Leukemia, Lymphoma and Myeloma: Targeted Therapy

Bernhard Lammle^*
*Correspondence: Bernhard Lammle, Department of Haematology, School of Clinical Sciences at Monash Health, Monash University, Australia, Email:

Editorial

Most improvements in cancer therapy have been pioneered by professionals who treat blood illnesses in the past. The use of radiotherapy in Hodgkin disease, the use of aminopterin to treat childhood lymphoblastic leukaemia, the discovery of the Philadelphia chromosome, identification of the translocation involving the ABL oncogene and targeting of the ABL tyrosine kinase in CML, monoclonal antibodies to target B cell lymphoma and leukaemia, proteasome inhibitors in myeloma, and the development of drugs that promote. While traditional cytotoxic chemotherapy continues to assist many patients, it is clear that additional advancements are unlikely to be achieved with current cytotoxic drugs, and that progress will be based on our understanding of tumour biology and immunology

Several medicines are now available that target specific genes and proteins involved in cancer cell growth and survival. This shift is especially noticeable in lymphoma, leukaemia, and myeloma, where treatments targeting Bruton tyrosine kinase, phosphatidylinositol 3-kinase, B-cell lymphoma 2, the proteasome, and the ubiquitin E3-ligase cereblon are currently available in clinics. Second-generation CD20 antibodies, bi-specific antibodies and T-cell engagers, chimeric antigen receptor T-cells, and treatments acting on important immunological checkpoints such as programmed cell death protein 1 have all been developed as a result of the immune system's role in tumour eradication (PD1). In some haemopoietic malignancies, agents that affect DNA methylation or histone protein modification are also active.

Cancer progress is slow, and despite the fact that many cancers share basic characteristics, each tumour is distinct. A single loss of a regulatory gene can have a significant impact on therapeutic responsiveness. While patients are physiologically identical, drug pharmacokinetics and pharmacodynamics vary widely, with efficacy and tolerability influenced by age, comorbidity, past therapy, and drug–drug interactions.

BCL2 inhibitors in B cell non-Hodgkin lymphoma, Multiple Myeloma, Chronic Lymphocytic Leukaemia, and Acute Myeloid Leukaemia]; hypomethylating agents in T cell lymphoma and Acute Myeloid Leukaemia]; BTK inhibitors in Chronic Lymphocytic Leukaemia and B cell lymphoma; Cereblon-Interacting Small Molecules in Folli Monoclonal antibodies and their derivatives are used in a variety of blood malignancies, including Acute Myeloid and Lymphocytic Leukemia, B-cell and T-cell Lymphoma, and Myeloma. Several of these drugs have been shown to be more effective than traditional chemoimmunotherapy, although they are not without danger.

Many more targets will be discovered as our understanding of tumour biology improves; however, much of the future debate will revolve around therapy sequencing, identification of rational combinations, the benefits of fixed duration versus continuously administered therapy, long-term toxicity, and cost With substantial paradigm shifts in therapy for leukaemia, lymphoma, and myeloma, it's tough to editorialise this issue due to its range of information. Although patient outcomes for blood cancers appear to be improving, more work remains to be done in order to determine the best therapy methods for a wide range of blood cancers in a diverse group of patients [1-5].

References

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3. Di Ciaccio, Pietro, Georgia McCaughan, Judith Trotman and Phoebe Joy Ho, et al. "Australian and New Zealand consensus statement on the management of lymphoma, chronic lymphocytic leukaemia and myeloma during the COVID‐19 pandemic."Inter Med J50 (2020): 667-679.

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5. Kong, Jung Hee, Youmi Hu, Sun‐Young Kong and Se‐Na Lee, et al. "Analysis of laboratory parameters for optimal autologous peripheral blood stem cell collection from lymphoma and myeloma patients." J Clin Apher 36 (2021): 135-142.

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