Acute Leukemia

Rose-Inman, Hayley; Kuehl, Damon R.

doi:10.1016/j.hoc.2017.08.006

Cited by 50 publications

(32 citation statements)

References 74 publications

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“…Therefore, we speculate that these characteristics might be considered as the active groups of cassaine diterpenoid amide which Human leukemia is a malignant disorder of lymphoid progenitor cells that impacts both children and adults [19]. The prognosis of leukemia patients has improved over the past decades [20]. Among the treatments, chemotherapy is frequently used as a main therapy for leukemia [21].…”

Section: Resultsmentioning

confidence: 99%

Cassaine Diterpenoid Amide from Stem Bark of Erythrophleum fordii Suppresses Cytotoxic and Induces Apoptosis of Human Leukemia Cells

Nguyen

Cuong

et al. 2020

Molecules

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Cassaine diterpenoids amides from the stem bark of Vietnamese Erythrophleum fordii Oliver were screened for their cytotoxic activity against human cancer cells. The cell proliferation assay results showed that, among the active compounds, 3β-acetyl-nor-erythrophlamide (3AEP) exhibited the most potential cytotoxicity against human leukemia HL-60 and KG cells with IC50 values of 12.0 ± 1.2 and 18.1 ± 2.7 µM, respectively. Treatment of 3AEP resulted in the apoptosis of HL-60 cells via the activation of caspase 3, and poly (ADP-ribose) polymerase (PARP). Molecular docking in silico results showed that the 3AEP can bind to both the procaspase-3 allosteric site and the PARP-1 active site, with binding energies of −7.51 and −9.63 kcal/mol respectively. These results indicated that the stem bark of Vietnamese E. fordii and its cassaine diterpenoid amides may be useful in the apoptosis induction of human leukemia cancer cells.

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Section: Resultsmentioning

confidence: 99%

Cassaine Diterpenoid Amide from Stem Bark of Erythrophleum fordii Suppresses Cytotoxic and Induces Apoptosis of Human Leukemia Cells

Nguyen

Cuong

et al. 2020

Molecules

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“…With the advancement of chemotherapy regimens, the 5-year disease-free survival rate of pediatric T-ALL has substantially improved (11)(12)(13). However, the adverse effects of the high-intensity chemotherapy regimen are unfavorable, including liver and kidney damage, as well as severe infections secondary to bone marrow suppression (14,15). Hematopoietic stem cell transplantation may maximize the treatment efficiency of refractory ALL, but due to the shortage of donor sources and low degree of matching, as well as insufficient economic resources, its benefit is limited in the majority of cases of pediatric T-ALL (16,17).…”

Section: Introductionmentioning

confidence: 99%

Hirsutanol A inhibits T‑acute lymphocytic leukemia Jurkat cell viability through cell cycle arrest and p53‑dependent induction of apoptosis

et al. 2021

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Acute lymphocytic leukemia (ALL) is a type of childhood leukemia with the highest incidence; T-acute lymphocytic leukemia (T-ALL) is far more difficult to treat than B-acute lymphocytic leukemia (B-ALL) and has a poor long-term prognosis. Therefore, there is an urgent requirement to develop effective drugs for the treatment of T-ALL. Hirsutanol A is a natural sesquiterpenoid compound. The aim of the present study was to evaluate the in vitro anticancer activity of hirsutanol A against T-acute lymphocytic leukemia Jurkat cells and investigate the mechanism of action. A Cell Counting Kit-8 assay demonstrated that hirsutanol A inhibited the viability of Jurkat cells in a dose-and time-dependent manner. In addition, hirsutanol A induced cell cycle arrest at the G 2 phase as determined via flow cytometry. Furthermore, Hoechst staining, Annexin V-FITC/propidium iodide double staining, mitochondrial membrane potential detection using JC-1 and western blot analysis of apoptotic proteins indicated that the inhibitory effect of hirsutanol A on Jurkat cells was associated with the induction of apoptosis. Of note, hirsutanol A induced the expression of the tumor suppressor p53, whereas simultaneous treatment with pifithrin-α, an inhibitor of p53, significantly reduced Jurkat cell apoptosis induced by hirsutanol A. In summary, the present study suggested that hirsutanol A inhibited Jurkat cell viability through induction of cell cycle arrest and p53-dependent initiation of apoptosis, thus hirsutanol may serve as a promising compound for the treatment of T-ALL. By screening a natural compound library owned by State Key Laboratory of Quality Research in Chinese Medicine (Macau, China), it was revealed that hirsutanol A exerted a clear inhibitory effect on the viability of the T-ALL cell line Jurkat. Hirsutanol A is a sesquiterpenoid compound initially

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“…In general, acute leukemia develops with symptoms accompanying pancytopenia, such as anemia, bleeding tendency and febrile neutropenia ( 1 ). It is therefore possible to miss leukemia if other organ symptoms are dominant.…”

Section: Introductionmentioning

confidence: 99%

Acute Myeloid Leukemia Developing with Acute Pancreatitis Mimicking Autoimmune Pancreatitis

et al. 2021

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A 33-year-old man was admitted to our hospital for fever and abdominal pain. A blood analysis revealed pancytopenia and increased serum pancreatic enzymes with disseminated intravascular coagulation. A detailed examination revealed acute pancreatitis, with diffuse swelling of the pancreas and diffuse beaded dilatation of the main pancreatic duct, which mimicked autoimmune pancreatitis complicated by acute myeloid leukemia. Systemic cytotoxic chemotherapy led to the remission of leukemia and pancreatitis. We hypothesized that the etiology of acute pancreatitis was invasion of leukemia cells. Acute pancreatitis is rare as a symptom of leukemia; however, we should consider the possibility of leukemia during the differential diagnosis of acute pancreatitis.

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Acute Leukemia

Cited by 50 publications

References 74 publications

Cassaine Diterpenoid Amide from Stem Bark of Erythrophleum fordii Suppresses Cytotoxic and Induces Apoptosis of Human Leukemia Cells

Cassaine Diterpenoid Amide from Stem Bark of Erythrophleum fordii Suppresses Cytotoxic and Induces Apoptosis of Human Leukemia Cells

Hirsutanol A inhibits T‑acute lymphocytic leukemia Jurkat cell viability through cell cycle arrest and p53‑dependent induction of apoptosis

Acute Myeloid Leukemia Developing with Acute Pancreatitis Mimicking Autoimmune Pancreatitis

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