bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 3761: Tissue processing time affects the expression of phosphoproteins after breast cancer resection
Authors: Gao Ming , Huang Ta-Chen , Chen Chi-Long , Tu Hui-Ching , Feng Wen-Chi , Lu Yen-Shen , Yeh Pei-Yen , Kuo Wun-Hon , Chang King-Jeng , Hsu Chih-Hung , Cheng Ann-Lii 
Published: February 2011

Abstract
Background: Many phosphoproteins are among the targeted pathways of cancer signal transduction and are therefore candidates for cancer biomarkers. However, the collection procedures of biospecimens might affect the expression of the phosphoproteins significantly because the time interval between surgical removal of tissues and fixation, i.e. warm ischemia time, are variable. This study aimed to evaluate the stability of phosphoprotein expression under the differential tissue processing time.
Materials and Methods: Specimens were obtained from patients who received mastectomy at National Taiwan University Hospital. Each specimen was cut into 5 pieces, stored at 4oC for 10 minutes, 2, 4, 6, and 24 hours before further processing. At each assigned time point, a small section of the specimen was fixed immediately in 10% buffered formalin, then paraffin embedded for immunohistochemical stains (IHC) of phospho-Akt (p-Akt) and phospho-Erk (p-Erk). The remaining specimens were snap frozen in liquid nitrogen, followed by homogenization in RIPA buffer. Western blot analysis was performed for phospho-Akt (p-Akt), total Akt, phospho-Erk (p-Erk), total Erk, phospho-STAT3 (p-STAT3), and total STAT3 staining.
Results: Western blot analysis showed that the expression of p-Erk declined significantly as early as 2 hours. The expression of p-Akt was relatively stable and decreased slightly after 24 hours. The expression of p-STAT3 gave variable results. The expression of total Akt, Erk, and STAT3 remain unchanged at each assigned time point. The immunohistochemical expression of p-ERK declined in a time-dependent manner whereas no obvious p-Akt decrease was detected.
Conclusions: Our results indicate that the expression of some phosphoproteins by IHC may be affected by warm ischemia time. Caution should be given to the interpretation of the results of these biomarkers.
(The study was supported by the grant NSC 98-3112-B-002-038)
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3761.
Abstract 3768: Comparison of breast density measured by dual energy x-ray Absorptiometry (DXA) with mammographic density among adult women
Authors: Maskarinec Gertraud , Morimoto Yukiko , Daida Yihe , Laidevant Aurelie , Shepherd John A. , Novotny Rachel 
Published: February 2011

Abstract
Mammographic density, the distribution of fat, connective, and epithelial tissues in the female breast, is strongly associated with breast cancer and has been used as a biomarker for breast cancer risk among adult women. While use of mammography is limited due to concerns about radiation exposure, Dual Energy X-ray Absorptiometry (DXA), commonly available in medical care settings, has very low radiation. In this analysis, we compared breast density measured by DXA with mammographic density among adult women. We recruited 101 participants aged 30 years and older with a normal mammogram (defined as BIRADS categories 1 through 3) through Kaiser Permanente Hawaii. After completing a questionnaire asking for demographic, reproductive, anthropometric, and medical information, all women received DXA scans of both breasts, as well as of the whole body, using a GE Lunar Prodigy Bone Densitometer. On the DXA scans, the breast image was manually outlined and the following measures were computed: percent fibroglandular volume density (% FGV), absolute fibroglandular volume, total breast area, and volume. After digitizing the most recent craniocaudal (CC) and mediolateral (ML) mammograms, total breast area, dense area, and percent density were estimated using a computer-assisted method (Cumulus). For the overall population, mean % FGV was 38.8±14.3%, and mean percent density was 31.9±18.2% for CC views and 28.3±16.2% for ML views. Both DXA and mammographic measures showed high correlations between left and right breasts ranging from 0.85 to 0.98 (p &lt;0.0001). When comparing DXA and mammographic measures, the correlation coefficients between % FGV and percent density were 0.76 for both CC and ML views (p &lt;0.0001). Associations with common risk factors showed similar patterns for DXA and mammographic densities; in particular, the inverse associations with BMI and age at menarche were evident for both methods. Multilinear regression with stepwise selection indicated an explained variance of 0.57 for % FGV alone and 0.58 for % FGV plus parity. The current comparison suggests that DXA has the potential to provide a low-radiation option to evaluate breast density for women who do not undergo mammography. This may allow improved individualized risk assessment to identify women for targeted prevention strategies.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3768.
Abstract 3769: Use of combined levels of dietary intake from FFQ and plasma biomarkers to assess association between antioxidant exposures and prostate cancer risk
Authors: Kong So Yeon J. , Goodman Michael , Bostick Roberd M. 
Published: February 2011

Abstract
Epidemiologic studies evaluating the relation between specific nutrients and risk of disease typically rely either on questionnaire-based or on biomarker-based measures of exposure; however both of these approaches may be affected by systematic error. In this study, we aim to improve assessment of antioxidant exposure through a combined measure reflecting both plasma measurements and food frequency questionnaire (FFQ)-derived levels of intake. This combined measure of exposure is examined in relation to risk of prostate cancer. In this community-based case-control study, dietary intake was assessed through the validated Block FFQ that allowed estimating daily intakes of various antioxidants. Archived plasma samples were analyzed using high performance liquid chromatography to determine circulating levels of carotenoids (lycopene, α-carotene, β-carotene, lutine, and β-cryptoxanthin), retinol (vitamin A), and α-tocopherol (vitamin E). Cases and controls were categorized as having “high” or “low” for each antioxidant's dietary intake and plasma level based on the median value among controls. Each participant was then included into one of the following four categories: (1) low dietary intake and low plasma level; (2) low dietary intake and high plasma level; (3) high dietary intake and low plasma level; and (4) high dietary intake and high plasma level. The combined measurements of high dietary intake and high plasma levels of lycopene, β-cryptoxanthin, and α-tocopherol demonstrated a statistically significant association with prostate cancer risk with adjusted odds ratios of 0.46 (0.23-0.91), 0.43 (0.22-0.84), and 0.32 (0.14-0.72), respectively. The combined measurements of high dietary intake and low plasma levels of β-carotene also demonstrated a statistically significant association (aOR = 0.43; 95% CI=0.20-0.91) with prostate cancer risk. These results tended to be stronger than the corresponding results for each measure of exposure considered individually. These findings provide evidence that the use of combined levels of dietary intake from FFQ and plasma biomarkers can improve the assessment of antioxidant exposure compared to use of either FFQ or plasma biomarkers separately.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3769.
Abstract 3770: Long-term variation in serum 25-hydroxyvitamin D concentration among participants in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial
Authors: Hofmann Jonathan N. , Yu Kai , Horst Ronald L. , Hayes Richard B. , Purdue Mark P. 
Published: February 2011

Abstract
Molecular epidemiologic studies of vitamin D and risk of cancer and other health outcomes usually involve a single measurement of the biomarker 25-hydroxyvitamin D [25(OH)D] in serum or plasma. However, the extent to which 25(OH)D concentration at a single time point is representative of an individual's long-term vitamin D status is unclear. To address this question, we evaluated within-person variability in 25(OH)D concentration across serum samples collected at three time points over a five year period among 29 participants in the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial. Serial blood samples in the PLCO Cancer Screening Trial were obtained from each subject at the same time of year for each of the three collection events. This sample collection protocol provided a unique opportunity to evaluate within-person temporal variability beyond seasonal effects, which have been well-characterized in previous studies. The within-person coefficient of variation (CV) and intraclass correlation coefficient (ICC) were calculated using variance components estimated from random effects models. Spearman rank correlation coefficients were calculated to evaluate agreement between measurements at different collection times (baseline, +1 year, +5 years). The within-subject CV was 14.9% [95% confidence interval (CI) 12.4%-18.1%] and the ICC was 0.71 (95% CI 0.63-0.88). Spearman rank correlation coefficients comparing baseline to +1 year, +1 year to +5 years, baseline to +5 years, and the average of baseline and +1 year to +5 years were 0.65 (0.37-0.82), 0.61 (0.29-0.81), 0.53 (0.17-0.77), and 0.65 (0.34-0.83) respectively. After restricting to 23 non-Hispanic Caucasian subjects, the ICC was 0.75 (0.64-0.90) and slightly stronger pairwise correlations were observed: the correlation coefficients were 0.72 (0.42-0.87) for baseline vs. +1 year, 0.69 (0.37-0.87) for +1 year vs. +5 years, 0.58 (0.18-0.81) for baseline vs. +5 years, and 0.70 (0.37-0.87) for the average of baseline and +1 year vs. +5 years. These findings suggest that serum 25(OH)D concentration at a single time point may be a useful biomarker of long-term vitamin D status in population-based studies of various diseases. When possible, investigators might also consider taking multiple measurements from each subject at different times to reduce misclassification of vitamin D status, thereby improving the validity of risk estimates.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3770.
Abstract 3776: Third follow-up of a Dutch cohort occupationally exposed to chlorophenoxy herbicides, chlorophenols and dioxins
Authors: Boers Daisy , Portengen Lutzen , Bueno-de-Mesquita Bas , Heederik Dick , Vermeulen Roel 
Published: February 2011

Abstract
A retrospective cohort study of workers exposed to phenoxy herbicides, chlorophenols, and contaminants (2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other polychlorinated dioxins and furans) has been conducted in two chemical factories in the Netherlands. TCDD levels at time of presumed last exposure were estimated based on back-extrapolation of predictive models derived from a cross-sectional survey on a sub-population of the full cohort. Analyses were done using Cox proportional hazard models, using attained age as the time-scale.
In analyses relating exposure to phenoxy herbicides to cancer mortality the previously reported increased risks for respiratory cancer, and non-Hodgkin's lymphoma in factory A could not be confirmed. However, increased risks were observed for all cancers in both factory A (HR=1.31; 95% CI 0.86-2.01) and factory B (HR=1.54; 95% CI 1.00-2.37). Increased risks for urinary cancers (HR=4.2; 95% CI 0.99-17.89) and genital cancers (HR=2.93; 95% CI 0.61-14.15) were observed in factory A, consistent with earlier reported results in this population. More detailed analyses showed that this increased risk for urinary and genital cancers in exposed workers was not due to selection of healthy controls and could not be attributed to specific products or departments.
The results of this study showed only slight increases in cancer mortality risk among phenoxy herbicide exposed workers. Analyses using estimated (back-extrapolated) TCDD are currently in progress. Preliminary analyses suggest an increased risk for non-Hodgkin lymphoma in TCDD exposed factory A compared to B.
Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3776.
Abstract 3778: Protein targets for prostate cancer prevention by α-keto acid metabolites of organoselenium compounds
Authors: Sinha Raghu , Sinha Indu , Pinto John 
Published: February 2011

Abstract
Our previous studies show that human glutamine transaminase K (GTK) and L-amino acid oxidase convert Se-methylselenocysteine (MSC) and selenomethionine (SM) to methylselenopyruvate (MSP) and α-keto-γ-methylselenobutyrate (KMSB), respectively. Further more, both of these α-seleno keto acids inhibit histone deacetylase (HDAC) activity in cultured human prostate cancer cells in a dose-dependent manner (Cancer Prev. Res. 2:683, 2009). Since human prostate cancer cells have GTK activity and can metabolize MSC to MSP but not SM to KMSB, we studied whether administration of SM and KMSB to human prostate cancer cells each function as direct-acting metabolites of organoselenium compounds and individually can result in differential regulation of protein targets critical for growth regulation. Using a 4-plex-iTRAQ proteomic approach, we examined the potential effects of either SM or KMSB on several protein targets in LNCaP prostate cancer cells. Analyses revealed significant changes (p&lt;0.05) in at least 68 proteins (1-60 peptide residue coverage) following 5 hr incubation of LNCaP cells with SM (200 μM), KMSB (50 μM) and Trichostatin A (TSA) (20 μM), an inhibitor of class I and II mammalian HDACs. The majority of observed protein changes were cytosolic (49%), nuclear (31%), then plasma membrane (4%) and the remainder was extracellular or unknown. Six proteins that included histone 1c, histone 2a, PARP1, and Epoxide hydrolase 1 microsomal (xenobiotic) were up regulated and two proteins, namely, ribosomal protein SA and hematological and neurological expressed-1 protein were down regulated in both KMSB and TSA-treated cells. A total of six proteins (including annexin VI and splicing factor 3a) were significantly altered by KMSB treatment alone while fifteen proteins (among which HSP90, 14-3-3ε, phosphoglycerate kinase 1, and eukaryotic translation initiation factor 4γ) were significantly changed by SM treatment alone. Collectively, our data reveal that several novel protein targets for prostate cancer prevention may be selective for either KMSB or SM alone. Several of these recognized targets will be investigated further to confirm the selectivity of seleno amino acids or seleno keto acids to function as direct-acting metabolites of naturally-occurring organoselenium compounds that can lead to de-repression of silenced tumor suppressor proteins and/or regulation of genes and signal factors.
The study was supported by NCI R01CA111842.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3778.
Abstract 3784: Caloric restriction inhibits 1, 2-dimethylhydrazine-induced aberrant crypt foci formation and induces differential expression of sirtuins in colonic mucosa of F344 rats
Authors: Tomita Mariko , Kanemoto Sayuri , Nakano Mayumi , Matsui Yuri , Morioka Takamitsu , Cui Changxu , Yoshimi Naoki 
Published: February 2011

Abstract
Caloric restriction (CR), a 20-40% lowering of caloric intake, is associated with longevity, and decreased incidences of age-related diseases including cancer. The sirtuins are a highly conserved family of nicotinamide adenine dinucleotide (NAD+)-dependent enzymes and have been implicated as a key mediator for the beneficial effects of CR on aging and longevity. However, the underlying mechanisms by which CR decreases cancer risk have not yet been elucidated. The present study was conducted to determine whether CR would modify the growth of preneoplastic colonic aberrant crypt foci (ACF), and whether sirtuin expression levels would be correlated with ACF formation. Five-week-old male F344 rats were randomly divided into four experimental groups. Groups 1 and 2 were given subcutaneous injection of 1, 2-dimethylhydrazine (DMH, 40 mg/Kg body weight), once a week for 2 weeks to induce ACF. Rats in groups 2 and 4 were fed a CR diet (60% of the ad libitum intake), and those in groups 1 and 3 were fed CE-2 diet (CLEA, Tokyo, Japan) ad libitum. All animals were sacrificed at 4 weeks after the first DMH injection. Rat colons were removed and fixed in 10% formalin. ACF were counted after 2% methylene blue staining. The expressions of sirt1 and sirt4 in the colonic mucosa were evaluated by RT-PCR. The number of ACF in colonic mucosa was significantly decreased in DMH-treated rats with CR (group 2) as compared to in DMH-treated rats without CR (group 1). No ACF was found in DMH-untreated animals with or without CR (groups 3 and 4). The expression levels of sirt1 and sirt4 in colonic mucosa were increased by CR (group 1 vs. group 2 and group 3 vs. group 4). Interestingly, DMH treatment also increased the expression of sirt1 and sirt4 (group 1 vs. group 3), and DMH-treated rats with CR (group 2) showed the highest expression levels of these genes. These results suggest that sirt1 and sirt4 induced by CR might inhibit colonic mucosa from formation and development of ACF. Our observations warranted further investigation of association between expression of sirtuins and prevention of colon carcinogenesis. We are currently analyzing the expression of other sirtuins and will compare the expression of all sirtuin family and ACF formation in colonic mucosa of the rats with or without CR.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3784.
Abstract 3798: Epigallocatechin-3-gallate and atorvastatin induce translocation of eGFP-LC3 in immortalized baby mouse kidney cells suggesting of a link between autophagy and apoptosis
Authors: Yang Zhihong , Huang Bridget , Strohecker Anne M. , White Eileen , Yang Chung S. 
Published: February 2011

Abstract
Epigallocatechin-3-gallate (EGCG), the major polyphenolic compound in green tea, and atorvastatin (ATST), a commonly used cholesterol-lowing medication, have been reported to have cancer preventive activities and to induce cancer cell apoptosis. However, the mechanisms of these activities are still unclear. Here we report that EGCG and ATST could induce cell autophagy, which may be linked to the induction of cell apoptosis. In immortalized baby mouse kidney (iBMK) cells that overexpress eGFP-tagged LC3, EGCG at 3, 6 and 12 μM exhibited a dose-dependent induction of the translocation of eGFP-LC3, an indicator of the formation of autophagosomes, as observed by fluorescent microscopy. ATST at 2 and 4 μM also induced the translocation of eGFP-LC3. Western-blot analysis showed that 25 μM EGCG and 4 μM ATST treatment for 24 h induced the appearance of LC3-II, a higher migrating band, indicating the occurrence of autophagy. Beclin +/− iBMK cells also displayed autophagy upon treatment with 25 μM EGCG for 24h, but to a less extent as compared to Beclin +/+ cells. The induction of the appearance of eGFP-LC3 puncta could not be eliminated by addition of superoxide dismutase plus catalase, enzymes that were used to inhibit the auto-oxidation of EGCG and the production of reactive oxygen species. The results suggest that the induction of autophagy is not caused by EGCG auto-oxidation produced oxidative stress. ATST inhibited the proliferation of iBMK cells in 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays, but the inhibition was to a less extent in Beclin +/− cells as compared to Beclin +/+ cells. EGCG and ATST treatment resulted in an increase of cleaved caspase 3, a hallmark of cell apoptosis, and a decrease of anti-apoptotic Bcl-2. Beclin +/+ iBMK cells showed stronger and earlier induction of these apoptotic markers than Beclin +/− cells, indicating that induction of apoptotic marker is correlated to the ability of cells to produce autophagy. EGCG at 25 μM and ATST at 2 μM also induced the appearance of endogenous LC3-II in human colon cancer HCT116 cells. The induction of autophagy may be a key mechanism for EGCG and ATST to inhibit cancer growth and formation (This research is supported by NIH grants CA 120915 and CA 133021).
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3798.