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Journal of Medical Oncology & Therapeutics | Volume 4
Oncology & Cancer Therapy
International Conference on
March 18-19, 2019 | London, UK
The JAK2V617F mutated trilinearmyeloproliferative neoplasms
include a broad spectrum of clinical laboratory and bone
marrow features in essential thrombocythemia, prodromal
polycythemia vera and erythrocythemic PV, classical PV
and advanced stages of masked PV and PV complicated by
splenomegaly and secondary myelofibrosis. Heterozygous
JAK2V617F mutated ET is associated with low JAK2 allele
and MPN disease burden and normal life expectance. In
combined heterozygous and homozygous or homozygous
JAK2V617F mutated trilinear MPN, the JAK2 mutation load
increases from less than 50% in prodromal and early stage
PV to above 50% up to 100% in classical PV, advanced PV and
PV with MF. Bone marrow histology features show various
degrees of diagnostic erythrocytic, megakaryocytic and
granulocytic myeloproliferation in JAK2V617F mutated trilinear
MPN clearly differ from monolinear megakaryocyticor dual
megakaryocytic granulocytic myeloproliferation in MPL or
calreticulin mutated thrombocythemia without features
of PV. The morphology of clustered large pleomorphic
megakaryocytes with hyperlobulated nuclei are similar in
JAK2V67F thrombocythemia, prodromal PV and classical PV
patients. Monolinear megakaryocytic myeloproliferation of
large to giant megakaryocytes with hyperlobulated staghorn
like nuclei is the hallmark of MPL515 mutated normocellular
thrombocythemia. CALR mutated thrombocythemia usually
presents with high platelet count around 1000x109/l and
normocellular megakaryocytic proliferation of immature
megakaryocyteswithcloud-likehyperchromaticnuclei followed
by dual megakaryocytic granulocytic myeloproliferation
followed by various degrees of bone marrow fibrosis. Natural
history and life expectancy of MPN patients are related to the
response to treatment and thedegreeof anemia, splenomegaly,
myelofibrosis and constitutional symptoms. The acquisition
of epigenetic mutations at increasing age on top of MPN
disease burden independently predict unfavorable outcome
in JAK2V617F , MPL515 and CALR mutated myeloproliferative
neoplasms, which mutually exclude each other.
Speaker Biography
Jan Jacques Michiels is a Lifestyle Physician and Medical Doctor, educated in Internal
Medicine, Hematology, blood coagulation and Vascular Medicine and graduated as PhD
at the Erasmus University Medical Center, Rotterdam. He frequently served as Guest
Editor and was the Founder and Editor in Chief of Seminars in Vascular Medicine. He is
the Founder of the Thrombocythemia Vera Study Group, the European Working Group
on Myeloproliferative Disorders and Myeloproliferative Neoplasms as scientific working
groups of the European Hematology Association. He is the founder of the Goodheart
Institute & Foundation in Nature Medicine & Health, Rotterdam, The Netherlands.
e:
Jan Jacques Michiels
Goodheart Institute, The Netherlands
Change of the 2008/16 WHO into 2018 clinical, laboratory, molecular and
pathobiological (WHO-CLMP) criteria for diagnosis of the meloproliferative neoplasms
JAK2 V617F trilinear polycythemia vera (PV), JAK2 exon 12 PV and JAK2V617F, CALR or
MPL515 mutated thrombocythemias and secondary myelofibrosis