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1.  Relationships of tumor inflammatory infiltration and necrosis with microsatellite instability in colorectal cancers 
AIM: The relationships between microsatellite instability (MSI) and survival in colorectal cancer patients are not consistent. The favorable survival of patient with MSI has been suggested to be related to pronounced inflammatory infiltration; however, the reason for non-association of MSI with survival is unclear. Our aims were to investigate the associations of inflammatory infiltration and tumor necrosis (TN) with microsatellite status and clinicopathological factors in colorectal cancer patients in whom MSI was not related to survival.
METHODS: Three hundred and one colorectal adenocar-cinomas were evaluated for inflammatory infiltration and 300 for TN under light microscope.
RESULTS: Low infiltration at invasive margin (χ2 = 3.94, P = 0.047) and in whole tumor stroma (χ2 = 3.89, P = 0.049) was associated with MSI, but TN was not (χ2=0.10, P = 0.75). Low infiltration was related to advanced stage (χ2 = 8.67, P = 0.03), poorer differentiation (χ2 = 8.84, P = 0.03), DNA non-diploid (χ2 = 10.04, P = 0.002), higher S-phase fraction (χ2 = 11.30, P = 0.004), positive p53 expression (χ2 = 7.94, P = 0.01), and worse survival (P = 0.03 for both univariate and multivariate analyses). Abundant TN was related to advanced stage (χ2 = 17.74, P = 0.001) and worse survival (P = 0.02 for univariate, and P = 0.05 for multivariate analysis).
CONCLUSION: The result that high inflammatory infiltration was not related to MSI might help explain the non-association of MSI with survival in colorectal cancer patients.
PMCID: PMC4305792  PMID: 15810089
Inflammatory infiltration; Necrosis; Microsatellite instability; Prognosis; Colorectal cancer
2.  An optimized method for detecting gamma-H2AX in blood cells reveals a significant interindividual variation in the gamma-H2AX response among humans 
Nucleic Acids Research  2007;35(5):e36.
Phosphorylation of histone H2AX on serine 139 (gamma-H2AX, γH2AX) occurs at sites flanking DNA double-strand breaks (DSBs) and can provide a measure of the number of DSBs within a cell. Here we describe a rapid and simple flow-cytometry-based method, optimized to measure gamma-H2AX in non-fixed peripheral blood cells. No DSB induced signal was observed in H2AX−/− cells indicating that our FACS method specifically recognized gamma-H2AX accumulation. The gamma-H2AX assay was capable of detecting DNA damage at levels 100-fold below the detection limit of the alkaline comet assay. The gamma-H2AX signal was quantitative with a linear increase of the gamma-H2AX signal over two orders of magnitude. We found that all nucleated blood cell types examined, including the short-lived neutrophils induce gamma-H2AX in response to DSBs. Interindividual difference in the gamma-H2AX signal in response to ionizing radiation and the DSB-inducing drug calicheamicin was almost 2-fold in blood cells from patients, indicating that the amount of gamma-H2AX produced in response to a given dose of radiation varies significantly in the human population. This simple method could be used to monitor response to radiation or DNA-damaging drugs.
PMCID: PMC1865071  PMID: 17284459

Results 1-2 (2)