16th Annual John Goldman Conference on Chronic Myeloid Leukemia: Biology and Therapy

Philadelphia, PA US
September 4, 2014 to September 7, 2014


Improved knowledge of the biology underlying CML has revolutionized the clinical management of the disease and introduced new therapeutic perspectives. Imatinib a direct BCR-ABL kniase inhibitor leads to durable cytogenetic remissions and improved survival. However many patients with CME are slow responders or develop resistance. Although monitoring is recognized as necessary, when adherence to guidelines deficient. The treatment goals and the significance of deeper mlecular response is still being debated. Second-generation TKIs including 2 FDA approved agents are available to overcome Bcr-Abl1 kinase domain mutations. Even so many patients fail subsequent treatment with these agents, as they can develop highly resistant mutations such as T315I. Newer data on the upfront use of newer second generation TKIs is changing the paradigm of CML therapy further and creating the need for newer modalities that can address resistance to these agents. We have also become aware of long-term adverse events of TKI creating a growing interest in treatment discontinuation. 

ACCME Accreditation Statement:
The Medical College of Wisconsin is accredited by the Accreditation Council for Continuing Medial Educaiton to provide ocntinuing medical education for physicians.

AMA Credit Designation Statement:
The Medical College of Wisconsin designates this live activity for a maximum of 23.35 AMA PRA Category 1 Credits
. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Hours of Participation for Allied Health Care Professionals:
The Medical College of Wisconsin designates this activity for up to 23.25 hours of participation for continuing education for allied health care professionals.



Target Audience

Physicians & Allied Health Care Professionals

Learning Objectives

1.  Understand something of the origin of the BCR-ABL fusion gene, the signal transduction pathways involved in producing the clinical picture of chronic myeloid leukemia (CML) and the mechanisms of action of tyrosine kinase inhibitors.

2.  Have some insight into the possible mechanisms of genomic instability that predisposes to formation of the BCR-ABL fusion gene and predisposes also to disease progression.

3.  Define a leukemia stem cell and its relationship to disease kinetics in so far as current knowledge permits.

4.  Discuss the role of the microenvironment and epigenetic mechanisms in the genesis and progression of CML.

5.  Evaluate the merits of various management decisions, eg., how to start treatment for patients in the different phases of CML, how to  assess success or failure of initial treatment, what approaches to consider for patients who have failed to respond well to initial treatment, including assessing the precise role of second generation TKIs and other non-molecular therapeutic approaches.

6.  Review new modalities of monitoring and mutation assessment and update the current understanding of proper monitoring, clinical significance of monitoring results at different time points, and the importance of timely assessments in the proper management of CML.

7.  Assess the role of allogeneic stem cell transplantation in the management of CML in 2014.

8.  Critically evaluate the possible role of the different immunotherapeutic approaches in the treatment of CML.

Additional information


D'Etta Waldoch, CMP
Phone Number: 
+1 (262) 827-4996
Course summary
Available credit: 
  • 23.25 AMA PRA Category 1 Credit(s)™
    AMA PRA Category 1 Credit(s)™
Course opens: 
Course expires: 
Event starts: 
09/04/2014 - 7:00am CDT
Event ends: 
09/07/2014 - 5:00pm CDT
Loews Philadelphia Hotel
1200 Market Street
Philadelphia, PA 19107
United States

Parameswaran Hari, MD, MRCP, MS


All persons in control of content have no relevant financial relationships to disclose.

Available Credit

  • 23.25 AMA PRA Category 1 Credit(s)™
    AMA PRA Category 1 Credit(s)™


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