Objectives: We conducted this study to identify factors influencing the burdens cancer brings to a patient’s family and to evaluate the association between the burdens and the caregiver’s quality of life (QOL). Methods: Participants were drawn from the primary family caregivers of cancer patients at 6 university hospitals and the National Cancer Center in Korea. Of the 738 eligible caregivers, 704 (95.4%) completed the questionnaire packets (Family Impact Questions and Caregiver’s QOL-Cancer). Results: Caregivers, who were poor (OR, 2.11; 95% CI, 1.44–3.10), whose health status was poor (OR, 1.87; 95% CI, 1.29–2.70), who were married (OR, 1.75; 95% CI, 1.12–2.72), who provided care for a long time (OR, 2.29; 95% CI, 1.59–3.28), who cared for patients with poor performance status (OR, 1.35; 95% CI, 1.00–1.82), and who paid high medical expenses (OR, 1.70; 95% CI, 1.21–2.40), were more likely to lose their family savings. In multiple regression analysis, most burden variables – including requiring caregiving assistance, major life change, inability to function normally, loss of savings, loss of income, and altered educational plans – were associated with caregiver QOL. Loss of family income, which was related to economic issues, was most strongly associated with it (16.0%). Conclusions: Our study suggests that to improve caregiver QOL, we should give priority to decreasing the economic burden that cancer places on patient’s family.

Purpose: Rho GDP dissociation inhibitor 2 (RhoGDI2) has been identified as a regulator of Rho family GTPase. However, there is currently no direct evidence suggesting whether RhoGDI2 activates or inhibits Rho family GTPase in vivo (and which type), and the role of RhoGDI2 in tumor remains controversial. Here, we assessed the effects of RhoGDI2 expression on gastric tumor growth and metastasis progression. Experimental Design: Proteomic analysis was done to investigate the tumor-specific protein expression in gastric cancer and RhoGDI2 was selected for further study. Immunohistochemistry was used to detect RhoGDI2 expression in clinical samples of primary gastric tumor tissues which have different pathologic stages. Gain-of-function and loss-of-function approaches were done to examine the malignant phenotypes of the RhoGDI2-expressing or RhoGDI2-depleting cells. Results: RhoGDI2 expression was correlated positively with tumor progression and metastasis potential in human gastric tumor tissues, as well as cell lines. The forced expression of RhoGDI2 caused a significant increase in gastric cancer cell invasion in vitro, and tumor growth, angiogenesis, and metastasis in vivo, whereas RhoGDI2 depletion evidenced opposite effects. Conclusion: Our findings indicate that RhoGDI2 is involved in gastric tumor growth and metastasis, and that RhoGDI2 may be a useful marker for tumor progression of human gastric cancer.

Pectolinarigenin (PEC), a natural flavonoid present in Cirsium chanroenicum and in some species of Citrus fruits, has various pharmacological benefits such as anti-inflammatory and anti-cancer activities. In the present study, we investigated the anti-cancer mechanism of PEC induced cell death caused by autophagy and apoptosis in AGS and MKN28 human gastric cancer cells. The PEC treatment significantly inhibited the AGS and MKN28 cell growth in a dose-dependent manner. Further, PEC significantly elevated sub-G1 phase in AGS cells and G2/M phase cell cycle arrest in both AGS and MKN28 cells. Apoptosis was confirmed by Annexin V and Hoechst 33342 fluorescent staining. Moreover, Immunoblotting results revealed that PEC treatment down-regulated the inhibitor of apoptosis protein (IAP) family protein XIAP that leads to the activation of caspase-3 thereby cleavage of PARP (poly-ADP-ribose polymerase) in both AGS and MKN28 cells in a dose-dependent manner. The autophagy-inducing effect was indicated by the increased formation of acidic vesicular organelles (AVOs) and increased protein levels of LC3-II conversion in both AGS and MKN28 cells. PEC shows the down regulation of PI3K/AKT/mTOR pathway which is a major regulator of autophagic and apoptotic cell death in cancer cells that leads to the down-regulation of p-4EBP1, p-p70S6K, and p-eIF4E in PEC treated cells when compared with the untreated cells. In conclusion, PEC treatment might have anti-cancer effect by down-regulation of PI3K/AKT/mTOR pathway leading to G2/M phase cell cycle arrest, autophagic and apoptotic cell death in human gastric cancer cells. Further studies of PEC treatment can support to develop as a potential alternative therapeutic agent for human gastric carcinoma.

The goal of this study was to evaluate the reliability and validity of the Korean version of the Brief Fatigue Inventory (BFI-K). One hundred seventy-eight cancer patients and the same number of age- and sex-matched control subjects completed the BFI-K, the European Organization for Research and Treatment of Cancer QLQ-C30 (EORTC QLQ-C30), the Beck Depression Inventory (BDI), and a Brief Pain Inventory (BPI). The Cronbach's alpha coefficient for the BFI-K was 0.956 in the cancer patient group and 0.955 in the control group. The global score and nine of the single item scores for the BFI-K were significantly correlated with the fatigue and global health status/QoL subscale of the EORTC QLQ-C30, BDI, and BPI (coefficient range 0.38-0.66). Discriminant validity showed that BFI-K could distinguish significant differences of performance status between subgroups of patients, and between the cancer patient group and the control group, as expected. Our study has shown that the BFI-K is a reliable, valid self-rating instrument in terms of its psychometric properties.