bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4686: MAL is down-regulated in oral squamous cell carcinoma and suppresses proliferation, invasion, tumorigenicity of oral cancer cells, in vitro and in vivo
Authors: Chen Wantao , Cao Wei , Zhang Ping 
Published: February 2011

Abstract
Purpose: The molecular mechanisms involved in oral squamous cell carcinoma (OSCC) still remain unclear to date. Our previous study revealed that MAL was down-regulated in the tissues of oral squamous cell carcinomas tested by cDNA microarray analysis. In order to identify the function of MAL, the effects on the proliferation, invasion and apoptotic potential in oral cancer cell lines were investigated, in vitro and in vivo.
Methods: Expression levels of MAL mRNA in oral squamous cell carcinoma (OSCC) tissues and oral cancer cell lines were examined by semi-quantitive reverse transcription (RT)-PCR and quantitive Real-time PCR. OSCC cell line, Tca cells, were transiently and stably transfected with the full-length MAL cDNA sequence or the empty expression vector pcDNA3.1. Transient and stable gene transfers were verified by Western blot analysis and RT-PCR. Subsequently, WST-8 assay, colony-formation assay, and flow cytometry were used to assess the effects of MAL on the proliferation of Tca cells. Furthermore, PI staining, 7-AAD and annexin V staining and detecting the level of cleavage PARP protein were used to examine apoptosis of Tca cells by MAL gene transfer. Finally, Invasion and tumorigenicity potential of MAL-expressing or MAL-nonexpressing Tca cells was investigated by invasion assay in vitro and tumorigenicity assay in vivo. All statistical tests were two-sided.
Results: Expression of MAL was decreased in 86.7% (26/30) OSCC tissues compared with the matched normal tissues by semi-quantitive RT-PCR (P=0.0004). In concordance with the results from OSCC tissues, the relative transcript levels of MAL gene were significantly five-fold lower in 9 OSCC cell lines than in normal oral epithelium cells by real-time PCR. A significant reduction in cell proliferation and a change in cell cycle phase were observed in MAL transfectants. Matrigel assays demonstrated that the OSCC cell invasiveness was significantly decreased. A strong increase in population of apoptotic cells by MAL gene transfer was also observed. Xenografts growth was inhibited in cells expressing MAL compared with cells not expressing MAL (P=0.018).
Conclusion: The results showed that MAL is able to suppress malignant phenotypes of OSCC, such as proliferation, apoptosis and invasion, and inhibit tumorigenicity in vivo by transient and stable transfection and suggested MAL might be a candidate of tumor suppression gene. This gene may become a promising target molecule for OSCC diagnosis and gene therapy.
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 4686.
Abstract 4687: Gene expression of breast cancer with CD44+CD24-/low genotype
Authors: Tsunoda Yuko , Sakamoto Masaaki , Suzuki Kenya , Sawada Terumasa , Sasaki Akiko , Yamamoto Gou , Isobe Tomohide , Tachikawa Tetsuhiko 
Published: February 2011

Abstract
Purpose: Breast cancer cells with a CD44+CD24-/low phenotype have been suggested to have tumor-initiating properties with stem cell-like. The purpose of this study is to clarify the gene expression profiling of cells with different CD44/CD24 genotypes within breast cancer.
Methods: Laser-captured microdissection was used to select the isolation of cancer cells in 36 frozen tissues of breast cancer, and RNA extracted from these cells was examined by real-time RT-PCR to quantify CD44 and CD24 expressions. Human stem cell RT2 profiler PCR array was used for gene expression analysis in the groups of different CD44/CD24 genotype. Associations between different CD44/CD24 genotypes and clinical variables were assessed by Fisher's exact test, and the Mann-Whitney U test was used for gene expression profiling. P&lt;0.05 was considered significant.
Results: Thirty-six tumors were divided into 3 groups. Group A was composed of CD44+CD24-/low genotype, in which the ratio of CD44/CD24 was &gt;1.0. Group B was composed of CD44+CD24+ genotype, in which that was 0.1 &lt; ratio ≤ 1.0. In group C of CD44-/lowCD24+ genotype, that was &lt; 0.1. The number of tumors in group A, B and C was 5, 29 and 2, respectively. Regarding the correlation of CD44/CD24 status with tumor characteristics, tumors of group A were significantly associated with lymph node metastasis compared with those of group B (P=0.029). The number of tumor with HER 2 score 3 within group A and B was 0 and 11, respectively. There was no significantly difference in ER status and tumor size. As far as the signaling pathways, the number of expression genes for Notch pathway in group A was significantly greater than in group B (P=0.028), and that for Wnt pathway was not significantly different between group A and B. Overexpressed gene in group A was NUMB, which is related to the programmed cell death. MYST1 and SOX2 tended to show higher levels of group A than of group B.
Conclusion: This study suggests that Notch pathway may be more important than Wnt pathway on breast cancer with CD44+CD24-/low genotype, and the CD44+CD24-/low status would be associated with low/negative HER2 expression. Moreover, the gene of self-renewal markers, such as MYST1, SOX2 and NUMB might be a target for therapy against breast cancer with low/negative HER2 expression.
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 4687.
Abstract 4691: Evaluating the effectiveness of community based breast cancer and prostate cancer interventions among African Americans
Authors: Louis Judithe , Brown Camille , Cannon Crystal , Wilkins Jeffrey , Cameron Amura , Patrice Jasmine , Livingston Jonathan , Singleton Dorothy 
Published: February 2011

Abstract
Health disparities among African Americans have been of key concern for the past decade. High rates of morbidity due to HIV/AIDS, heart disease, and cancer have led to the creation of new and more innovative efforts to educate African Americans about health disparities. The current paper is an assessment of the use of Community Theater to educate African Americans about breast and prostate cancers. To assess the effectiveness of theater, a team of health professionals, psychologists, and biomedical scientists were convened to develop two scripts written by a local playwright: “Stealing Clouds” which focused on breast cancer and “Fourth and a Mile” which focused on prostate cancer. A retrospective pre/post-test design with a 3-month delayed time series follow up was employed using surveys from participants upon viewing the plays. Results of both theatre presentations indicated that the plays were significant in increasing knowledge and awareness about both breast and prostate cancers. Furthermore, results indicated that participants, as a result of viewing the plays, reported increased likelihood of engaging in healthier behaviors (i.e., physician visits, testing). To assess the impact of Community Theatre as an effective medium, data was collected from a local health center indicating higher increases in mammography and prostate cancer exams as results of the plays. Given the high rates of cancer among African Americans, continued creation and evaluation of the effectiveness of such community-based efforts should be of key import in reducing and addressing cancer disparities.
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 4691.
Abstract 4695: Elevated levels of biomarkers of volatile organic carcinogens and toxicants in Chinese women who regularly cook at home
Authors: Carmella Steven G. , Hecht Stephen S. , Seow Adeline , Wang Mingyao , Wang Renwei , Meng Lei , Koh Woon-Puay , Chen Menglan , Han Shaomei , Yu Mimi C. , Yuan Jian-Min 
Published: February 2011

Abstract
Chinese women in Asia have higher rates of lung cancer than in many other places in the world. In China, the age standardized incidence rate for female lung cancer is 19.9 per 100,000 and in Singapore it is 17.5, while rates are far lower (1.5-9.2) in countries such as Vietnam, Indonesia, India, and Russia. Cigarette smoking is not the major risk factor for lung cancer in these women, nor is secondhand tobacco smoke exposure. Some studies demonstrate the role of fumes from indoor heating under special circumstances. However, multiple epidemiologic studies document an association between lung cancer in Chinese women and Chinese-style cooking with oils heated at high temperatures. Carcinogens and toxicants have been identified in fumes generated during high temperature cooking with various oils but there have been no biomarker studies to assess carcinogen and toxicant uptake in Chinese women who regularly cook at home. We quantified urinary mercapturic acid biomarkers of exposure to the volatile compounds acrolein, crotonaldehyde, benzene, 1,3-butadiene, and ethylene oxide; and urinary metabolites of the non-volatile combustion products pyrene and phenanthrene in 54 non-smoking, non alcohol-drinking Chinese women who reported regularly doing home cooking and 50 non-smoking, non-alcohol drinking women randomly selected from the Singapore Chinese Health Study as controls. Compared with controls, women who engaged in regular home cooking had significantly higher levels of mercapturic acids of acrolein [geometric mean 1959 pmol/mg creatinine (95% CI 1554-2467) vs.1370 (95% CI 1077-1742), P = 0.038], crotonaldehyde [geometric mean 231.6 pmol/mg creatinine (95% CI 193-277) vs. 142.2 (95% CI 118-171) P = 0.0004], and benzene [geometric mean 0.58 pmol/mg creatinine (95% CI 0.44-0.78) vs. 0.18 (95% CI 0.14-0.24) P &lt; 0.0001]. No significant differences were found in levels of mercapturic acids of 1,3-butadiene or metabolites of pyrene and phenanthrene between the two groups whereas levels of the ethylene oxide mercapturic acid were significantly higher in the controls than in the cooking group. The higher levels of the mercapturic acid of benzene, a multi-organ carcinogen, in the women who cooked, are particularly notable. The results of this study showing increased exposure to the volatile toxicants and carcinogens acrolein, crotonaldehyde, and benzene in Chinese women who regularly cook provide a plausible lead for further investigating the role of volatile compounds generated during cooking as causes of lung cancer.
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 4695.
Abstract 4697: Liquid chromatography-electrospray ionization tandem mass spectrometry analysis of 7-ethylguanine in human urine
Authors: Balbo Silvia , Hochalter J. Bradley , Villalta Peter W. , Carmella Steven G. , Hecht Stephen S. 
Published: February 2011

Abstract
Considerable evidence in the literature demonstrates the exposure of humans to an unknown ethylating agent. Previous studies have demonstrated the presence of 3-ethyl-Ade in urine, 7-ethylguanine (7-ethyl-Gua) in urine and human liver DNA, 7-ethyldGuo and O4-ethyl-dThd in human lung DNA, and ethylvaline in hemoglobin. Some studies also report higher levels of ethyl adducts in smokers compared to nonsmokers, and there is convincing evidence for an uncharacterized ethylating agent in cigarette smoke. To further investigate this question and evaluate the potential role of ethylating agents in smoking-induced cancer we have developed a liquid chromatography-electrospray ionization tandem mass spectrometry-selected reaction monitoring (LC-ESI-MS/MS-SRM) method for analysis of 7-ethyl-Gua in human urine.
A two-dimensional chromatography approach was used with [15N5]7-ethyl-Gua as the internal standard. Human urine was diluted with 15 mM ammonium acetate and partially purified by a solid-phase extraction cartridge (Strata-X 33 µm, 30 mg/1 mL, Phenomenex) and a mixed mode cation exchange reversed-phase extraction cartridge (Oasis MCX, 30 mg/cartridge, Waters). The fraction from this last purification step containing the analyte (30% MeOH, 5% NH4OH) was dried and redissolved in 80% acetonitrile, 0.1% formic acid and purified by HPLC on a YMC Polyamino II column (150 × 1.0 mm I.D. 5 μm). The fraction containing 7-ethyl-Gua was collected, dried, dissolved in H2O and analysed by LC-ESI-MS/MS-SRM using a Thermo Hypersil Gold PFP column (150 × 0.5 mm I.D. 3 μm). The analysis was carried out using the transition m/z 180 [M + H]+ → m/z 152 [Gua+ H]+ for 7-ethyl-Gua and m/z 185 → m/z 157 for the internal standard. Recovery was about 50%. The detection limit was approximately 10 fmol on column. The peaks attributed to 7-ethyl-Gua and the labeled internal standard had identical retention time and were observed in most of the human urine samples analyzed. The identity of the peak was confirmed by re-injecting the samples after spiking with a standard solution of 7-ethyl-Gua. Twenty-one human urine samples (1 mL) from 11 smokers and 10 nonsmokers were analyzed. 7-Ethyl-Gua was clearly detected in 8 out of 11 samples from smokers and 5 out of 10 samples from nonsmokers. These results strongly indicate that 7-ethyl-Gua is present in human urine and demonstrate that it can be detected and quantified. Further investigation is required to clarify its relationship to cigarette smoking.
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 4697.
Abstract 47: Pyruvate kinase M2 is a target of the tumor-suppressive microRNA-326 and regulates the survival of glioma cells
Authors: Kefas Benjamin A. 
Published: February 2011

Abstract
Emerging studies have identified microRNAs as possible therapeutic tools for the treatment of glioma, the most aggressive brain tumor. Their important targets in this tumor are not well understood. We recently found that the Notch pathway is a target of microRNA-326. Ectopic expression of microRNA-326 in glioma and glioma stem cells induced their apoptosis and reduced their metabolic activity. Computational target gene prediction revealed pyruvate kinase type M2 (PKM2) as another target of microRNA-326. PKM2 has recently been shown to play a key role in cancer cell metabolism. To investigate whether it might be a functionally important target of miR-326, we used RNA interference to knock down PKM2 expression in glioma cells. Transfection of established glioma and glioma stem cells with PKM2 siRNA reduced their growth, cellular invasion, metabolic activity with decreased ATP and glutathione levels, and activated AMP-activated protein kinase. The cytotoxic effects exhibited by PKM2 knockdown in glioma and glioma stem cells were not observed in transformed human astrocytes. Western blot analysis of human glioblastoma specimens showed high levels of PKM2 protein but none was observed in normal brain samples. Our data suggest PKM2 inhibition as a therapy for glioblastoma, with the potential for minimal toxicity to the brain.
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 47.
Abstract 4701: DNA-adducts levels and chromosomal aberrations in relation to smoking history and topography in smokers
Authors: Dumitrescu Ramona G. , Zheng Yun-Ling , Yang Yang , Seillier-Moiseiwitsch Francoise , Spernak Stephanie M. , Loffredo Christopher , Phillips David H. , Shields Peter G. 
Published: February 2011

Abstract
Introduction: Tobacco smoking is the major cause of morbidity and mortality in developed countries. Important determinants of tobacco carcinogen exposure include the smoking history and smoking topography. Tobacco carcinogens-induced DNA adducts and chromosomal aberrations have been associated with cancer development. It is unknown if the choice of cigarettes and smoking topography lead to differences in carcinogen-DNA adduct levels and chromosomal aberrations.
Methods: We studied 207 population-based smokers (97 Caucasians and 110 African Americans). The subjects smoked two cigarettes, one hour apart, and the smoking topography was measured. We assessed three parameters of smoke exposure (serum cotinine, nicotine boost and carbon monoxide boost) in order to collect corroborative evidence that reflect different types of exposure. Carcinogen-DNA adducts and chromosomal aberrations in lymphocytes were determined by using the 32P-postlabeling analysis and standard cytogenetic method, respectively.
Results: The chance of having high level of DNA-adducts was significantly higher in males than females (OR: 1.9; 95%CI: 1.09-3.31). Weakly associations of the DNA-adducts were observed with age and race (higher in older people and African-Americans smokers) (OR: 1.7; 95%CI: 0.97-2.90; OR: 1.5; 95%CI: 0.87-2.60). DNA-adducts were significantly associated with the baseline and post cigarette CO level for the first (p-value=0.001; 0.007 respectively) and second cigarette (p-value=&lt;0.001; 0.001 respectively), with the total number of puffs for the second cigarette (p-value=0.04) and with the cumulative topography (p-value=0.03). Marginal associations were observed for the changes in CO2 pre and post cigarettes (p-value=0.08), the average inter-puff interval and the total puff volume for the second cigarette (p-value=0.06; 0.07 respectively). The changes in CO2 pre and post first and second cigarette were significantly associated with the mean number of chromosomal aberrations per cell (p-value=0.05; 0.01 respectively).
Conclusion: In this study we observed potentially important associations of smoking topography with both DNA adduct levels and chromosomal aberrations. Larger study sets will be necessary to clarify the magnitude of these associations and to account for baseline differences related to gender, age, and race. Such an approach could provide useful information for understanding differential susceptibility to lung cancer among smokers.
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 4701.
Abstract 4704: Racial/ethnic differences in double-strand-break repair signaling in breast cancer
Authors: Rodriguez-Gil Jorge L. , Hill Jeff W. , Allen Glenn O. , Thomas Venetta , Hu Jennifer J. 
Published: February 2011

Abstract
To evaluate whether deficient DNA repair contributes to elevated DNA damage and breast carcinogenesis, we used a newly developed flow-cytometry assay for rapid assessment of H2AX phosphorylation (gamma-H2AX) in response to double strand breaks (DSBs) in peripheral lymphocytes from 64 breast cancer cases and 71 controls. Basal or ionizing radiation (IR)-induced gamma-H2AX was not influenced by age, smoking status, family history (FH), age at menarche, age at first birth or parity and body mass index (BMI). With limited sample size, basal or IR-induced gamma-H2AX level did not differ between breast cancer cases (mean+SD, 6.65+1.18; 29.23+6.88) and controls (6.48+0.95; 27.19+7.26). In subgroup analysis of women with younger age at first live birth (&lt;24), breast cancer cases have a significantly higher IR-induced gamma-H2AX level (29.87+6.45) than that in controls (26.60+7.19). In cases, African Americans (AA) had a significantly higher IR-induced gamma-H2AX level (32.17+6.76) than that in Caucasians (28.08+6.65), particularly in the younger age group (&lt;50), never smokers, negative FH, and higher BMI (&gt;25 kg/m2). In younger cases, a higher gamma-H2AX was observed in AA (p=0.042) compared to Caucasians (32.71+5.43 vs. 27.32+5.33). In never smokers, AA cases had a significantly higher level of IR-induced gamma-H2AX than Caucasians (32.70+5.77 vs. 27.58+6.41, p=0.03). In cases without FH, AA had a significantly higher level of IR-induced gamma-H2AX than Caucasians (32.38+6.90 vs. 28.02+7.09, p=0.044). In cases with a higher BMI, AA had a significantly higher level of IR-induced gamma-H2AX than Caucasians (33.36+5.94 vs. 26.93+6.00, p=0.001). Our results, although based on a relatively small group of subjects, indicate that DSBs response is significantly higher in AA breast cancer cases. Future larger studies are warranted to test whether this racial/ethnic difference in IR-induced gamma-H2AX levels contribute to breast cancer risk, tumor phenotypes, treatment response, and/or clinical outcome.
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 4704.
Abstract 4709: NXF2 is a Candidate Biomarker of Mechanical Stress in Breast Cancer
Authors: Wang Jiaxu , Barnes Rebecca , West Nathan , Watson Peter 
Published: February 2011

Abstract
Mechanical stress has been implicated as an important factor influencing tumour cell biology. Due to the nature of early stages of breast cancer and its ductal environment and associated stromal changes, origins in ductal changes in gland tension are likely to occur and the associated mechanical forces may contribute to the progression of breast cancer. To identify specific changes in gene expression that might serve as biomarkers of mechanical stress in breast cancer, we applied static tensile forces (0.65 pN/μm2) to breast cancer cell lines via collagen-coated magnetite beads, profiled gene expression changes by Microarray chips, validation by RT-PCR and immunoblotting. Our results showed that mechanical stretch forces altered cell signaling in both MDA-MB-231 and MDA-MB-468 breast cancer cell lines by array chip analysis and 7.24.% genes (4.67% up and 2.57% down regulation) were regulated by mechanical stress in 16822 profiling genes in MDA-MB-231 cell line and 5.79% genes (2.22% up and 3.57% down regulated) was regulated in MDA-MB-468 cell lines. The 0.48% (82/16822) up regulation and the 0.125% (21/16822) down regulation was in complete concordance with Microarray in both cell lines. The validation of the gene expression with significant changes of &gt;1.5-fold in MDA-MB-231 cell line, RT-PCR revealed the up-regulation of LCE2D and NXF2 and down-regulation of PIGH and RAPD1B and confirmed the force-induced genes identified by Microarray. Mechanical stress also increased 2.75 fold NXF2 protein expression level with confirmation of immunoblotting. There were no significant expression changes found relating to hypoxia stress control gene NDRG1, which changed the highest gene in hypoxia control chip. We conclude that mechanical stress promotes early breast cancer progression mediated by multiple signal transduction pathways and that NXF2 is a potential mechanical stress marker in breast cancer progression.
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 4709.