bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 2500: Analysis of protein biomakers in prostate and colorectal tumor lysates.
Authors: Stephen Laurie L. , Damour Marc , Kemp Josh , Ballard Karri L. , McDade Ralph L. , Mapes James P. 
Published: August 2014

Abstract
Traditional tumor biomarkers are proteins that have been shed in the bloodstream and have been critical in identifying and treating cancer. We sought to survey proteins relevant to oncology in colon and prostate tumors; in order to identify potential proteins of interest for cancer research. Four colon and three prostate tumors were homogenized and 115 proteins were analyzed from the Oncology MAP 2.0. Each tumor had 2 fractions homogenized to look at heterogeneity of the protein with the tumor. In all of the samples measured 102 of the 115 protein showed levels above the LLOQ. Five proteins (PSP94, Tenascin-X, lipocalin-1, Tie-1 and BAFF) were 100 fold higher in prostate tumors compared to colon tumors (P&lt;0.001). PSP94 has been shown to be a prostate cancer marker in serum; however, none of the other markers have been shown to be markers of prostate tumors. Eight proteins (PECAM-1, CA 72-4, Eotaxin-2, HGF-R, CA 15-3, TATI, CEACAM6 and CEA) were greater than 10 fold higher in colon tumors compared to prostate tumors (P&lt;0.001). Although oncology MAP 2.0 was developed for serum biomarkers, it may provide a valuable tool for examining proteins biomarkers in tumors.
Citation Format: Laurie L. Stephen, Marc Damour, Josh Kemp, Karri L. Ballard, Ralph L. McDade, James P. Mapes. Analysis of protein biomakers in prostate and colorectal tumor lysates. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2500. doi:10.1158/1538-7445.AM2013-2500
Abstract 2501: Differential protein signatures in cancer cell lines after dosing with anticancer molecules in vitro and in vivo.
Authors: Swift Robert , Ayers Deb , Chang Ying , Perry Darryl , Routt Sheri , Wilcox Sheri , Lollo Bridget , Saccomano Nick 
Published: August 2014

Abstract
Using a sensitive proteomics platform that can precisely and simultaneously measure 1129 distinct proteins (SOMAscan™), we profiled the proteomic changes in cancer cell lines and xenograft models following exposure to several oncological agents. Our goals were to identify novel biomarkers and drug targets, and to map out pharmacological MOA, with the ultimate goal of assessing the translatability of in vitro and preclinical models to human patients. We have generated multiple successful examples of using our platform in this manner. We treated a breast cancer cell line MCF-7 with eight pharmacological agents, including TamoxifenTM and TaxolTM. We have assessed PKC-δ resistant and sensitive lung cancer cell lines with a PKC-δ inhibitor, and profiled protein changes in response to these compounds. To assess how well in vitro models translate to preclinical models, we profiled protein changes in HCC827 (sensitive) or H1299 (resistant) cell lines treated with erlotinib (TarcevaTM), and NOD/SCID mice implanted with HCC827 cells and dosed with erlotinib. We observed good concordance of the protein changes in the HCC827 cell-lines and the xenograft models, which included cyclin A and p27KIP1 expression levels (proteins previously associated with erlotinib sensitivity) as well as additional protein changes with highly plausible connections to erlotinib's mode of action. These newly identified proteins may have implications for treating patients that develop resistance to erlotinib in the clinic, and suggest new targets for drug development. A human clinical study is underway to explore how the proteomic changes seen in this study translate to erlotinib treatment of NSCLC patients in the clinic.
Citation Format: Robert Swift, Deb Ayers, Ying Chang, Darryl Perry, Sheri Routt, Sheri Wilcox, Bridget Lollo, Nick Saccomano. Differential protein signatures in cancer cell lines after dosing with anticancer molecules in vitro and in vivo. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2501. doi:10.1158/1538-7445.AM2013-2501
Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Abstract 2530: Incidence trends of childhood and adolescent melanoma in the United States from 1973-2009.
Authors: Wong Jeannette , Harris Jenine , Rodriguez-Galindo Carlos , Johnson Kimberly 
Published: August 2014

Abstract
OBJECTIVE: Melanoma in children and adolescents is rare but, similar to adults, has been reported to be increasing. To gain insight into possible reasons underlying increased number of cases, we analyzed trends in melanoma incidence diagnosed between the ages of 0-19 years among United States whites by sex, stage, age at diagnosis, and primary site. We also investigated incidence trends by ultraviolet B radiation (UVB) exposure levels.
METHODS: Using Surveillance, Epidemiology, and End Results (SEER) program data (1973-2009), we calculated age-adjusted incidence rates, annual percent changes, and 95% confidence intervals (CIs) for each category of interest. Incidence trends were also evaluated using joinpoint and loess regression models. SEER registries were categorized with respect to low or high UVB radiation exposure.
RESULTS: From 1973-2009, 1,230 children of white race were diagnosed with malignant melanoma. Overall, pediatric melanoma increased by an average of 2% per year (95% CI, 1.4%-2.7%). Females, 15-19 year olds, and individuals with low UVB exposure had significantly higher incidence rates than males, younger children, and those living in SEER registries categorized as high UVB. Over the study period, males experienced increased incidence rates for melanoma on the face and trunk, and females on the lower limbs and hip. The only decreased incidence trend we observed was among 15-19 year olds in the high UVB exposure group from 1985-2009. Loess curves indicated similar patterns.
CONCLUSIONS: These results may help elucidate possible risk factors for adolescent melanoma, but further individual-level studies will be necessary to determine the reasons for increasing incidence trends.
Citation Format: Jeannette Wong, Jenine Harris, Carlos Rodriguez-Galindo, Kimberly Johnson. Incidence trends of childhood and adolescent melanoma in the United States from 1973-2009. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2530. doi:10.1158/1538-7445.AM2013-2530
Abstract 2539: Survival of lymphoma and beverages consumptions; alcohol, tea and coffee: results from National Cancer Centre, Singapore lymphoma cohort.
Authors: Lee Yin Leng , Tay Kevin Kuang Wei , Tan Soo Yong , Tan Leonard , Quek Richard Hong Hui , Tao Miriam , Ha Tam Cam , Lim Soon Thye 
Published: August 2014

Abstract
Background: In 2008, Singapore Cancer Registry reported lymphoma age-standardized rate (ASR) among males and females was 11.2 per 100,000 and 7.5 per 100,000, respectively with highest incidence observed in Malays, followed Chinese and Indians. Lymphoma incidence rates have been increasing since 1968 (female; ASR: 1.8 per 100,000) and is now the seventh and ninth most common cause of cancer for both men and women, respectively. Lymphoma is widely studied but the cause is yet to be ascertained. Epidemiological studies have shown modifiable behaviour such as heavy alcohol use results in poorer survival across various cancer types in Western population while reviews of tea and coffee consumptions in association with survival are limited. Here, we examined the impact of beverages consumption; alcohol, tea and coffee on lymphoma survival in South East Asia.
Methods: A cohort of 384 lymphoma patients with confirmed histology was recruited from January 2004 to December 2009 and was prospectively followed through till July 2012. At diagnosis, lifestyle characteristics were assessed using a structured questionnaire. Cox proportional hazards regression was used to estimate the prognostic value of three beverages; alcohol, tea and coffee, on lymphoma survival adjusted for other clinical prognostic factors; LDH, ECOG, Ann Arbor stage and extra-nodal sites.
Results: The overall median follow-up was 4.2 years (range: 0.02 to 8.3). Among all lymphoma subtypes, the most prevalent was DLBCL, 183 (47.7%) with highest incidence among Chinese, 305 (79.4%) followed by Malay 53 (13.8%) and Indian 24 (6.3%). Alcohol consumptions were associated with poorer survival for all lymphoma (ptrend=0.004) with increasing alcohol use whereas female black tea (plog-rank=0.0063) and coffee (plog-rank=0.018) consumptions had lower risk of death compared to non-drinkers. Full model including alcohol (one or more drinks per day; HR=2.35, 95% CI: 1.38-4.00, p=0.002) and clinical prognostic factors results in c index, 0.75 and 0.72, for overall survival and progression free survival, respectively.
Conclusion: Alcohol consumption in our cohort is predictive of survival while tea and coffee had a weak survival association among lymphoma. This model warrant external validation.
Citation Format: Yin Leng Lee, Kevin Kuang Wei Tay, Soo Yong Tan, Leonard Tan, Richard Hong Hui Quek, Miriam Tao, Tam Cam Ha, Soon Thye Lim. Survival of lymphoma and beverages consumptions; alcohol, tea and coffee: results from National Cancer Centre, Singapore lymphoma cohort. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2539. doi:10.1158/1538-7445.AM2013-2539
Abstract 2541: A prospective study of medical diagnostic x-rays and risk of thyroid cancer.
Authors: Neta Gila I. , Rajaraman Preetha , Berrington de Gonzalez Amy , Doody Michele , Alexander Bruce , Simon Steve , Freedman D. Michal , Linet Martha , Sigurdson Alice 
Published: August 2014

Abstract
While diagnostic x-rays provide important medical benefits, cancer risks associated with their exposure are also possible. The thyroid gland is the most radiosensitive organ, and radiotherapy to the head and neck is associated with an increased risk of thyroid cancer. However, it is not known whether diagnostic x-rays, which yield a lower dose of ionizing radiation to the thyroid gland than radiotherapy, also increase the risk. The United States Radiological Technologists study (1983-2006) is a nationwide, prospective cohort with extensive questionnaire data on history of personal diagnostic imaging procedures collected prior to cancer diagnosis. Cox proportional hazards were used to estimate thyroid cancer (TC) risks related to the number and type of selected procedures. Potential modifying effects of age and calendar year of the first x-ray in each category of procedures were assessed. Incident thyroid cancers (n=251) were diagnosed among 75,494 technologists (1.3 million person-years, mean follow-up=17 years). Overall, there was no clear evidence of TC risks associated with diagnostic x-rays, except for dental x-rays. The authors observed a 13% increase in TC risk for every 10 reported dental x-rays (95%CI: 1.01-1.26), driven by dental x-rays first received before 1970, but no evidence that the relationship between dental x-rays and TC was associated with childhood or adolescent exposures as would have been anticipated. The lack of association of TC with x-rays which expose the thyroid to higher radiation doses than dental x-rays underscores the need to conduct a detailed radiation exposure assessment to enable quantitative evaluation of risk.
Citation Format: Gila I. Neta, Preetha Rajaraman, Amy Berrington de Gonzalez, Michele Doody, Bruce Alexander, Steve Simon, D. Michal Freedman, Martha Linet, Alice Sigurdson. A prospective study of medical diagnostic x-rays and risk of thyroid cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2541. doi:10.1158/1538-7445.AM2013-2541
Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Abstract 2581: Intervention of chronically-induced human breast cell carcinogenesis.
Authors: Choudhary Shambhunath , Sood Shilpa , Wang Hwa-Chain Robert 
Published: August 2014

Abstract
The purpose of our study was to investigate the ability of dipyridamole (DPM) [2,6-bis(diethanolamino)-4,8-dipiperidinopyrimido-(5,4-d)-pyrimidine] to intervene in breast cell carcinogenesis induced by chronic exposure to environmental carcinogens. More than 85% of breast cancers are sporadic and attributable to long-term exposure to environmental carcinogens through a multistep and multiyear disease process. Therefore, it is urgent to identify preventive agents effective in intervention of cellular carcinogenesis. DPM, an antioxidant and a synthetic inhibitor of phosphodiesterase, is approved by the Food and Drug Administration to inhibit platelet aggregation and vasoconstriction. DPM is also able to enhance the cytotoxicity of anticancer agents, such as cisplatin, adriamycin, and 5-fluorouracil, in various cell types. However, its ability to block breast cell carcinogenesis has not been determined. Using our chronically-induced breast cell carcinogenesis model as a target system, we found that DPM, at a non-cytotoxic physiologically-achievable dose of 10 nmol/L, effectively blocked breast cell carcinogenesis induced by chronic exposure to three unrelated carcinogens: 2-amino-1-methyl-6-phenylimidazo[4,5- b]pyridine (PhIP), benzo[a]pyrene (B[a]P), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The ability of DPM to block H-Ras upregulation, thus blocking ERK pathway activation, reactive oxygen species (ROS) elevation, and DNA damage in each exposure, may account for its mechanisms in intervention of carcinogenesis induced by chronic exposures to PhIP. Likewise, DPM's ability to block ROS elevation and DNA damage may account for its mechanisms in intervention of carcinogenesis chronically induced by NNK and B[a]P, as well. Our study revealed, for the first time, the novel ability of DPM to block breast cell carcinogenesis induced by three unrelated carcinogens. DPM should be seriously considered as a chemopreventive agent in development of strategies for reducing the risk of sporadic breast cancer associated with long-term exposure to environmental carcinogens.
Citation Format: Shambhunath Choudhary, Shilpa Sood, Hwa-Chain Robert Wang. Intervention of chronically-induced human breast cell carcinogenesis. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2581. doi:10.1158/1538-7445.AM2013-2581
Abstract 2599: Inhibitory effects of new 1H-pyrrolo[3,2-c]pyridine derivative, KIST101029, on AP-1 activity and neoplastic cell transformation induced by insulin-like growth factor 1.
Authors: Yun Hyo Jeong , Choi Hong Seok 
Published: August 2014

Abstract
Diarylureas and diarylamides derivatives are reported to have antitumor activity. Encouraged by the interesting antiproliferative activity of diarylurea and diarylamide derivatives, we synthesized a new series of diarylureas and diarylamides containing pyrrolo[3,2-c]pyridine scaffold. In this study, we demonstrate that a new 1H-pyrrolo[3,2-c]pyridine derivative, KIST101029, inhibits neoplastic cell transformation induced by insulin-like growth factor 1 (IGF-1) in mouse epidermal JB6 Cl41 cells. The KIST101029 compound inhibited mitogen-activated protein kinase/extracellular signal-regulated kinase kinases (MEK), c-jun N-terminal kinases (JNK), and mechanistic target of rapamycin (mTOR) signaling pathways induced by IGF-1 in JB6 Cl41 cells, resulting in the inhibition of c-fos and c-jun transcriptional activity. In addition, the KIST101029 inhibited the associated activator protein-1 (AP-1) transactivation activity and cell transformation induced by IGF-1 in JB6 Cl41 cells. Consistent with these observations, in vivo chorioallantoic membrane assay also showed that the KIST101029 inhibited IGF-1-induced tumorigenicity of JB6 Cl41 cells. Taken together, these results indicate that a new 1H-pyrrolo[3,2-c]pyridine derivative, KIST101029, might exert chemopreventive effects through the inhibition of phosphorylation of MAPK and mTOR signaling pathway.
Citation Format: Hyo Jeong Yun, Hong Seok Choi. Inhibitory effects of new 1H-pyrrolo[3,2-c]pyridine derivative, KIST101029, on AP-1 activity and neoplastic cell transformation induced by insulin-like growth factor 1. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2599. doi:10.1158/1538-7445.AM2013-2599
Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Abstract 2600: Polyunsaturated omega-3 fatty acids and their metabolites preferentially inhibit cell proliferation and motility in triple negative over luminal breast cancer cells.
Authors: Pogash Thomas J. , Lopez de Cicco Ricardo , Pressly Benjamin , Russo Irma H. , Himmelberger Julie A. , Amin Shantu , Gowda Krishne , El-Bayoumy Karam , Manni Andrea , Russo Jose 
Published: August 2014

Abstract
The role of diet as a preventive measure in breast cancer remains controversial. Current literature suggests that the risk of developing breast cancer may decrease or increase with the intake of omega-3 (n-3) and omega-6 (n-6) fatty acids, respectively. Omega 3 polyunsaturated fatty acids (PUFAs) exert an anticancer effect by affecting multiple cellular mechanisms leading to inhibition of proliferation and induction of apoptosis. It is well known that breast cancer comprises distinct molecular subtypes which differ in their responsiveness to therapeutic and preventive agents. In these experiments, we tested the hypothesis that n-3FA may preferentially affect triple negative breast cancer cells for which no targeted intervention is presently available. The in vitro effects of n-3 PUFA Docosahexaenoic acid (DHA) and its metabolites, 4-OH-DHA and 4-OXO-DHA, were tested on proliferation and motility of seven triple negative human basal breast cell lines at different stages of transformation (MCF-10F, trMCF, bsMCF, caMCF, MDA-MB-231, Hs-578T, and BT-549), and three luminal breast cancer cell lines (MCF-7, T-47D, and SK-BR-3). Cell proliferation was measured with the tetrazolium MTT (3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide) assay and cell migration was assessed using the wound healing assay via time lapse microscopy with MetaMorph 7.7.7.8. All assays were performed in quadruplicate. Statistical significance was assessed using Student's t-test (p&lt;0.05). DHA and its metabolites significantly inhibited cell proliferation (20-90% reduction) of both basal and luminal breast cancer cell lines. The inhibitory effect was more pronounced on triple negative basal breast cancer cell lines as compared to luminal breast cancer cell lines. DHA did not produce an inhibitory effect on cell migration. However, the metabolites of DHA significantly reduced (20-60% reduction) cell migration on the bsMCF cell line. Our data provide novel information regarding the preferential antitumor effect of DHA and its metabolites on basal type breast cancer. (This project was supported by the Komen Foundation (KG081632).
Citation Format: Thomas J. Pogash, Ricardo Lopez de Cicco, Benjamin Pressly, Irma H. Russo, Julie A. Himmelberger, Shantu Amin, Krishne Gowda, Karam El-Bayoumy, Andrea Manni, Jose Russo. Polyunsaturated omega-3 fatty acids and their metabolites preferentially inhibit cell proliferation and motility in triple negative over luminal breast cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2600. doi:10.1158/1538-7445.AM2013-2600
Abstract 2624: Sodium butyrate induced cellular senescence and inhibited invasion of cancer cells with distinct mechanism.
Authors: Itoh Kazuyuki , Yoshioka Kiyoko , Nakagawa Hidemitsu 
Published: August 2014

Abstract
Sodium butyrate (SB) -C-4 saturated fatty acid (short-chain fatty acids) present in the human bowel membrane in the quite high concentration (2 mM) as food metabolites. It was previously reported that SB showed anti-tumor effect as HDAC inhibitor, however, the precise mechanism has not been elucidated yet. Here, we focused on the role of SB on cancer cell growth, motility and invasion. Physiological concentration of SB (0.25-4 mM) induced inhibition of cell growth (2D), colony formation in soft agar, in vitro motility and invasiveness with Boyden chamber and wound healing assay in a dose-dependent fashion using human fibrosarcoma (HT1080), glioblastoma (A172) cells and rat mammary Walker 256 cells. SB also affected the morphology of HT1080, A172 and Walker 256 cells, namely spread out with marked stress fibers bridging focal adhesions. Phosphorylation levels of focal adhesion kinase (Y577 and Y397 sites) were increased but that of myosin light chain (S19 site) was not altered. All of these biological effects of SB were reversible, and recovered after withdrawal. In contrast, HDAC inhibitor trichostatinA inhibited cancer cell growth irreversibly but not affected motility, invasiveness and morphology. In addition, HT1080 and A172 cells treated with SB showed positivity for senescence-associated β-gal (SA-β gal) staining with elevated expression levels of p53 and p21 proteins in a time and dose-dependent manner. In contrast, mRNA level of p21 was sharply declined after the treatment with SB. Knocking down of p21 protein expression by siRNA reversed both the growth inhibition and positivity for SA-β gal staining but not the inhibition of invasiveness. Thus p21 was required for cellular senescence but not for the decrease in motility induced by SB. Further, proteasome inhibitor, MG132 decreased the cellular growth and inhibited motility and invasiveness of the HT1080 and A172 cells, and showed similar all these biological effects of SB. Finally, intrathecal administration of SB effectively inhibited the invasion of Walker256 cells into the brain and elongated the animal (rat) survival in vivo. Collectively, SB inhibited growth with induced cellular senescence, inhibited invasion by distinct mechanism, and thus would be a good candidate for anti-invasive therapy without severe adverse effects.
Citation Format: Kazuyuki Itoh, Kiyoko Yoshioka, Hidemitsu Nakagawa. Sodium butyrate induced cellular senescence and inhibited invasion of cancer cells with distinct mechanism. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2624. doi:10.1158/1538-7445.AM2013-2624