The Modelled Effectiveness of Ruxolitinib on Survival in Polycythemia Patients with Hydroxyurea Resistance/Intolerance in Turkey

Büyükaşık, Yahya; Haznedaroğlu, İbrahim C.; Özet, Gülsüm; Ar, Muhlis Cem; Ozcan, MA; Güvenç, Birol; Yaşar, Nurgül; Parali, E; Ozkan, Beyza Nur; Özdemir, Oktay

doi:10.1016/j.jval.2017.08.832

Cited by 1 publication

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“…Hence, we fully agree with Porpaczy et al that the detection of a preexisting B-cell clone may identify individuals at risk for lymphoma development and any ruxolitinib candidate should undergo a bone marrow biopsy procedure for the evaluation of clonal lymphoid baseline proliferation (6). This suggestion is particularly helpful for early stage myelofibrosis or PV since those patients potentially have decades for survival (7,18,19). Ruxolitinib is administered for PV just for the control of symptoms, but if lymphoma due to ruxolitinib complicates the clinical picture, the survival could be decreased from about two decades to several months in a given PV patient.…”

Section: Discussionsupporting

confidence: 82%

“…Table 3 summarizes the list of genes present in lymphoid cancer stem cells that were affected by ruxolitinib usage and their clinical correlations. Thus, ruxolitinib may potentially lead to the pathological expression of the transcription factors important in lymphomagenesis, neoplastic commitment on the progenitor lymphoid cells, inhibition of repressor transcriptions protective for lymphoma development, inhibition of apoptosis, promotion of neoplastic proliferation, transcriptional (7,18,19). Ruxolitinib is administered for PV just for the control of symptoms, but if lymphoma due to ruxolitinib complicates the clinical picture, the survival could be decreased from about two decades to several months in a given PV patient.…”

Section: Discussionmentioning

confidence: 99%

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The impact of JAK/STAT inhibitor ruxolitinib on the genesis of lymphoproliferative diseases

Turk¹,

Okay²,

Turk³

et al. 2019

Turk J Med Sci

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Background/aim: Ruxolitinib, a JAK/STAT signaling pathway inhibitor targeted drug, has been approved for the controlling of disease symptoms and splenomegaly in patients with myeloproliferative neoplastic diseases. Recently, it has been proposed that ruxolitinibinduced JAK/STAT pathway inhibition in myelofibrosis is associated with an elevated frequency of aggressive B-cell lymphomas. However, the biological basis and significance of this pharmacobiological adverse event is unknown. The aim of this bioinformatics study is to detect any possible confounding effects of ruxolitinib on the genesis of lymphoproliferative disorders. Materials and methods: The gene expression data were retrieved from the E-MTAB-783 Cancer Genome Project database. Gene expression data for all available genes in 26 cell lines belonging to various types of lymphomas were chosen for use in this in silico analysis. Results: We identified genes that were significant in developing resistance to ruxolitinib in lymphoma cell lines. Conclusion: Based on the results of our present study, ruxolitinib may potentially lead to the pathological expression of the transcription factors important in lymphoma genesis, neoplastic commitment on the progenitor lymphoid cells, inhibition of repressor transcriptions protective for lymphoma development, inhibition of apoptosis, promotion of neoplastic proliferation, transcriptional activation, and proliferation of malignant neoplastic B cells.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%