期刊
CANCERS
卷 14, 期 4, 页码 -出版社
MDPI
DOI: 10.3390/cancers14040972
关键词
myeloproliferative neoplasms; JAK2; Aurora A; ROCK; drug resistance; cell signaling
类别
资金
- AIRC [IG 24930, 25254]
Aberrant signaling in myeloproliferative neoplasms can result from genetic alterations, and the cooperation between mutated and normal cells leads to persistent inflammation. Despite hopes for targeted therapies, these diseases remain incurable.
Aberrant signaling in myeloproliferative neoplasms may arise from alterations in genes coding for signal transduction proteins or epigenetic regulators. Both mutated and normal cells cooperate, altering fragile balances in bone marrow niches and fueling persistent inflammation through paracrine or systemic signals. Despite the hopes placed in targeted therapies, myeloid proliferative neoplasms remain incurable diseases in patients not eligible for stem cell transplantation. Due to the emergence of drug resistance, patient management is often very difficult in the long term. Unexpected connections among signal transduction pathways highlighted in neoplastic cells suggest new strategies to overcome neoplastic cell adaptation.
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