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Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

Mutational profiling in myelofibrosis: implications for management.

Prithviraj Bose¹, Srdan Verstovsek²

¹Department of Leukemia, University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Unit 428, Houston, TX, 77030, USA.

International Journal of Hematology

|October 21, 2019

Summary

This summary is machine-generated.

Mutational profiling in myelofibrosis (MF) identifies key driver mutations like JAK2, MPL, and CALR. These genetic markers, along with others, impact prognosis and transplant decisions in MF patients.

Keywords:

Epigenetic JAK–STAT Mutations Myelofibrosis Splicing

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Database-guided Flow-cytometry for Evaluation of Bone Marrow Myeloid Cell Maturation

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Published on: November 3, 2018

Area of Science:

Hematology
Oncology
Molecular Biology

Background:

Myelofibrosis (MF) is a myeloproliferative neoplasm often associated with specific genetic mutations.
Mutational profiling is becoming standard for patients with primary MF (PMF) and secondary MF (post-PV/ET MF).

Purpose of the Study:

To review the role of mutational profiling in diagnosing and managing myelofibrosis.
To highlight the prognostic significance of various mutations in MF.
To discuss the implications of mutational status for treatment decisions, particularly for stem cell transplantation.

Main Methods:

Targeted next-generation sequencing (NGS) is the primary method for mutational profiling.
Analysis of mutations in genes including JAK2, MPL, CALR, ASXL1, EZH2, TET2, DNMT3A, SRSF2, U2AF1, and IDH1/2.

Main Results:

JAK2, MPL, and CALR mutations are the main "driver" mutations in most PMF and post-ET MF cases.
CALR type 1/-like mutations are associated with a favorable prognosis in PMF and post-ET MF.
Non-driver mutations (e.g., ASXL1, EZH2, TET2) are common and can indicate inferior survival, influencing prognostic models.
IDH1/2 mutations are more prevalent in blast phase MF and are therapeutically targetable.

Conclusions:

Mutational profiling is crucial for understanding MF pathogenesis and prognosis.
While not currently guiding drug choice in chronic-phase MF, high molecular risk genotypes inform transplant decisions.
Further research into CALR mutation subtypes and therapeutic targeting of mutations like IDH1/2 is ongoing.