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Emerging therapeutic targets in myeloproliferative neoplasms and peripheral T-cell leukemia and lymphomas
Anna Orlova1,2, Bettina Wingelhofer1,2, Heidi A Neubauer1,2
1a Institute of Animal Breeding and Genetics , University of Veterinary Medicine Vienna , Vienna , Austria.
Introduction:
Hematopoietic neoplasms are often driven by gain-of-function mutations of the JAK-STAT pathway together with mutations in chromatin remodeling and DNA damage control pathways. The interconnection between the JAK-STAT pathway, epigenetic regulation or DNA damage control is still poorly understood in cancer cell biology. Areas covered: Here, we focus on a broader description of mutational insights into myeloproliferative neoplasms and peripheral T-cell leukemia and lymphomas, since sequencing efforts have identified similar combinations of driver mutations in these diseases covering different lineages. We summarize how these pathways might be interconnected in normal or cancer cells, which have lost differentiation capacity and drive oncogene transcription. Expert opinion: Due to similarities in driver mutations including epigenetic enzymes, JAK-STAT pathway activation and mutated checkpoint control through TP53, we hypothesize that similar therapeutic approaches could be of benefit in these diseases. We give an overview of how driver mutations in these malignancies contribute to hematopoietic cancer initiation or progression, and how these pathways can be targeted with currently available tools.
Insights
Hematopoietic neoplasms like myeloproliferative neoplasms and T-cell lymphomas share common driver mutations. Targeting interconnected JAK-STAT, epigenetic, and DNA damage pathways offers potential therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Hematopoietic neoplasms frequently involve mutations in the JAK-STAT pathway, chromatin remodeling, and DNA damage control.
- The interplay between these pathways in cancer cell biology remains incompletely understood.
- Recent sequencing efforts reveal shared driver mutations across diverse hematopoietic malignancies.
Purpose of the Study:
- To explore mutational insights into myeloproliferative neoplasms and peripheral T-cell leukemia/lymphomas.
- To summarize the interconnectedness of JAK-STAT, epigenetic, and DNA damage pathways in normal and cancer cells.
- To provide an overview of how these mutations drive cancer initiation and progression.
Main Methods:
- Review of sequencing data identifying common driver mutations.
- Analysis of pathway interconnections in normal and malignant hematopoietic cells.
- Literature review on current therapeutic tools targeting these pathways.
Main Results:
- Identified similar combinations of driver mutations in myeloproliferative neoplasms and T-cell leukemias/lymphomas.
- Highlighted the role of these pathways in loss of differentiation and oncogene transcription.
- Demonstrated the contribution of driver mutations to cancer initiation and progression.
Conclusions:
- Similarities in driver mutations (epigenetic enzymes, JAK-STAT activation, TP53 mutations) suggest shared therapeutic vulnerabilities.
- Hypothesized that comparable therapeutic approaches could benefit patients across these distinct malignancies.
- Outlined strategies for targeting these interconnected pathways with existing tools.
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