Over the past few years, the use of targeted therapies has proven effective for various forms of hematological neoplasia, and increasingly become routine. The rational molecular design of such active substances allows for the targeted blocking of intracellular signal chains in malignant cells, resulting e.g. in cell cycle arrest or ideally apoptosis.
Unfortunately, resistance occurs even against such tailored therapies. It has increasingly become possible to explain their molecular mechanisms. For one, under therapy are a growing number of new mutations in various target genes of targeted drugs or in the genes of associated molecular pathways which could lead to a loss of effectiveness.
The targeted analysis of such resistance mutations can, particularly in the event of the absence of a response or a decreasing response, be proof of potential drug resistance and provide a rationale for the modification of the therapy. Naturally, patient compliance should be ensured before this is done.
Accordingly, MLL strives to offer the analysis of such resistance mutations in the target genes of various active substances according to the state of the art, and recently expanded its portfolio to this effect.
Currently, the following analyses are being offered in this context:
- IDH2 mutations for Enasidenib resistance in AML
- BCR-ABL1 mutations for resistance to common tyrosine kinase inhibitors or against the new allosteric Abl inhibitor Asciminib in CML and ALL
- BCL2 mutations for Venetoclax resistance (e.g. in CLL, mantle cell lymphoma and follicular lymphoma)
- BTK mutations and PLCG-2 mutations for Ibrutinib resistance in CLL
On our order form (current version at www.mll.com), these analyses can be found under the sections for the respective disease. The same applies for our digital order entry system. Please feel free to contact us for any suggestions or questions regarding this.