Inositol Hexaphosphate and Inositol Inhibit Colorectal Cancer Metastasis to the Liver in BALB/c Mice.

Inositol hexaphosphate (IP6) and inositol (Ins), naturally occurring carbohydrates present in most mammals and plants, inhibit the growth of numerous cancers both in vitro and in vivo. In this study, we first examined the anti-metastatic effects of IP6 and Ins using a liver metastasis model of colorectal cancer (CRC) in BALB/c mice. CT-26 cells were injected into the splenic capsule of 48 BALB/c mice. The mice were then randomly divided into four groups: IP6, Ins, IP6 + Ins and normal saline control (n = 12 per group). IP6 and/or Ins (80 mg/kg each, 0.2 mL/day) were injected into the gastrointestinal tracts of the mice on the second day after surgery. All mice were sacrificed after 20 days, and the tumor inhibition rates were determined. The results demonstrated that the tumor weights of liver metastases and the tumor inhibition rates were reduced in the experimental groups compared to the control group and that treatment with the combination of IP6 and Ins resulted in greater inhibition of tumor growth than treatment with either compound alone. These findings suggest that IP6 and Ins prevent the development and metastatic progression of colorectal cancer to the liver in mice by altering expression of the extracellular matrix proteins collagen IV, fibronectin and laminin; the adhesion factor receptor integrin-ß1; the proteolytic enzyme matrix metalloproteinase 9; and the angiogenic factors vascular endothelial growth factor, basic fibroblast growth factor, and transforming growth factor beta in the tumor metastasis microenvironment. In conclusion, IP6 and Ins inhibited the development and metastatic progression of colorectal cancer to the liver in BALB/c mice, and the effect of their combined application was significantly greater than the effect of either compound alone. This evidence supports further testing of the combined application of IP6 and Ins for the prevention of colorectal cancer metastasis to the liver in clinical studies.

64-Slice spiral computed tomography and three-dimensional reconstruction in the diagnosis of cystic pancreatic tumors.

The present study aimed to describe the characteristics of cystic pancreatic tumors using computed tomography (CT) and to evaluate the diagnostic accuracy (DA) of post-imaging three-dimensional (3D) reconstruction. Clinical and imaging data, including multi-slice spiral CT scans, enhanced scans and multi-faceted reconstruction, from 30 patients with pathologically confirmed cystic pancreatic tumors diagnosed at the Linyi People's Hospital between August 2008 and June 2014 were retrospectively analyzed. Following the injection of Ultravist® 300 contrast agent, arterial, portal venous and parenchymal phase scans were obtained at 28, 60 and 150 sec, respectively, and 3D reconstructions of the CT images were generated. The average age of the patients was 38.4 years (range, 16-77 years), and the cohort included 5 males and 25 females (ratio, 1:5). The patients included 8 cases of mucinous cystadenoma (DA), 80%]; 9 cases of cystadenocarcinoma (DA, 84%); 6 cases of serous cystadenoma (DA, 100%); 3 cases of solid pseudopapillary tumor (DA, 100%); and 4 cases of intraductal papillary mucinous neoplasm (DA, 100%). 3D reconstructions of CT images were generated and, in the 4 cases of intraductal papillary mucinous neoplasm, the tumor was connected to the main pancreatic duct and multiple mural nodules were detected in one of these cases. The DA of the 3D-reconstructed images of cystic pancreatic tumors was 89.3%. The 64-slice spiral CT and 3D-reconstructed CT images facilitated the visualization of cystic pancreatic tumor characteristics, in particular the connections between the tumor and the main pancreatic duct. In conclusion, the 3D reconstruction of multi-slice CT data may provide an important source of information for the surgical team, in combination with the available clinical data.

Application of apparent diffusion coefficient and exponent apparent diffusion coefficient values in magnetic resonance imaging diffusion-weighted imaging to differentiate benign and malignant ovarian epithelial tumors.

OBJECTIVE: The aim of this study was to investigate the value of two quantitative indicators, the apparent diffusion coefficient (ADC) and the exponent apparent diffusion coefficient (EADC), of magnetic resonance imaging (MRI) diffusion-weighted imaging (DWI) in the differential diagnosis of ovarian epithelial tumors. MATERIALS AND METHODS: Clinical and MRI data from ovarian epithelial tumors were analyzed after pathology confirmation of 85 lesions from 76 cases (47 lesions from 41 benign cases; 38 lesions from 35 malignant cases). Patients underwent routine MRI examination and DWI before surgery. The average ADC and EADC values of the solid sections of the tumors were measured when the b value was 1000 s/mm 2. RESULTS: The mean ADC value of the solid sections in the benign group was 1.28 ± 0.23 × 10-3 mm 2/s; the average EADC value was 27.96 ± 5.78 × 10-2. In the malignant group, the mean ADC value of the solid sections was 0.86 ± 0.17 × 10-3 mm 2/s; the average EADC value was 42.37 ± 5.96 × 10-2. When the b value was 1000 s/mm 2, there was a statistically significant difference in ADC and EADC values between benign and malignant ovarian tumors (P < 0.05). CONCLUSION: ADC and EADC values of DWI can be used to differentiate benign and malignant ovarian epithelial tumors.

Diagnostic utility of diffusion-weighted magnetic resonance imaging in two common renal tumors.

The aim of the present study was to evaluate the utility of diffusion-weighted magnetic resonance imaging (DWI) in the diagnosis of common renal tumors. Conventional magnetic resonance imaging and DWI were performed on 85 patients with renal lesions (54 renal carcinoma and 31 renal angiomyolipoma cases). The apparent diffusion coefficient (ADC) values in each case at b=800 sec/mm2 were measured in the ADC maps using a statistical software package. The 54 cases of renal cell carcinoma showed a high signal intensity in the parenchyma, and the 31 renal angiomyolipoma cases showed a well-defined mixed signal intensity on DWI. The soft-tissue component showed a high signal intensity and the fat tissue showed a low signal intensity on DWI. When the b-value was set to 800 sec/mm2, the mean ADC was significantly lower in the renal carcinoma cases than in the renal angiomyolipoma cases. In conclusion, the measurement of ADC on DWI can reveal the structure of renal tumors, which is beneficial in diagnosing and determining the prognosis of benign and malignant renal tumors.

Inositol hexaphosphate suppresses growth and induces apoptosis in HT-29 colorectal cancer cells in culture: PI3K/Akt pathway as a potential target.

BACKGROUND: Inositol hexaphosphate (IP6) is a polyphosphorylated carbohydrate that is present in high amounts in almost all plants and mammalian cells. IP6 induces apoptosis in multiple types of cancer cells, including prostate cancer, breast cancer, skin tumor, liver cancer and colorectal cancer. However, little is known regarding the molecular mechanisms of its anticancer effects. Therefore, this study was conducted to investigate the activity of IP6 against human colorectal cancer cells (HT-29) and to determine whether the IP6 regulates apoptosis in HT-29 cells by inhibiting the PI3K/Akt signaling pathway. METHOD: A human colorectal cancer cell line (HT-29) was used for the study. HT-29 cells were treated with 0, 50, 100, 200, and 400 µg/mL of IP6. The MTT colorimetric assay was used to observe the proliferation of HT-29 in vitro, and flow cytometry (FCM) was used to analyze the apoptosis of the HT-29 cells. The relative mRNA expression was determined by real-time PCR, and relative protein levels were analyzed by Western blot analysis. RESULT: The results of MTT showed that HT-29 cells underwent inhibition of proliferation after exposure to IP6 (100-400 µg/mL) for 12 and 48 h, and this inhibition clearly relied on time and dosage. IP6 induced apoptosis in HT-29 cells in a dose-dependent manner. The mRNA and protein expression of PI3K and Akt decreased in the groups treated with IP6, and IP6 inhibited the phosphorylation of Akt (pAkt), whereas increased the expression of its downstream effector, caspase-9. CONCLUSION: Our results suggested that by targeting PI3K/Akt pathway, IP6 suppresses cell survival and proliferation, but induces death in HT-29 cells.