Medicines

In brief: Cellular model tracks evolution of AML; Trial identifies optimum time to review patients on warfarin; Fibrinogen has an anti-inflammatory role

Thursday, 11 Feb 2021


Cellular model tracks the evolution of leukaemia

Scientists have built the first cellular model to depict the evolution of acute myeloid leukaemia, from its early to late stages using gene editing technology.

Using CRISPR gene editing the researchers altered DNA sequences in induced pluripotent stem cells to create a model that showed progressive malignant features that correspond to their human counterparts in myeloid disease.

“By creating the first cellular model to track the evolution of human leukaemia, we believe we’ve taken an important step toward unraveling the cellular biology of this disease. We’ve identified molecular vulnerabilities that occur early in the disease process which could potentially lead to improved biomarkers and novel treatments for AML–goals that have proven so elusive to medical science in the past,” the authors from the Icahn School of Medicine at Mount Sinai said.

The study is published in Cell Stem Cell.


Trial identifies optimum time to review patients on warfarin 

The majority of patients can achieve a stable TiTR above 65% within six months, a study reports.

The retrospective Australian study of 566 patients found patients had a Time in therapeutic range (TiTR) of 64.9±16.5% at month three and median TtSTR of six months.

Patients with mean time to stable therapeutic range (TtSTR) of ≤6 months achieved a mean TiTR of 68.9±12.8% at month two and maintained a TiTR over 75% from month 3 to 24. Patients with a TtSTR>6 months obtained a TiTR of 66.4±10.6% at month nine and continued to achieve lower TiTR throughout the 24 months study period. On the basis of their findings the authors suggest that clinicians review their patients at 6 to 9 months to determine if they need to switch to a different anticoagulant.


Fibrinogen has an anti-inflammatory role

Fibrinogen can act as an antioxidant in blood plasma by protecting against hypochlorite, a chemical created by the body in response to inflammation, researchers report.

The study published in Redox Biology found that the protein doesn’t harm cells in the same way as hypochlorite-modified albumin which can exacerbate conditions like kidney and heart disease.

“When we figure out precisely how these distinctly different protein molecules behave, then it might be possible to block the disease-promoting activities of hypochlorite-modified albumin using drugs,” says the Flinders University research group.

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