News by Subject Medicine & Health

Oncotarget Volume 11, Issue 12 reported outside its natural niche, the cultured prostate cancer stem cells lost their tumor-inducing capability and stem cell marker expression after approximately 8 transfers at a 1:3 split ratio.

Oncotarget Volume 11, Issue 12 reported that using the HL-60 human non-APL AML model where ATRA causes nuclear enrichment of c-Raf that drives differentiation/G0-arrest, the research team now observe that roscovitine enhanced nuclear enrichment of certain traditionally cytoplasmic signaling molecules and enhanced differentiation and cell cycle arrest.

With so much genetic information packed in such a tiny space, how cells access DNA when it needs it is something of a mystery. Research published today by Professor Joel Mackay and colleagues has revealed the role played by motor protein CHD4 that allows the DNA to remodel when the information is needed -- and it will help us understand diseases connected to when that process goes wrong.

Oncotarget Volume 11, Issue 11 reported that relapsed APL, particularly in the high-risk subset of patients, remains an important clinical problem. The probability of relapse is significantly higher in the high-risk subset of patients undergoing treatment for APL; overall approximately 10-20% of APL patients relapse regardless of their risk stratification.

Oncotarget Volume 11, Issue 11 reported that at clinical progression, 64 EGFR T790M plasma positive patients were subjected to second line-treatment with osimertinib and strictly monitored during the first month of therapy. Plasma analysis by the EGFR Cobas test showed in 57 cases a substantial decrease in the levels of the sensitizing EGFR mutant allele, down to a not detectable value.

Oncotarget Volume 11, Issue 11 reported that in order to understand the molecular mechanism of the dependency in MM, the research team examined gene expression changes upon DOT1L inhibition in sensitive and insensitive cell lines and discovered that genes belonging to the endoplasmic reticulum stress pathway and protein synthesis machinery were specifically suppressed in sensitive cells.

Oncotarget Volume 11, Issue 11 reported that in this preclinical study, we characterized the binding affinity and selectivity of quizartinib, a small-molecule inhibitor of FLT3, and AC886, the active metabolite of quizartinib, compared with those of other FLT3 inhibitors. Dr. Takeshi Isoyama from Daiichi Sankyo Co., Ltd. said, "FMS like tyrosine kinase 3 (FLT3) is a receptor tyrosine kinase expressed by acute myeloid leukemia (AML) cells in 70% to 90% of patients."

The cover for issue 11 of Oncotarget features Figure 6, 'Effects of AZD8186 in combination with anti-PD1 on syngeneic models,' by Owusu-Brackett, et al. In vitro cell viability assay and immunoblotting demonstrated that PTEN loss was significantly correlated with AZD8186 sensitivity in triple-negative breast cancer cell lines.