Publications by authors named "C Demur"

Dendrogenin A (DDA) is a newly discovered cholesterol metabolite with tumor suppressor properties. Here, we explored its efficacy and mechanism of cell death in melanoma and acute myeloid leukemia (AML). We found that DDA induced lethal autophagy in vitro and in vivo, including primary AML patient samples, independently of melanoma Braf status or AML molecular and cytogenetic classifications.

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Long non-coding RNAs are defined as transcripts larger than 200 nucleotides but without protein-coding potential. There is growing evidence of the important role of long non-coding RNAs in cancer initiation, development and progression. In this study, we sought to evaluate the long non-coding RNA expression profile of patients with cytogenetically normal acute myeloid leukemia (AML).

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Optimal treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN), a rare entity of dismal prognosis previously described as CD4+/CD56+ hematodermic malignancies, is not defined. We report five cases of relapsed BPDCN treated with bendamustine hydrochloride, a well-tolerated bifunctional drug acting as an alkylating and antimetabolite agent. All patients were above the age of 50 years and in advanced disease (early first relapse in two, subsequent relapse in three; multi-organ involvement in four; previous intensive chemotherapy in five; and stem cell transplantation in four).

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Objectives: To assess the prevalence of tobacco consumption in patients with inflammatory arthritis treated in our department and to raise awareness against tobacco in order to reduce the maximum number of active smokers.

Method: A tobacco consumption survey was conducted to patients with inflammatory arthritis treated at the department of Rheumatology. Variables assessed: demographics, diagnosis, treatment, and current smoking.

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Article Synopsis
  • The study focuses on how the FLT3-ITD mutation in acute myeloid leukemia (AML) cells affects cell cycle regulation, particularly through the control of the CDC25A protein.
  • Upon inhibition of FLT3, CDC25A levels dropped quickly, revealing that its regulation is linked to FLT3-ITD signaling via STAT5.
  • CDC25 inhibitors not only halted cell growth and caused cell death in FLT3-ITD cells but also promoted differentiation, highlighting CDC25A as a potential therapeutic target in treating FLT3-ITD AML.
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