Publications by authors named "A Parolia"
Objectives: This study evaluated the number and quality of working length (WL) and master cone (MC) radiographs taken during root canal treatment by dental undergraduates, and their associations with the technical quality of root canal fillings (TQRCF) and endodontic outcomes (EO).
Methods: A retrospective evaluation of radiographs from 303 root canal-treated teeth in 231 patients was conducted, with 72 patients attending recall visits to assess EO. The chi-square and one-way analysis of variance tests were performed.
Article Synopsis
- 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.
Article Synopsis
- 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.
The POU2F3-POU2AF2/3 transcription factor complex is the master regulator of the tuft cell lineage and tuft cell-like small cell lung cancer (SCLC). Here, we identify a specific dependence of the POU2F3 molecular subtype of SCLC (SCLC-P) on the activity of the mammalian switch/sucrose non-fermentable (mSWI/SNF) chromatin remodeling complex. Treatment of SCLC-P cells with a proteolysis targeting chimera (PROTAC) degrader of mSWI/SNF ATPases evicts POU2F3 and its coactivators from chromatin and attenuates downstream signaling.
View Article and Find Full Text PDF