Mitotic index

About: Mitotic index is a research topic. Over the lifetime, 3914 publications have been published within this topic receiving 101766 citations.

IDH mutation status and role of WHO grade and mitotic index in overall survival in grade II-III diffuse gliomas

Abstract: Diffuse gliomas are up till now graded based upon morphology. Recent findings indicate that isocitrate dehydrogenase (IDH) mutation status defines biologically distinct groups of tumors. The role of tumor grade and mitotic index in patient outcome has not been evaluated following stratification by IDH mutation status. To address this, we interrogated 558 WHO grade II–III diffuse gliomas for IDH1/2 mutations and investigated the prognostic impact of WHO grade within IDH-mutant and IDH-wild type tumor subsets independently. The prognostic impact of grade was modest in IDH-mutant [hazard ratio (HR) = 1.21, 95 % confidence interval (CI) = 0.91–1.61] compared to IDH-wild type tumors (HR = 1.74, 95 % CI = 0.95–3.16). Using a dichotomized mitotic index cut-off of 4/1000 tumor cells, we found that while mitotic index was significantly associated with outcome in IDH-wild type tumors (log-rank p < 0.0001, HR = 4.41, 95 % CI = 2.55–7.63), it was not associated with outcome in IDH-mutant tumors (log-rank p = 0.5157, HR = 1.10, 95 % CI = 0.80–1.51), and could demonstrate a statistical interaction (p < 0.0001) between IDH mutation and mitotic index (i.e., suggesting that the effect of mitotic index on patient outcome is dependent on IDH mutation status). Patient age, an established prognostic factor in diffuse glioma, was significantly associated with outcome only in the IDH-wild type subset, and consistent with prior data, 1p/19q co-deletion conferred improved outcome in the IDH-mutant cohort. These findings suggest that stratification of grade II–III gliomas into subsets defined by the presence or absence of IDH mutation leads to subgroups with distinct prognostic characteristics. Further evaluation of grading criteria and prognostic markers is warranted within IDH-mutant versus IDH-wild type diffuse grade II–III gliomas as independent entities.

The effects of nano-TiO2 on seed germination, development and mitosis of root tip cells of Vicia narbonensis L. and Zea mays L

Abstract: This study aimed to provide new information about phyto-toxicology of nano-TiO2 on plant systems. To contribute to the evaluation of the potential harmful effects of the nanoparticles on monocots and dicots we considered their effects on seed germination and root elongation applying a concentration range from 0.2 to 4.0‰ in the plants Zea mays L. and Vicia narbonensis L. Moreover, we achieved a genotoxicity study at cytological level in root meristems by means of traditional cytogenetic approach, to evidence possible alterations in mitotic activity, chromosomal aberrations, and micronuclei release. From these analyses it comes out that nano-TiO2 particles, after short-term exposure and under our experimental conditions, delayed germination progression for the first 24 h in both materials. Root elongation was affected only after treatment with the higher nano-TiO2 concentration. Further significant effects were detected showing mitotic index reduction and concentration-dependent increase in the aberration emergence that evidenced a nano-TiO2-induced genotoxic effect for both species.

Effects of Hyperthermia on Survival and Progression of Chinese Hamster Ovary Cells

Abstract: In general, the survival of Chinese hamster ovary cells exposed to hyperthermic temperatures of 42.5–46.0° decreases exponentially as a function of duration of heat exposure in a manner quite similar to survival as a function of radiation dose. The data indicate that above 43° a 1° change in temperature requires a 2-fold change in time to achieve the same degree of killing, whereas below 43° the same 2-fold change in time requires only a 0.5° change in temperature for the same effect. An Arrhenius-type plot of the logarithm of the rate of killing as a function of reciprocal temperature exhibits linearity with a change in slope at 43°. This change in slope suggests either a change in the mechanism of cell killing below this temperature or a manifestation of thermal tolerance that is readily observed when the duration of heating exceeds 4 to 5 hr. Thermotolerance to 45.5°, as evidenced by a 3- to 4-fold increase in D0, is observed in synchronous G1 cells exposed to heat 20 hr after an initial heat dose. This thermotolerance develops, although no progression of cells into S phase occurs during this period. In addition, thermotolerance develops in both asynchronous and synchronous G1 cells exposed to single heat doses between 41.5 and 42.5° for periods exceeding 4 to 5 hr, i.e., survival decreases exponentially as a function of duration of heating up to 4 to 5 hr, after which survival decreases very little. At 42.0–42.5°, survival is extremely sensitive to changes in temperature, with as much as a 10-fold difference in survival for a 0.1° difference in temperature with heat exposures greater than 4 hr. The above data indicate the importance of careful treatment design and precise temperature control if hyperthermia is to be used for cancer therapy. No progression of synchronous G1 cells into S phase is observed for cells continuously exposed to temperatures of 42.0° and above. However, computer simulation of sequential DNA histograms from flow cytometry of synchronous cells continuously exposed to 41.5° indicates that cell cycle delays of 5.4 and 2.4 hr for G1 and S, respectively, occurred for cells for which exposure began in G1, and delays of 0.5 and 5.4 hr for S and G2 plus mitosis, respectively, occurred for cells for which exposure began in late S. Normal cell cycle phase transit times for G1, S, and G2 plus mitosis are 4.3, 7.1, and 2.4 hr, respectively. In addition, mitotic indices and increases in cell number of asynchronous populations of cells continuously exposed to 41.5° indicate that entry into mitosis is delayed for approximately 2 hr. Following this delay, cells begin to enter mitosis and accumulate from 2 to 6 hr in metaphase; after about 6 hr, they begin to progress into G1. However, comparison of flow cytometry data and mitotic index data suggests that during the initial 6 hr of heating, the majority of cells accumulating in G2 plus mitosis are actually delayed in G2.