Publications by authors named "J Tien"
Inadequate response to androgen deprivation therapy (ADT) frequently arises in prostate cancer, driven by cellular mechanisms that remain poorly understood. Here, we integrated single-cell RNA sequencing, single-cell multiomics, and spatial transcriptomics to define the transcriptional, epigenetic, and spatial basis of cell identity and castration response in the mouse prostate. Leveraging these data along with a meta-analysis of human prostates and prostate cancer, we identified cellular orthologs and key determinants of ADT response and resistance.
View Article and Find Full Text PDFWe present a high-sensitivity fiber optic soil moisture sensor based on side-polished multimode fibers and lossy mode resonance (LMR). The multimode fibers (MMFs), after side-polishing to form a D-shaped structure, are coated with a single-layer SnO thin film by electron beam evaporation with ion-assisted deposition technology. The LMR effect can be obtained when the refractive index of the thin film is positive and greater than its extinction coefficient and the real part of the external medium permittivity.
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- Biallelic loss of CDK12 is linked to a specific subtype of metastatic castration-resistant prostate cancer (mCRPC), raising questions about its role in cancer development versus exposing drug targets.
- Research shows that loss of CDK12 leads to early cancer-like changes and enhances cancer cell growth when combined with mutations in other genes like Trp53, while it inhibits tumor growth in the absence of another tumor suppressor gene, Pten.
- CDK12 loss causes genomic instability and makes tumors sensitive to treatments targeting another protein, CDK13, highlighting CDK12 as a crucial tumor suppressor and suggesting new therapeutic approaches for CDK12-mutant mCRPC.
Cyclin-dependent kinases 12/13 play pivotal roles in orchestrating transcription elongation, DNA damage response, and maintenance of genomic stability. Biallelic CDK12 loss has been documented in various malignancies. Here, we develop a selective CDK12/13 PROTAC degrader, YJ9069, which effectively inhibits proliferation in subsets of prostate cancer cells preferentially over benign immortalized cells.
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- The androgen receptor (AR) is important for prostate cell differentiation, but its role changes in cancer, leading to enhanced tumor traits due to altered chromatin interactions.
- This study reveals that the NSD2 enzyme, which is overexpressed in prostate cancer, is crucial for the function of tumor-specific AR enhancers by affecting their chromatin makeup.
- Targeting both NSD1 and NSD2 may provide an effective treatment strategy for advanced prostate cancer, especially seen with a specialized degrader that shows strong effects in AR-driven cancer models.