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During our third symposium, we bring together national and international acclaimed leukemia scientists to discuss recent advances in clonal hematopoiesis, low/high risk myelodysplastic syndrome, targeted AML therapy with emphasis in novel HMA plus BCL-2 inhibitor combination, advances in P53 myeloid malignancies therapies. During our 2021 symposium, we incorporate State-of- the-Art Lectures on post induction HMA treatment, mechanisms of FLT3 inhibition resistance and how to manage elderly AML patients. A highly interactive update on HMA plus BCL-2 inhibitor therapy will be followed by a panel discussion on post induction AML maintenance. Additionally, the symposium will provide important novel development in MDS and AML pathogenesis leading to unique opportunity for clinical trial design ideas.

TARGETED AUDIENCE

This course is designed for practicing hematologists, oncologists, physician assistants, basic scientists, nurse practitioners, registered nurses, hematology and oncology fellows, residents and students.

EDUCATIONAL OBJECTIVES

At the conclusion of the conference, participants should be able to:

• Describe the mechanisms leading to clonal hematopoiesis progression
• Compare laboratory and genomic factors that predict response to immunosuppressive therapy and thrombopoietin (TPO) mimetic
• Discuss how targeted therapy has improved the outcome of low risk myelodysplastic syndrome
• Predict the response to hypomethylating agent plus venetoclax based on genomic subtype
• Outline recent advances in tumor suppressor gene, TP53, acute myeloid leukemia (AML) therapy

ACCREDITATION

Baylor College of Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. Baylor College of Medicine designates this live activity for a maximum of 5.00 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

 For more information please visit the official event page.