the MAPK and cell cycle pathways, and potential demographic-specific molecular signatures. These findings support the need for expanded molecular profiling to improve prognostic accuracy and identify targets for future therapy.

Sequential treatment with genotoxic agents followed by CDK4/6 inhibitors preserves the cytotoxic efficacy of DNA-damaging drugs while simultaneously blocking entry into the endoreplication cycle and WGD-driven evolutionary rescue. These findings reveal the molecular rules governing the switch from the mitotic to endoreplication cycle and highlight the potential of WGD-blocking drugs as adjuvant therapies to inhibit drug resistance and suppress tumor evolution.

Moreover, Z. jujuba increased pro-apoptotic factors caspas3 and caspase9. The results demonstrated the therapeutic potential of Z. jujuba in CRC through anti-proliferative, and anti-inflammatory properties, indicating its potential value in the treatment of CRC.

Conversely, SOX4 also acts as an oncogene, and TFF3 as a potential tumor suppressor, both linked to OS. Targeting CCND1 and its OS-mediated regulatory pathways offers a promising therapeutic strategy for PTC.CCND1, oxidative stress, papillary thyroid carcinoma, single-cell RNA sequencing, SOX4, TFF3.

Definitive diagnosis relies on molecular testing (such as FISH or NGS), which is crucial for differential diagnosis and prognostic evaluation. This subtype of CCSK is commonly associated with advanced clinical stage and early metastasis/recurrence, highlighting the necessity for improving risk stratification and clinical management.

In CRC, however, SLC46A1 downregulation induces intracellular folate deficiency, triggering locus-specific DNA hypomethylation at the FOS promoter, which activates oncogenic transcription of key downstream effectors (CCND1, BCL2, PLAU), driving tumor progression. The graphical abstract illustrates the differential impact of SLC46A1 on folate metabolism and gene expression in normal versus tumor cells, highlighting its potential as a therapeutic target in CRC.

Drug sensitivity analysis showed that the DSN1 high expression group was resistant to drugs such as Epirubicin, Cyclophosphamide, Ribociclib, and Palbociclib, but relatively sensitive to tamoxifen and lapatinib. DSN1 contributes to breast cancer progression by modulating cell cycle pathways, making it a potential diagnostic and therapeutic target with clinical applicability.

P3, N=182, Recruiting, Hoffmann-La Roche | Trial completion date: Sep 2027 --> Mar 2028 | Trial primary completion date: Feb 2027 --> Aug 2027

Beyond histological grade, proliferative signaling and M2 macrophage polarization strongly influence recurrence risk in ESS. These findings highlight potential diagnostic and therapeutic targets, suggesting integration of immune and cell-cycle biomarkers into future risk stratification models.