Publications by authors named "D S Chandrashekar"

Androgen receptor (AR)-negative triple-negative breast cancer (TNBC), often termed quadruple-negative breast cancer (QNBC), disproportionately impacts women of African descent, leading to poorer overall survival (OS). MiRNAs regulate the expression of gene drivers involved in critical signaling pathways in TNBC, such as the gene, and their expression varies across races and breast cancer subtypes. This study investigates whether differentially expressed miRNAs influence AR transcription, potentially contributing to the observed disparities between African American (AA) and European American (EA) QNBC patients.

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Breast cancer (BCa) is one of the most common malignancies among women worldwide. It is a complex disease that is characterized by morphological and molecular heterogeneity. In the early stages of the disease, most BCa cases are treatable, particularly hormone receptor-positive and HER2-positive tumors.

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Human papillomaviruses (HPV), most commonly HPV16, are associated with a subset of head and neck squamous cell carcinoma (HNSCC) tumors, primarily oropharyngeal carcinomas, with integration of viral genomes into host chromosomes associated with worse survival outcomes. We analyzed TCGA data and found that HPV+ HNSCC expressed higher transcript levels of the bromodomain and extra terminal domain (BET) family of transcriptional coregulators. The role of BET protein-mediated transcription of viral-cellular genes in the viral-HNSCC genomes needs to be better understood.

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Article Synopsis
  • The BET family of proteins, particularly BRD4, plays a significant role in cancer development by binding to acetylated proteins and regulating cell cycle processes.
  • Recent studies have identified JQ1 as the first effective inhibitor that targets BRD4, but resistance to treatment is a common issue.
  • The research highlights potential combination therapies targeting overexpressed kinases like FYN and NEK9 alongside BRD inhibitors to improve cancer treatment outcomes.
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Background: Treatment with regorafenib, a multiple-kinase inhibitor, to manage metastatic colorectal cancers (mCRCs) shows a modest improvement in overall survival but is associated with severe toxicities. Thus, to reduce regorafenib-induced toxicity, we used regorafenib at low concentration along with a dual JAK/HDAC small-molecule inhibitor (JAK/HDACi) to leverage the advantages of both JAK and HDAC inhibition to enhance antitumor activity. The therapeutic efficacy and safety of the combination treatment was evaluated with CRC models.

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