Evaluation of immunohistochemical and gene expression of Janus kinase1 and Janus kinase3 in the skin of different clinical types of mycosis fungoides patients – Part II: reverse transcriptase–polymerase chain reaction

TL;DR

This study found that JAK1 and JAK3 genes are overactive in skin samples from mycosis fungoides patients, suggesting they may contribute to the disease and could be targets for treatment.

Contribution

The study provides new evidence on the role of JAK1 and JAK3 gene expression in different stages of mycosis fungoides.

Findings

JAK1 and JAK3 were significantly upregulated in lesional MF skin compared to healthy controls.

JAK1 showed higher upregulation in early-stage MF than JAK3.

The findings suggest JAK1 and JAK3 inhibitors could be potential treatments for MF.

Abstract

Mycosis Fungoides (MF) is the commonest type of primary cutaneous T-Cell lymphomas representing about 50% of all lymphomas arising primarily in the skin. Janus kinases are non-receptor intracellular tyrosine kinases that play an important role in the pathogenesis of variant skin disorders and several hematological malignancies.

The aim of this study was to investigate the gene expression of Janus Kinase-1 (JAK1) and Janus Kinase-3 (JAK3) in the skin of different types of MF patients using Real-time Quantitative Reverse Transcription Polymerase Chain Reaction (RT-PCR).

The current study included 53 patients with MF, and 53 control samples. RT-PCR for JAK1 and JAK3 was done in the skin specimens obtained from patients and controls.

Both JAK1 and JAK3 fold changes showed stepwise upregulation in lesional MF skin than normal control skin, with statistically significant increase in MF patients than healthy controls (p < 0.001 and < 0.001 respectively). JAK1 was significantly upregulated in early-stage MF than JAK3 (p < 0.001).

Limitations of this study include the small sample size of some mycosis fungoides variants, such as erythrodermic MF. Further studies are needed to clarify the functional role of Janus kinase signaling pathways in MF pathogenesis.

Both JAK1 and JAK3 play a role in the pathogenesis of MF. JAK1 may have a pathogenic role, particularly in the early stage of cutaneous T-cell lymphoma. This potentiates the idea of using JAK1 and JAK3 inhibitors for MF treatment.

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