<b>Conclusions:</b> These results may prove an important role of miR-34a expression as a predictor of apoptosis, even in cases when other risk factors like cytogenetic abnormalities are absent.
<b>HIGHLIGHTS</b> - Cytogenetic abnormalities and innate immune activation are seen in myelodysplasia- The NLRP3 inflammasome is a core element generating marrow failure of myelodysplasia- In April 2018 methylene blue was reported to potently inhibit NLRP3 inflammasome function- Methylene blue has benign side effects and has been in human use for a century- Study of methylene blue treatment of myelodysplasia would be a low-risk intervention.
<b>Materials and methods:</b> The effect of five days oral administration of TiO<sub>2</sub>NPs (21 and 80 nm) with different doses (50, 250 and 500 mg/kg body weight) was assessed in mice via measurement of oxidative stress markers; glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) and nitric oxide (NO), liver function indices; aspartate and alanine aminotransferases (AST and ALT), chromosomal aberrations and liver histopathological pattern.
(3) The mean indices for chromosomal aberrations and micronuclei end-points in ELF-EMF-exposed and control cells were within the spontaneous levels reported in historical database.
* Imatinib inhibits the breakpoint cluster region-Abelson (BCR-ABL) tyrosine kinase, which is produced by the chromosomal abnormality known as the Philadelphia (Ph) chromosome in patients with Ph chromosome-positive acute lymphoblastic leukaemia (Ph+ ALL).
11q23 translocations (t(11q23)) are recurring cytogenetic abnormalities in both acute myeloid leukemia (AML) and acute lymphoblastic leukemia, involving the same gene, ALL1 (or MLL).
11q23 translocations (t(11q23)) are recurring cytogenetic abnormalities in both acute myeloid leukemia (AML) and acute lymphoblastic leukemia, involving the same gene, ALL1 (or MLL).
5' (bcr 3) breakpoints in PML were over represented among the group and three patients had complex cytogenetic abnormalities suggesting both factors may increase the risk of relapse.
Cytogenetic aberrations were confirmed using fluorescent in situ hybridization with probes for the MDR gene and the tumor suppressor genes p16 and DCC.
Cytogenetic aberrations were confirmed using fluorescent in situ hybridization with probes for the MDR gene and the tumor suppressor genes p16 and DCC.
Chromosomal aberrations in humans induced by urban air pollution: influence of DNA repair and polymorphisms of glutathione S-transferase M1 and N-acetyltransferase 2.
Cytogenetic abnormalities were found in 81 of 2,757 cases (2.93%) screened for both cytogenetic and FMR-1 mutations because of mental retardation from 1992 to 1997.
Cytogenetic abnormalities were found in 81 of 2,757 cases (2.93%) screened for both cytogenetic and FMR-1 mutations because of mental retardation from 1992 to 1997.
Cytogenetic abnormalities were found in 81 of 2,757 cases (2.93%) screened for both cytogenetic and FMR-1 mutations because of mental retardation from 1992 to 1997.
Chromosomal aberrations were mostly found in older pts (12/14 >60 years; p=0.03) and in pts with CD34 positive leukemic blasts (13/14 coexpressed CD34, p=0.0004).
Chromosomal aberrations in breast tumors from BRCA1 and BRCA2 germ-line mutation carriers are considerably more frequent than what is seen in sporadic breast tumors.