Gliomas of frontal and temporal origin had significantly different incidences of IDH1/2 mutation irrespective and in respective of tumor pathology.

<p>The regional incidences of IDH1/2 mutation in all gliomas of the region irrespective of pathology were labeled with “All”. The regional incidences of IDH1/2 mutation in respective of pathology were labeled with “A+AA, O+AO and OA+AOA” respectively. *The incidence of IDH1/2 mutation in this region is significantly higher or lower than that in other regions (p<0.05, chi-square test).</p

Regional frequencies of 1p/19q co-deletion and IDH1/2 mutation in glioma subsets.

<p>A: astrocytomas; AA: anaplastic astrocytoma; G: glioblastoma; O: oligodendrogliomas; AO: anaplastic oligodedroglioma; OA: oligoastrocytomas; AOA: anaplastic oligoastrocytoma; IDH: isocitrate dehydrogenase gene; (-): no data available. Numbers of cases with alterations are given in respect to cases examined.</p

Regional molecular heterogeneity about chromosome 1p/19q and IDH1/2 in gliomas reported in English literature.

<p>Regional molecular heterogeneity about chromosome 1p/19q and IDH1/2 in gliomas reported in English literature.</p

Gliomas of frontal and temporal origin had significantly different incidences of 1p/19q co-deletion irrespective and in respective of tumor pathology.

<p>The regional incidences of 1p/19q co-deletion in all gliomas of the region irrespective of pathology were labeled with “All”. The regional incidences of 1p/19q co-deletion in respective of pathology were labeled with “A+AA+G, O+AO and OA+AOA” respectively. *The incidence of 1p/19q co-deletion in this region is significantly higher or lower than that in other regions (<i>p</i><0.05, chi-square test).</p

Additional file 1: of Influence of diet on leukocyte telomere length, markers of inflammation and oxidative stress in individuals with varied glucose tolerance: a Chinese population study

Table S1. Characteristics of different glucose tolerance statuses. Table S2. Correlation of carbohydrate/fat/protein proportion with oxidative stress and inflammatory indicators. Table S3. Correlation of diet ingredients with HbA1c, FPG. (DOCX 20 kb

A Key Role of microRNA-29b for the Suppression of Colon Cancer Cell Migration by American Ginseng

<div><p>Metastasis of colon cancer cells increases the risk of colon cancer mortality. We have recently shown that American ginseng prevents colon cancer, and a Hexane extract of American Ginseng (HAG) has particularly potent anti-inflammatory and anti-cancer properties. Dysregulated microRNA (miR) expression has been observed in several disease conditions including colon cancer. Using global miR expression profiling, we observed increased miR-29b in colon cancer cells following exposure to HAG. Since miR-29b plays a role in regulating the migration of cancer cells, we hypothesized that HAG induces miR-29b expression to target matrix metalloproteinase-2 (MMP-2) thereby suppressing the migration of colon cancer cells. Results are consistent with this hypothesis. Our study supports the understanding that targeting MMP-2 by miR-29b is a mechanism by which HAG suppresses the migration of colon cancer cells.</p></div

Hexane fraction of American Ginseng (HAG) represses HCT116 colon cancer cell migration <i>in vitro.</i>

<p>Collagen type-I (15 µg/mL) coated transwell chamber were applied with 5×10⁴ HCT116 cells (A/B) for 12 h. The lower chamber contains SFM/Serum (10%) or HAG (260 µg/mL in complete medium). (A) 5×10⁴ HCT116 WT cells were applied to the upper chamber of the transwell membrane. (B) 5×10⁴ HCT116 (transfected with mirvana miR-29b, 10 nM, 48 h) cells were applied to the upper chamber of transwell membrane. After 12 h incubation at 37°C, the cells migrated to the inside (lower membrane) of transwell membrane was counted using ImageJ software (7 random microscopic fields (100X) were evaluated for cell counting). (C) Depicts the representative picture of HCT116 WT cell migration from each treatment. (D) Depicts the representative picture of HCT116 (transfected with mirvana miR-29b, 10 nM, 48 h) cell migration from each treatment. The background in the picture shows the 8 μm pore in the transwell membrane. *, indicates significant difference (pvalue <0.005) when compared to SFM. #, indicates significant difference (pvalue <0.005) when compared to 10% Serum.</p

MicroRNA expression changes with exposure to HAG (260 μg/ml): Trend Change Analysis.

<p>MicroRNA expression changes with exposure to HAG (260 μg/ml): Trend Change Analysis.</p

Hexane fraction of American Ginseng (HAG) represses DLD-1 colon cancer cell migration <i>in vitro.</i>

<p>Collagen type-I (15 µg/mL) coated transwell chamber were applied with 5×10⁴ DLD-1 cells (A/B) for 12 h. The lower chamber contains SFM/Serum (10%) or HAG (260 µg/mL in complete medium). (A) 5×10⁴ DLD-1 WT cells were applied to the upper chamber of the transwell membrane. (B) 5×10⁴ DLD-1 (transfected with mirvana miR-29b, 10 nM, 48 h) cells were applied to the upper chamber of transwell membrane. After 12 h incubation at 37°C, the cells migrated to the inside (lower membrane) of transwell membrane was counted using ImageJ software (7 random microscopic fields (100X) were evaluated for cell counting). (C) Depicts the representative picture of DLD-1 WT cell migration from each treatment. (D) Depicts the representative picture of DLD-1 (transfected with mirvana miR-29b, 10 nM, 48h) cell migration from each treatment. The background in the picture shows the 8 μm pore in the transwell membrane. *, indicates significant difference (pvalue <0.005) when compared to SFM.</p

MicroRNA expression changes with exposure to HAG (260 μg/ml): Fold Change Analysis (Untreated Vs Treated).

*<p>, Indicates False Discovery Rate.</p