Case reports in hematology · 2026
Development of Colonic Polyposis in a Woman With Chronic Myeloid Leukemia Treated With Dasatinib.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Pelaez Guido, Yildiz Behram Suha, Candan Mert, Ismail Mohammad, Vacca Francesca, Ruzinova Marianna B, Ballentine Samuel, Byrnes Kathleen, Ghobadi Armin
Аннотация
INTRODUCTION: Chronic myeloid leukemia (CML) is a hematopoietic malignancy driven by constitutive tyrosine kinase activity. Dasatinib, a second-generation (2G) tyrosine kinase inhibitor (TKI), is a preferred treatment due to its superior, durable, and rapid response rates. While dasatinib has known gastrointestinal (GI) side effects, colonic polyposis is a rare complication, not well described in the literature.
CASE PRESENTATION: Upon routine colonoscopy, a 66-year-old woman with chronic-phase CML was incidentally discovered to have asymptomatic colonic polyposis after 11 months of dasatinib therapy. Histopathology revealed reactive inflammatory changes without evidence of dysplasia or neoplasia. The polyposis resolved completely after cessation of dasatinib.
CONCLUSION: The mechanism behind dasatinib-induced polyposis is unclear. We hypothesize a role of dasatinib's differential inhibition of multiple kinase pathways, regulatory T cells, and STAT5 signaling in the intestinal epithelium, causing an unregulated inflammatory state. This case underscores the need for awareness of this rare adverse effect and further research into its pathogenesis.
CASE PRESENTATION: Upon routine colonoscopy, a 66-year-old woman with chronic-phase CML was incidentally discovered to have asymptomatic colonic polyposis after 11 months of dasatinib therapy. Histopathology revealed reactive inflammatory changes without evidence of dysplasia or neoplasia. The polyposis resolved completely after cessation of dasatinib.
CONCLUSION: The mechanism behind dasatinib-induced polyposis is unclear. We hypothesize a role of dasatinib's differential inhibition of multiple kinase pathways, regulatory T cells, and STAT5 signaling in the intestinal epithelium, causing an unregulated inflammatory state. This case underscores the need for awareness of this rare adverse effect and further research into its pathogenesis.