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Background: This study investigated the role of cyclin-dependent kinase 9 (CDK9) expression levels and prognosis in acute myeloid leukemia (AML) by examining its expression at the time of initial diagnosis.
Methods: Bone marrow samples from 60 AML patients were collected for the observation group, with 20 normal human bone marrow samples serving as controls. Clinical and pathological data were gathered from the AML pa-tients. Real-time quantitative PCR (RT-qPCR) was employed to measure CDK9 expression levels in both groups, and the association between CDK9 expression, clinical characteristics, and prognosis in AML patients was analyzed. Kaplan-Meier curves were used to assess the impact of CDK9 on overall survival (OS) in AML, while Cox regression analysis was performed to identify prognostic factors in AML patients.
Results: The expression of CDK9 was significantly elevated in AML patients, compared to the control group (p < 0.05). High CDK9 expression was associated with increased white blood cell (WBC) count, poor treatment response, and worse prognosis compared to low expression (p < 0.05). Additionally, patients with high CDK9 expression exhibited significantly shortened OS compared to those with low expression (p < 0.05). High CDK9 expression emerged as an independent risk factor influencing prognosis in AML.
Conclusions: CDK9 is markedly upregulated in AML patients, suggesting its potential utility as both a prognostic indicator and a therapeutic target, particularly for patients with unfavorable clinical and pathological characteristics and poor prognosis.
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http://dx.doi.org/10.7754/Clin.Lab.2024.240416 | DOI Listing |
Theranostics
August 2025
State Key Laboratory of Membrane Biology, School of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing, 100084, China.
Despite advancements in EGFR- and KRAS-targeted therapies for lung adenocarcinoma (LUAD), novel targets are needed for patients unresponsive or resistant to current treatments. This study demonstrates the critical role of CREPT in modulating ERK-downstream gene transcription in LUAD progression. CREPT expression and function were investigated using human LUAD tissues, EGFR/KRAS mutant LUAD cell lines, and mouse models.
View Article and Find Full Text PDFMol Cell
September 2025
The Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC 3052, Australia; Peter MacCallum Cancer Centre, Laboratory Research Division, Parkville, VIC 3052, Australia. Electronic address:
Controlled gene expression is achieved through the intricate regulation of RNA polymerase II (Pol II) progression through transcription-cycle checkpoints. While the contribution of CDK9 for Pol II pause-release is well established, the requirement for other cyclin-dependent kinases (CDKs) has not been fully elucidated. In this study, we propose a critical role for CDK11 in the Pol II pausing-to-elongation transition at a checkpoint that precedes and is independent from CDK9.
View Article and Find Full Text PDFEur J Pharmacol
August 2025
Department of Translational Orthopedic Research, Houston Methodist Research Institute, Houston, TX, 77030, USA; Orthopedics & Sports Medicine, Houston Methodist Hospital, Houston, TX, 77030, USA. Electronic address:
Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive lung disease with limited therapeutic options. Cyclin-dependent kinase 9 (CDK9), a key transcriptional regulator, has been implicated in fibrotic diseases, but no therapies targeting CDK9 have been developed for IPF. This investigation found that CDK9 expression was significantly elevated in IPF lung fibroblasts, correlating with an enhanced fibrogenic transcriptional profile and phenotype.
View Article and Find Full Text PDFBlood Neoplasia
August 2025
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.
The antiapoptotic protein myeloid cell leukemia 1 (Mcl-1) promotes cell survival in acute myeloid leukemia (AML), and its overexpression is associated with resistance to venetoclax. Voruciclib, an oral cyclin-dependent kinase 9 inhibitor, indirectly decreases Mcl-1 protein expression and has synergistic activity with venetoclax in AML preclinical models. We hypothesized that voruciclib in combination with venetoclax would induce responses in patients with AML with disease progression after venetoclax therapy.
View Article and Find Full Text PDFCancer Cell Int
July 2025
Cancer Research Institute, Seoul National University, Seoul, Republic of Korea.
Background: Cyclin-dependent kinase 9 (CDK9) is a crucial regulator of transcriptional progression of RNA polymerase-II (RNAP2). RNA polymerases trapped in DNA can be a source of transcription-replication conflict (T-R conflict), which is a common source of replication stress. AZD4573, a highly selective CDK9 inhibitor, has been shown to induce apoptosis in leukemia cell lines, while its anti-tumor potential in breast cancer has yet to be elucidated.
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