bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 3457: Social support as emotional adjustment determinant of breast cancer patients after surgery in selected hospitals in Nigeria
Authors: Oyewusi Christiana Oluseun , Oyewusi Samuel Oyebode 
Published: July 2016

Abstract
Breast cancer is the most common invasive cancer and a leading cause of premature mortality for females worldwide. It accounts for 16% of all female cancers; 18.2% of all cancer deaths globally are from breast cancer. Social support plays a major role in modifying negative effect of this disease on affected individuals. It is an important psychosocial resource for coping with stressful life events. This study was carried out to examine social support as determinant of emotional adjustment of breast cancer patients after surgery in selected hospitals in Ibadan, Nigeria.
This cross-sectional descriptive survey utilized a quantitative approach. A sample of two hundred and eighteen patients was randomly selected from hospitals in Ibadan. The respondents were reassured of confidentiality of the data. The instrument used basically was self-structured questionnaire. Data were collected, coded and analyzed using Pearson correlation coefficient.
The respondents’ ages were between 21- 51 years; 87.2% were females, majority of them (81.6%) were Christians, more than half (62.4%) were married, about one third (31.2%) had higher qualifications, 55.0% were civil servants and 74.3% were living with other family members. Result findings show that instrumental support had significant effect on emotional adjustment of the breast cancer patients after surgery. Family and friends helping the patients had a positive effect on their emotional adjustment. Therefore, it was revealed that instrumental support had a positive effect on emotional adjustment of the patients (r.cal = .217, r. critical = .195, P &lt; 0.05). Also, emotional support had a significant effect on emotional adjustment of the patients after surgery. Having family members and friends to talk to and help with personal problems was helpful to emotional adjustment. Thus it was evident that emotional support had a positive effect on emotional adjustment (r. cal = .250, r. critical = .195, P &lt; 0.05)
The patients admitted that they had friends and family members who helped them and were a source of comfort to them. This helped them to show a better psychological and emotional adjustment to breast cancer than those who did not have support. It is recommended that adequate attention be given to financial, material and emotional needs of the breast cancer patient.
Keywords: Social support, determinant, emotional adjustment, breast cancer patients.
Citation Format: Christiana Oluseun Oyewusi, Samuel Oyebode Oyewusi. Social support as emotional adjustment determinant of breast cancer patients after surgery in selected hospitals in Nigeria. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3457.
Abstract 3467: Moderate-intensity exercise to reduce radiation therapy-related fatigue in black breast cancer patients: A feasibility trial
Authors: Dash Chiranjeev , Mills Mary , Watkins Vivian , Randolph-Jackson Pamela , Isaacs Claudine , Makambi Kepher , Adams-Campbell Lucile L. 
Published: July 2016

Abstract
Background: Fatigue is an important side-effect of radiation therapy (RT) for treatment of early stage breast cancer. Evidence on the efficacy of physical activity (PA) interventions in reducing fatigue among Black cancer patients undergoing RT is lacking. In a randomized controlled trial we tested the efficacy of a structured PA intervention, coinciding with the start of RT, in reducing cancer-related fatigue among Black patients undergoing RT for breast cancer.
Methods: We randomly assigned 30 Black, sedentary, RT-naïve, non-pregnant patients diagnosed with stage 0-IIIA breast cancer who had completed adjuvant or neo-adjuvant chemotherapy and were scheduled for RT to the PA intervention (n = 15) and control groups (n = 15). PA intervention was an 8-week structured, moderate-intensity aerobic exercise regimen (75 minutes/week) using PEDLARS (portable stationary cycle ergometers) concurrent with RT. Fatigue was measured by using the Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-Fatigue) survey, a 13-item scale whose score ranges from 0 to 52 with a higher score denoting lower fatigue. We used ANCOVA to compare fatigue levels between the groups at T8 weeks after adjusting for baseline (T0) fatigue levels. We also compared change in fatigue scores (T8 weeks - T0) using 2-sample t-tests. All tests were double-sided with alpha = 0.05.
Results: 27 women completed baseline and follow-up assessments. After adjusting for baseline fatigue scores, intervention group participants reported lower fatigue at T8 weeks than the control group (42.53 vs. 37.12; P = 0.17). Intervention group participants improved their fatigue scores at T8 weeks compared to T0 (mean change +1.3) but the control group did not (mean change -1.91; P = 0.42).
Conclusion: Although statistically not significant, moderate-intensity exercise regimen among Black breast cancer patients undergoing RT was associated with lower RT-associated fatigue. This trial demonstrated the feasibility and acceptability of conducting a randomized clinical trial of a moderate-intensity exercise program among women initiating RT for breast cancer.
Citation Format: Chiranjeev Dash, Mary Mills, Vivian Watkins, Pamela Randolph-Jackson, Claudine Isaacs, Kepher Makambi, Lucile L. Adams-Campbell. Moderate-intensity exercise to reduce radiation therapy-related fatigue in black breast cancer patients: A feasibility trial. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3467.
Abstract 3474: Prevalence of BRCA1 and BRCA2 small mutation and large genomic rearrangements in breast cancer patients visiting a genetic counseling clinic
Authors: Sohn Ji Yeon , Park Boyoung , Yoon Kyong-Ah , Park Soo Jin , Lee Moo Hyun , Cho Eun Hae , Lee Keun Seok , Lim Myong Cheol , Kong Sun-Young , Lee Eun Sook 
Published: July 2016

Abstract
BACKGROUND: This study was conducted to investigate mutation prevalence of the BRCA1 and BRCA2 genes in breast cancer patients, including both small mutations and large genomic rearrangements (LGRs) following the patients in the process of genetic counseling.
METHODS: A total of 358 breast cancer patients who visited genetic counseling clinic and screened for BRCA1/2 mutation at the National Cancer Center were included. Among the non-carriers by direct sequencing, a subset of patients who were agreed on participation of the research were screened for the presence of LGRs using a multiple ligation-dependent probe amplification (MLPA) assay. Clinico-pathologic characteristics of cancer were evaluated thorough medical record review and characteristics for those who found BRCA mutation through MLPA were described.
RESULTS: 53 (14.8%) mutation carriers were identified. The frequency of BRCA small mutations in specific subgroups was as follows: 18.0% of patients with a family history, 12.8% of early-onset breast cancer, and 20.6% of bilateral breast cancer patients. MLPA identified BRCA1 LGRs in 3 (1.5%) out of 204 patients with BRCA1 and BRCA2 small mutation-negative results. Those with LGRs showed higher probabilities of BRCA mutation carriers estimated by risk assessment models and receptor negatives of tumor immunohistochemistry.
CONCLUSIONS: The prevalence of BRCA1/2 mutation prevalence in breast cancer patients with family history or personal risk factors were comparable to previous Korean studies. MLPA to screen for mutations in the BRCA1 gene could be recommended for breast cancer patients negative for small mutations. To specify proper targets of MLPA, probabilities of carrying BRCA1/2 mutation and tumor receptor status could be considered.
Citation Format: Ji Yeon Sohn, Boyoung Park, Kyong-Ah Yoon, Soo Jin Park, Moo Hyun Lee, Eun Hae Cho, Keun Seok Lee, Myong Cheol Lim, Sun-Young Kong, Eun Sook Lee. Prevalence of BRCA1 and BRCA2 small mutation and large genomic rearrangements in breast cancer patients visiting a genetic counseling clinic. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3474.
Abstract 3481: Kisspeptin regulates the invasiveness of endometrial cancer cells through FAK/ Src signaling-dependent activation of matrix metalloproteinase (MMP)-2
Authors: Wu Hsien-Ming , Liang Yung-Yu , Chiu Wei-Jung , Wang Hsin-Shih , Huang Hong-Yuan , Lai Chyong-Huey , Soong Yung-Kuei 
Published: July 2016

Abstract
Introduction:
More than 25% of patients diagnosed with endometrial carcinoma have an invasive primary cancer accompanied by metastasis. The kisspeptin has an important role in reproduction. In mammals, kisspeptin may regulate tumor progression of endometrial cancer. FAK and Src signaling have been considered important components of tumor progression. MMPs are largely implicated in promoting angiogenesis and tumor metastasis. In the present study, we examined the action of kisspeptin-promoted motility of endometrial cancer cells and the mechanisms of the action in endometrial cancer.
Materials and methods:
Endometrial cancer cell line Ishikawa and ECC-1 were derived from an endometrial adenocarcinoma. Kisspeptin agonist and antagonist were synthetic peptides. Cell motility was estimated by invasion and migration assay. The activities of MMP-2 was assessed by gelatin zymography. Immunoblot analysis was done to study the expression of kisspeptin receptor and the effects of kisspeptin in the activation of FAK,Src and MMP-2. Human FAK siRNA and Src siRNA were used to knock down the expression of FAK and Src to evaluate the effects of FAK and Src. MMP-2 inhibitor (OA-Hy) was pretreated for 30 min to evaluate the effects of MMP-2 in cell motility.
Results:
The kisspeptin regulated cell motility in a dose-dependent manner. Kisspeptin activated the phosphorylation of FAK and Src signaling and the phosphorylation was abolished by FAK siRNA and Src siRNA. Kisspeptin-regulated cell motility was suppressed in cells pretreated with FAK siRNA and Src siRNA. Moreover, FAK siRNA and Src siRNA abolished kisspeptin-induced activation of MMP-2. Inhibition of MMP-2 with 10μM OA-Hy suppressed cell motility in response to kisspeptin.
Conclusion:
Our study shows that the kisspeptin regulated the cell motility of endometrial cancer cells through the kisspeptin receptor, and the phosphorylation of FAK and Src-dependent activation of MMP-2. Our findings represent a new concept regarding the mechanisms of kisspeptin-regulated cell motility in endometrial cancer cells, suggesting the possibility of kisspeptin analogues as a potential therapeutic intervention for the treatment of human endometrial cancer.
Citation Format: Hsien-Ming Wu, Yung-Yu Liang, Wei-Jung Chiu, Hsin-Shih Wang, Hong-Yuan Huang, Chyong-Huey Lai, Yung-Kuei Soong. Kisspeptin regulates the invasiveness of endometrial cancer cells through FAK/ Src signaling-dependent activation of matrix metalloproteinase (MMP)-2. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3481.
Abstract 3497: Metformin enhances TRAIL-induced apoptosis by Mcl-1 degradation via Mule in colorectal cancer cells
Authors: Park Seong Hye , Lee Dae-Hee , Kim Jung Lim , Lee Sun Il , Kim Bo Ram , Na Yoo Jin , Lee Suk Young , Kim Hong-Jun , Joung Sung Yup , Kang Sanghee , Oh Sang Cheul 
Published: July 2016

Abstract
Recent studies have reported that metformin is an anti-diabetic drug, and is the potential a promising anti-cancer agent. The purpose of this study is to evaluate whether metformin effectively sensitize human colorectal cancer (CRC) cells to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Metformin alone did not induce apoptosis, but significantly potentiated TRAIL-induced apoptosis in CRC cells. CRC cells treated with metformin and TRAIL activated the intrinsic and extrinsic pathways of caspase activation. To elucidate the underlying mechanism, we found that metformin significantly reduced the protein levels of Mcl-1 (Myeloid cell leukemia 1) in CRC cells, and overexpression of Mcl-1 attenuated the cell death by metformin alone, or in combination with TRAIL. Further experiments revealed that metformin did not affect the mRNA level, but proteasomal degradation and protein stability of Mcl-1. The metformin-induced degradation of Mcl-1 required the E3 ligase Mule, which is responsible for the polyubiquitination of Mcl-1. Taken together, our study is the first report indicating that metformin enhances TRAIL-induced apoptosis through the degradation of Mcl-1 by the proteasome machinery.
Citation Format: Seong Hye Park, Dae-Hee Lee, Jung Lim Kim, Sun Il Lee, Bo Ram Kim, Yoo Jin Na, Suk Young Lee, Hong-Jun Kim, Sung Yup Joung, Sanghee Kang, Sang Cheul Oh. Metformin enhances TRAIL-induced apoptosis by Mcl-1 degradation via Mule in colorectal cancer cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3497.
Abstract 3509: Knockdown of RNF2 induces apoptosis by regulating MDM2 and p53 stability
Authors: Wen Weihong , Peng Cong , Kim Myoung Ok , Jeong Chul Ho , Zhu Feng , Yao Ke , Zykova Tatyana , Ma Wei-Ya , Carper Andria , Langfald Alyssa , Bode Ann M. , Dong Zigang 
Published: July 2016

Abstract
RNF2, also known as Ring1B/Ring2, is a component of the polycomb repression complex 1 (PRC1). RNF2 is highly expressed in many tumors, suggesting that it might have an oncogenic function, but the mechanism is unknown. Here we show that knockdown of RNF2 significantly inhibits both cell proliferation and colony formation in soft agar, and induces apoptosis of cancer cells. Knockdown of RNF2 in HCT116 p53+/+ cells resulted in significantly more apoptosis than was observed in RNF2 knockdown HCT116 p53−/− cells, indicating that RNF2 knockdown-induced apoptosis is partially dependent on p53. Various p53-targeted genes were increased in RNF2 knockdown cells. Further studies revealed that in RNF2 knockdown cells, the p53 protein level was increased, the half-life of p53 was prolonged and p53 ubiquitination was decreased. In contrast, cells overexpressing RNF2 showed a decreased p53 protein level, a shorter p53 half-life and increased p53 ubiquitination. Importantly, we found that RNF2 directly binds with both p53 and MDM2 and promotes MDM2-mediated p53 ubiquitination. RNF2 over-expression could also increase the half-life of MDM2 and inhibit its ubiquitination. The regulation on p53 and MDM2 stability by RNF2 was observed during the etoposide-induced DNA damage response. These results provide a possible mechanism explaining the oncogenic function of RNF2, and because RNF2 is important for cancer cell survival and proliferation, it might be an ideal target for cancer therapy or prevention.
Keywords: RNF2, p53, apoptosis
Citation Format: Weihong Wen, Cong Peng, Myoung Ok Kim, Chul Ho Jeong, Feng Zhu, Ke Yao, Tatyana Zykova, Wei-Ya Ma, Andria Carper, Alyssa Langfald, Ann M. Bode, Zigang Dong. Knockdown of RNF2 induces apoptosis by regulating MDM2 and p53 stability. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3509.
Abstract 3512: Cyclopamine enhances TRAIL-induced apoptosis by induction of DR5 via ER stress in gastric cancer cells
Authors: Na Yoo Jin , Lee Dae-Hee , Kim Jung Lim , Kim Bo Ram , Park Seong Hye , Min Byung-Wook , Lee Sun Il , Kang SangHee , Joung Sung Yup , Lee Suk Young , Kim Hong-Jun , Oh Sang Cheul 
Published: July 2016

Abstract
Activation of sonic hedgehog (Shh) signaling has been involved in progression of various cancers. Cyclopamine uses as effective treatment for cancers in which hedgehog signaling is overexpressed. In this study, we elucidated that cyclopamine sensitizes to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in gastric cancer cells. Single treatment with cyclopamine or TRAIL could not induce significant cytotoxicity in gastric cancer cells. However, combination treatment of TRAIL with cyclopamine effectively led to caspase dependent apoptosis. We found that cyclopamine increased ER (Endoplasmic Reticulum) stress level in gastric cancer cells, and using ER stress inhibitor attenuated the cell death by cyclopamine. As further underlying mechanism, induction of ER stress by cyclopamine caused upregulation of JNK (c-Jun N-terminal kinases) protein, and then accumulation of p53 protein. We conducted experiment using p53 wild-type and p53-mutated gastric cancer cells, and this of particular importance since p53 wild-type gastric cancer cells had more significant efficacy than p53-mutated cells by cyclopamine. Accumulation of p53 increased DR5 protein. Taken together, we showed that cyclopamine sensitizes to TRAIL-induced apoptosis in gastric cancer cells.
Citation Format: Yoo Jin Na, Dae-Hee Lee, Jung Lim Kim, Bo Ram Kim, Seong Hye Park, Byung-Wook Min, Sun Il Lee, SangHee Kang, Sung Yup Joung, Suk Young Lee, Hong-Jun Kim, Sang Cheul Oh. Cyclopamine enhances TRAIL-induced apoptosis by induction of DR5 via ER stress in gastric cancer cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3512.
Abstract 3519: Paroxetine induces apoptosis in human breast cancer MCF-7 cells through mitochondrial dysfunction and modulation of K+ channels
Authors: Kang Kee R. , Cho Young-Woo , Ryu Ji Hyun , Kim Eun-Jin , Han Jaehee , Kang Dawon 
Published: July 2016

Abstract
Purpose: Selective serotonin reuptake inhibitors (SSRIs) are widely used for the treatment of patients with depression. Approximately 60% of women with breast cancer suffer from depression. This study was performed to investigate the effect of SSRIs on cell viability of human breast cancer MCF-7 cells.
Methods: Cell viability, ROS generation, and Ca2+ increase were quantified using MTT, H2DCFDA, and Fluo-3 AM. Apoptotic signaling pathways were analyzed by immuno-blotting and -staining. Plasma and mitochondrial membrane potentials were determined by DiO PMP and JC-1 dyes, respectively. K+ channel activity was analyzed by whole-cell and single-channel recordings.
Results: Of the antidepressants tested in this study, paroxetine most reduced the viability of MCF-7 cells. Paroxetine (10 and 30 μM) treatment resulted in a significant increase in the number of apoptotic cells, an increase in Bax/Bcl-2 ratio, an activation of caspase-8, 9, and PARP, and a release of cytochrome c from mitochondria. In addition, paroxetine markedly increased ROS generation and intracellular Ca2+ levels. Moreover, paroxetine blocked K+ channels, such as large conductance Ca2+-activated K+ channel and TASK-3 channel, which are present in plasma membrane and mitochondria. The paroxetine-induced apoptosis was reduced by antioxidants, in particular NAC. Combination with SB202190 (a p38 MAPK inhibitor) prevented cells from undergoing apoptosis.
Conclusion: Our findings show that apoptotic effect of paroxetine is mediated by mitochondrial dysfunction and modulation of K+ channels in MCF-7 cells. We suggest that paroxetine could be an agent for anti-tumor therapy in breast cancer.
Citation Format: Kee R. Kang, Young-Woo Cho, Ji Hyun Ryu, Eun-Jin Kim, Jaehee Han, Dawon Kang. Paroxetine induces apoptosis in human breast cancer MCF-7 cells through mitochondrial dysfunction and modulation of K+ channels. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3519.
Abstract 3524: D-glucose exposure induced DNA damage and apoptosis in MCF-7 cells
Authors: Farah Ibrahim O. , Tchounwou Christine K. , Yedjou Clement G. , Tchounwou Paul B. 
Published: July 2016

Abstract
D-glucose is the simple carbohydrate sugar that our bodies rely on to produce ATP energy. It has been shown that sustained high glucose burden is related to the promotion of many long-term health problems to various vital target organs including the kidneys, nervous system, eyes, heart (failure and stroke), erectile dysfunction in men and pregnancy complications in women. Epidemiological data have suggested an increased cancer rates in diabetic patients, for which the underlying mechanism is poorly understood. Furthermore, the D-glucose paradox as cancer-promoting energy source as well as being toxic to cancer cells is puzzling. Therefore in the present study, we will investigate the mechanisms of glucose-induced toxicity in MCF-7 cells as an in vitro cellular model to simulate diabetic complications in tumor cells using trypan blue exclusion and MTT assays. Mechanisms of DNA damage and apoptosis were tested by alkaline single cell gel electrophoresis (Comet) assay, and flow cytometry analysis using Annexin V FITC/PI and caspase-3 analysis. The MTT assay indicated that low dose (5 mg/mL) of D-glucose slightly increase cell viability upon 2 h of exposure. On the other hand, high doses (10-80 mg/mL) of D-glucose significantly reduced the viability of MCF-7 cells in a dose and time-dependent manner. Similar trends were seen with the trypan blue exclusion test. Data obtained from the comet assay indicated that D-glucose caused DNA damage in MCF-7 cells in a dose-dependent manner. The flow cytometry assessment (Annexin V FITC/PI) showed a strong dose-response relationship between high glucose exposure and Annexin V positive MCF-7 cells undergoing early stage apoptosis. Similarly, a statistically significant and concentration-dependent increase (p &lt;0.05) were recorded for caspase-3 activity in MCF-7 cells undergoing late apoptosis. Based on these in vitro findings, our study provides clear evidence that elevated level of D-glucose induced cytotoxicity to MCF-7 cells via induction of DNA damage, externalization of phosphatidylserine and caspase-3 activation as indicators for the apoptotic mechanisms of D-glucose exposure.
This research is supported by a grant from the National Institutes of Health-NIH (Grant No. NIMHD-G12MD007581).
Citation Format: Ibrahim O. Farah, Christine K. Tchounwou, Clement G. Yedjou, Paul B. Tchounwou. D-glucose exposure induced DNA damage and apoptosis in MCF-7 cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3524.