Publications by authors named "M A Bassal"
Article Synopsis
- β-thalassemia and sickle cell disease are common genetic blood disorders caused by mutations in the β-globin gene, leading to anemia and requiring treatments like blood transfusions and bone marrow transplants.
- New research is exploring the potential of inducing ε-globin expression, which was previously thought non-inducible postnatally, as a way to improve treatment outcomes for these conditions.
- The review highlights the need for further research into the mechanisms of ε-globin silencing and suggests future drug development initiatives to harness its therapeutic benefits.
DNA methylation and mRNA expression correlations are often presented with inconsistent evidence supporting causal regulation. We hypothesized that causal regulatory methylation elements would exhibit heightened demethylation sensitivity. To investigate, we analyzed 20 whole-genomic bisulfite sequenced samples before and after demethylation and identified narrow-width (45-294 bp) elements within a short plateau, termed Methylation Mesa (MM).
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- * Recent studies indicate that a specific TE-derived gene, POGK, functions as a tumor suppressor in triple-negative breast cancer (TNBC) by interfering with the expression of ribosomal genes.
- * POGK’s deactivation occurs through isoform switching in patients with clinical TNBC, highlighting its importance in regulating tumor development.
Background: Asparaginases are a mainstay treatment for pediatric acute lymphoblastic leukemia (ALL). Recent reports identified hypoglycemia associated with asparaginases. Other reports describe hypoglycemia associated with 6-mercaptopurine (6-MP), another fundamental ALL therapy.
View Article and Find Full Text PDFImmunomodulatory imide drugs (IMiDs) degrade specific C2H2 zinc finger degrons in transcription factors, making them effective against certain cancers. SALL4, a cancer driver, contains seven C2H2 zinc fingers in four clusters, including an IMiD degron in zinc finger cluster two (ZFC2). Surprisingly, IMiDs do not inhibit growth of SALL4 expressing cancer cells.
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