# JAK2 as Predictor of Therapeutic Response in Patients with Chronic Myeloid Leukemia Treated with Imatinib

**Authors:** Indra Wijaya, Muhammad H. Bashari, Lelani Reniarti, Anita Rahmawati, Rully M. A. Roesli

PMC · DOI: 10.1155/2024/2906566 · Disease Markers · 2024-04-12

## TL;DR

This study shows that lower JAK2 levels in patients with chronic myeloid leukemia are linked to better responses to imatinib treatment.

## Contribution

The study identifies JAK2 as a potential predictor of therapeutic response to imatinib in CML patients.

## Key findings

- Baseline JAK2 levels were significantly lower in patients achieving complete hematological and early molecular responses.
- JAK2 gene expression and protein levels were negatively correlated with treatment response outcomes.
- JAK2 may serve as a potential biomarker for evaluating imatinib efficacy in CML.

## Abstract

Chronic myeloid leukemia (CML) or chronic granulocytic leukemia is a myeloproliferative neoplasm indicated by the presence of the Philadelphia (Ph+) chromosome. First-line tyrosine kinase inhibitor, imatinib, is the gold standard for treatment. However, there has been known unresponsiveness to treatment, especially due to the involvement of other genes, such as the Janus kinase 2 (JAK2) gene. This study aimed to evaluate the relationships between JAK2 levels and complete hematological response (CHR), as well as early molecular response (EMR) after 3 months of imatinib treatment in patients with chronic phase CML.

Patients with Ph+ CML in the chronic phase (n = 40; mean age, 40 ± 11 years) were recruited to complete assessments consisting of clinical examination and blood test, including evaluation of complete blood counts and the JAK2 levels, at baseline and following 3 months of therapy with imatinib (at an oral dose of 400 mg per day). Subjects were divided into two groups according to the presence of CHR and EMR.

JAK2 gene levels, phosphorylated, and total JAK2 proteins at baseline were significantly lower in the group with the presence of CHR and EMR. In addition, baseline JAK2 levels, including JAK2 gene expression, phosphorylated, and total JAK2 proteins, were negatively correlated with the presence of CHR and EMR.

Based on these findings, JAK2 levels may be a potential indicator for evaluating treatment response on imatinib due to its role in the pathophysiology of CML.

## Linked entities

- **Genes:** JAK2 (Janus kinase 2) [NCBI Gene 3717]
- **Chemicals:** imatinib (PubChem CID 5291)
- **Diseases:** Chronic myeloid leukemia (MONDO:0011996), CML (MONDO:0011996)

## Full-text entities

- **Genes:** TXK (TXK tyrosine kinase) [NCBI Gene 7294] {aka BTKL, PSCTK5, PTK4, RLK, TKL}, JAK2 (Janus kinase 2) [NCBI Gene 3717] {aka JTK10}
- **Diseases:** myeloproliferative neoplasm (MESH:D009369), CML (MESH:D015464), Ph+ (MESH:D010677)
- **Chemicals:** Imatinib (MESH:D000068877)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

52 references — full list in the complete paper: https://tomesphere.com/paper/PMC11074917/full.md

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Source: https://tomesphere.com/paper/PMC11074917