Researchers led by a UCLA bioengineer have developed a therapy — based on two types of cells joined into a single unit — that could help strengthen existing treatments for acute myeloid leukemia. One of the cells is a blood platelet that carries a drug that attacks cancer cells; the other is a stem cell that guides the platelet into bone marrow, the spongy tissue inside bone where new blood cells are made and where leukemia begins. The researchers found that when injected into mice that had acute myeloid leukemia, the combination therapy halted the disease from developing any further. Of the mice that received the treatment, 87.5 percent were cured by 80 days after the combination cells were injected. Those mice also were all resistant to leukemia cells that were re-injected two months after the 80-day period.The study was published in Nature Biomedical Engineering.Zhen Gu, a professor of bioengineering at theUCLA Samueli School of Engineering who led the study, said the approach could be used in concert with other therapies, such as chemotherapy and stem cell treatment, to improve their effectiveness. Gu said the approach would have to be tested in human clinical trials and then approved for use before it could be incorporated in treatments for people with leukemia.Acute myeloid leukemia is a cancer that starts in bone marrow and affects the precursor stem cells to white blood cells, which are a key part of the immune system. The cancer can spread to the blo…
(University of Texas M. D. Anderson Cancer Center) A combination of the standard-of-care chemotherapy drug known as azacitidine, with nivolumab, an immune checkpoint inhibitor, demonstrated an encouraging response rate and overall survival in patients with relapsed or refractory acute myeloid leukemia (AML) according to findings from a Phase II study at The University of Texas MD Anderson Cancer Center.
In conclusion, the present study demonstrates the C/EBPα expression was correlated with CRT expression in vitro and in vivo and the molecular mechanism of DADS-induced leukaemic cell differentiation.
PMID: 30394654 [PubMed – as supplied by publisher]
Conclusion: The current study was designed to focus on the allosteric regulation (autoinhibition) of the of Shp2 protein. Subsequently, it will cover the last 10-year recap of Shp2 protein, their role in cancer, and regulation in numerous ways (allosteric regulation).
PMID: 30398108 [PubMed – as supplied by publisher]
The presence of internal tandem duplications (ITDs) in the FLT3 receptor tyrosine kinase gene have long been known to confer a poor prognosis to acute myeloid leukemia (AML) patients. Now, specific structural features of the ITD are also suggested to alter patient outcome, including sensitivity to targeted therapies, prompting their evaluation in therapeutic algorithms.
PMID: 30389660 [PubMed – as supplied by publisher]
This report provides a comprehensive assessment of recent tobacco-associated cancer incidence for each cancer type by sex, age, race/ethnicity, metropolitan county classification, tumor characteristics, U.S. census region, and state. These data are important for initiation, monitoring, and evaluation of tobacco prevention and control measures.
PERIOD COVERED: 2010-2014.
DESCRIPTION OF SYSTEM: Cancer incidence data from CDC’s National Program of Cancer Registries and the National Cancer Institute’s Surveillance, Epidemiology, and End Results program were used to calculate average annual age-adjusted incidence rate…
(UCLA Samueli School of Engineering) A cancer therapy based on fusing two types of cells into a single unit shows promise in strengthening existing treatments for acute myeloid leukemia. The approach joins blood platelets that carry cancer drugs with stem cells that guide the platelets into bone marrow where leukemia begins.
Pediatric Blood&Cancer, EarlyView.
Mutations affecting the spliceosomal protein U2AF1 are commonly found in myelodysplastic syndromes (MDS) and secondary acute myeloid leukemia (sAML). We have generated mice that carry Cre-dependent knock-in alleles of U2af1(S34F), the murine version of the most common mutant allele of U2AF1 encountered in human cancers. Cre-mediated recombination in murine hematopoietic…