?? Exploring Decitabine's Efficacy in DLBCL: Experimental Insights & Challenges

As part of my dissertation, I experimented to examine the effects of the hypomethylating agent decitabine on the KIS-1 cell line of Diffuse Large B-cell Lymphoma (DLBCL). My goal was to understand why this agent's efficacy is limited in certain DLBCL subtypes. However, the results were surprising! ??

The KIS-1 cell line comprises two serotypes, and intriguingly, the Germinal Center B-cell-like (GCB) subtype showed no significant response to decitabine. This brings forward the complex nature of DLBCL treatment, where different subtypes of the disease respond differently to therapies.

So, why is decitabine not practical for GCB-DLBCL? ??

One possible explanation is the epigenetic resistance mechanisms that vary between subtypes. While decitabine acts by inhibiting DNA methyltransferase (DNMT) enzymes to induce hypomethylation and reactivate silenced tumour suppressor genes, several factors may interfere:

• Reduced DNMT activity in the GCB subtype could mean less target availability for decitabine to exert its effects.
• Distinct methylation patterns in GCB-DLBCL might make this subtype less susceptible to decitabine-induced changes, limiting its therapeutic potential.

These results highlight the need for a deeper understanding of DLBCL heterogeneity and epigenetic landscapes to develop effective, targeted treatments. While the experiment didn't yield the expected outcomes, it raises critical questions about resistance mechanisms and the importance of personalized medicine approaches in hematologic malignancies.

The journey continues in uncovering the complexities of cancer biology to drive better outcomes for patients! ????

#CancerBiology #Epigenetics #DLBCL #Decitabine #HematologyResearch #PrecisionMedicine #BiomedicalScience