from yahoo board...
2014 Published Findings by Tefferi and Team
You may already be aware of:
Multivariable analysis distinguished CALR(-)ASXL1(+) mutational status as the most significant risk factor for survival: HR 3.7 vs 2.8 for age 65 years vs 2.7 for unfavorable karyotype. These observations signify immediate clinical relevance and warrant i) CALR and ASXL1 mutation screening in all patients with PMF and ii) molecular revision of DIPSS-plus.Leukemia accepted article preview online, 5 February 2014; doi:10.1038/leu.2014.57.
U2AF1 mutations in primary myelofibrosis are strongly associated with anemia and thrombocytopenia despite clustering with JAK2V617F and normal karyotype. Leukemia 2014]
Chronic neutrophilic leukemia with concurrent CSF3R and SETBP1 mutations: single colony clonality studies, in vitro sensitivity to JAK inhibitors and lack of treatment response to ruxolitinib. Leukemia. 2014 Jan 21. doi: 10.1038/leu.2014.39. [Epub ahead of print]
CALR mutation studies in chronic neutrophilic leukemia. Am J Hematol. 2014 Jan 13. doi: 10.1002/ajh.23665. [Epub ahead of print]
CALR vs JAK2 vs MPL-mutated or triple-negative myelofibrosis: clinical, cytogenetic and molecular comparisons. Leukemia. 2014 Jan 9. doi: 10.1038/leu.2014.3. [Epub ahead of print]
Drug-drug interaction between bosutinib and warfarin. Leuk Lymphoma. 2014 Jan 28. [Epub ahead of print]
----------------------------------------------------------------
Irish, tying Imetelstat success to genetic characteristics of each patient's mutation was expected by me. I wasn't sure Tefferi was doing that because I thought it was a bit too expensive for a study by Mayo where it did not have any funding help and as mayo is involved in many other such trials and studies to concentrate that much on Imetelstat. If he did that despite the financial difficulty (if any) or other resources-related restrictions, it shows how interested he and Mayo are in the success of Imetelstat. In my view, it's certainly a plus for Geron's effort to proceed with further studies to get the license. Thanks for posting the data.
----------------------------------------------------------------
Yes, Dr. Tefferi is definitely going to correlate genetic markers with imetelstat efficacy and identify the myelofibrosis patients for which it will work to achieve complete or partial remission.
To this extent, it is personalized medicine, and effective for a subset of myelofibrosis patients.
Imetelstat is also effective for essential thrombocythemia, and it may prove effective in combination with other drugs for solid tumors.
Imetelstat is not a "cure all" or "one size fits all" medicine, but it is a valuable therapy that will saves the lives of people for which it is effective. I look forward to it being on the shelf as soon as possible.
-------------------------------------------------------------------
The whole universe is changing with the discovery of God's particle (Higgs Boson). We finding out about black matter, and about speeds faster than light. This is the age of "The 3rd Industrial Revolution". Bio-discoveries and Imetelstat are part of that new science (which appears to be a miracle from God). Genetic codes and markers are a vital part of the Imetelstat discussion. Thanks to those that are helping the rest of us understand the implications.
"evil flourishes when good people fail to act"
