bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1905: Influence of serum and oxygen on lipid biosynthesis and energy metabolism in murine glioblastoma.
Authors: Ta Nathan , Seyfried Thomas 
Published: August 2014

Abstract
Glucose and glutamine are essential energy metabolites for brain tumor growth and survival under both normoxic and hypoxic conditions. Carbons derived from either metabolite can be used for lipid synthesis. Here, we used uniformly labeled C14-glucose and C14-glutamine to examine de novo lipid synthesis in the VM-M3 murine glioblastoma cells. The major lipids synthesized included phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylinositol (PI), phosphatidylserine (PS), sphingomyelin (SM), phosphatidic acid (PA), cholesterol (Chol), and cardiolipin (CL). De novo lipid synthesis was greater with glucose than with glutamine as the metabolic substrate under normoxia. Conversely, glutamine was the preferred substrate for lipid synthesis under anoxia. Lactate was produced largely from glucose carbons with minimal lactate derived from glutamine. Total lipid synthesis, using either glucose or glutamine, was greater in media without serum than in media containing 10% FBS under normoxia. Significant triglyceride accumulation was observed only under anoxia. Our findings show that lipid biosynthesis using glucose or glutamine is dependent on the type of growth environment, and that the VM-M3 glioblastoma cells can grow under anoxia only through acquisition of lipids, especially cholesterol, from serum. Supported in part from Boston College Res. Expense Fund.
Citation Format: Nathan Ta, Thomas Seyfried. Influence of serum and oxygen on lipid biosynthesis and energy metabolism in murine glioblastoma. [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 1905. doi:10.1158/1538-7445.AM2013-1905
Abstract 1917: Loss of steroid sulfotransferase (SULT) in human prostate cancer: Potential implications for SULT as a biomarker and therapeutic target.
Authors: Mirkheshti Nooshin , Song Chung S. , Chatterjee Bandana 
Published: August 2014

Abstract
Purpose: Reactivated androgen receptor, fueled by elevated tumor tissue 5α-dihydrotestosterone (DHT), plays a key role in the reemergence of prostate cancer. Primary prostate cancer almost always regresses in response to androgen deprivation therapy. The disease, however, recurs and progresses to therapy resistance and death in ∼30% patients. New-generation drugs that inhibit androgen receptor (MDV3100™) or enzymes involved in androgen biosynthesis (Zytiga™, TAK-700™, Dutasteride™) extend survival of post-chemotherapy patients for a limited period following which therapy resistance emerges– hence the challenge to develop alternate means for reducing intra-tumor androgen signaling.
Design and Results: 3β-sulfation of dehydroepiandrosterone (DHEA), mediated by the prostate-expressed sulfotransferase SULT2B1b (hereon SULT), is likely to reduce intra-prostate androgen levels since sulfated DHEA cannot be converted to androstenedione and thus to testosterone and DHT. We tested whether enzyme-catalyzed sulfation of DHEA, the obligate precursor steroid for androgen synthesis, is targetable to inhibit prostate cancer. Results show that SULT silencing increased prostate cancer cell proliferation. Clinical prostate cancer specimens showed markedly reduced SULT expression, revealed by immunohistochemistry, western blotting and mRNA quantification. 1,25-dihydroxy vitamin D3 (D3) and sterols enhanced SULT expression due to induction of the SULT2B-encoding gene by D3-activated vitamin D receptor (VDR) and sterol-activated liver X receptor (LXRα).
Conclusion: Tumor SULT levels may be a marker for predicting prostate cancer recurrence and progression. We also anticipate that enhancement of SULT activity in tumors by activating VDR and LXRα through combined therapeutic intervention with D3 and sterols would limit the tumor androgen pool and inhibit recurrent, therapy-resistant prostate cancer.
Citation Format: Nooshin Mirkheshti, Chung S. Song, Bandana Chatterjee. Loss of steroid sulfotransferase (SULT) in human prostate cancer: Potential implications for SULT as a biomarker and therapeutic target. [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 1917. doi:10.1158/1538-7445.AM2013-1917
Abstract 1921: Mutational and expressional analyses of DICER1 gene in ovarian stromal tumors and other common tumors.
Authors: Kim Min Sung , Je Eun Mi , Choi Youn Jin , Yoo Nam Jin , Lee Sug Hyung 
Published: August 2014

Abstract
Recurrent missense somatic mutations in DICER1 gene affecting exons 25 and 26 have recently been reported in non-epithelial tumors of ovary, especially in Sertoli-Leydig cell tumors (SLCT). Such a recurrent nature of the mutations strongly suggests that DICER1 mutation may play an important role in the development of ovarian non-epithelial tumors. The aim of this study was to further characterize the DICER1 mutations in human tumor tissues. We analyzed the DICER1 mutations in 2,819 tumor tissues from ovary and other organs by single-strand conformation polymorphism analysis. We found the DICER1 exon 25 and 26 hot-spot mutations in 2 of 14 SLCT (14.3%) and one of 132 non-Hodgkin lymphomas (0.8%), but none in other tumors. In SLCT, DICER1 expression was observed in Sertoli cells, but neither in Leydig nor spindle-shaped cells. We also analyzed DICER1 expression in lung, stomach, colon and prostate cancer tissues. DICER1 expression was lost in 37% of prostate cancers, but not in lung, stomach and colon cancers. Our data indicate that DICER1 recurrent mutations commonly occur in SLCT, but the incidence was significantly lowerthan that in the earlier study. Our data suggest that both DICER1 mutation and its expression loss may be important in tumor pathogenesis and that they are tumor type-specific.
Citation Format: Min Sung Kim, Eun Mi Je, Youn Jin Choi, Nam Jin Yoo, Sug Hyung Lee. Mutational and expressional analyses of DICER1 gene in ovarian stromal tumors and other common tumors. [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 1921. doi:10.1158/1538-7445.AM2013-1921
Abstract 193: Effect of omega-3 fatty acid and dietary energy restriction on mammary carcinogenesis, circulating biomarkers and molecular regulators in rats.
Authors: Jiang Weiqin , Zhu Zongjian , McGinley John N. , Manni Andrea , Thompson Henry J. 
Published: August 2014

Abstract
Available evidence indicates that diets enriched in the ratio of n-3 fatty acids or dietary energy restriction (DER) have a broad range of health-related benefit including prevention of breast cancer. However, the number of studies in the combined effects of these intervention strategies have been investigated is limited. The objective of this investigation was to determine the effect of the combination of dietary n-3 and DER on mammary carcinogenesis, on plasma levels of cancer associated growth factors and cytokines and on molecular regulators in mammary carcinomas using a pre-clinical rat model for breast cancer. Female Sprague Dawley rats were injected with 1-methyl-1-nitrosourea (50 mg/kg) and 7 days thereafter randomized to four groups (n=30/group), 1) control (dietary n-6/n-3=1:1); 2) high n-3 (dietary n-6/n-3=1:10); 3) 20%DER (dietary n-6/n-3=1:1); 4) high n-3 + 20%DER (dietary n-6/n-3=1:10). Rats were fed a modification of the AIN-93G diet formulation that contained 30% of dietary calories from fat (currently recommended in the US Dietary guidelines). It was observed that mammary cancer incidence, cancer multiplicity and tumor burden were reduced and cancer latency was elongated for the rats in groups 2-4 compared to the rats in group 1, and the significant differences were observed between group 1 (n-6/n-3=1:1) and 4 (n-6/n-3=1:10 + 20%DER). The protective dietary combination of high n-3 and DER was associated with significant reductions in plasma IGF-1, insulin, and leptin and increased adiponectin compared to rats fed the control diet (n-6/n-3=1:1, p&lt;0.01). Carcinomas induced in the protected animals were smaller in mass with altered levels of proteins in the PPAR and mTOR pathways on which plasma insulin had the most impact. This work was supported by grant KG081632 from the Susan G. Komen Foundation.
Citation Format: Weiqin Jiang, Zongjian Zhu, John N. McGinley, Andrea Manni, Henry J. Thompson. Effect of omega-3 fatty acid and dietary energy restriction on mammary carcinogenesis, circulating biomarkers and molecular regulators in rats. [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 193. doi:10.1158/1538-7445.AM2013-193
Abstract 1930: The unknown piece of the pie: Molecular markers in triple-negative lung cancer.
Authors: Schweitzer Brock L. , Lawrence Kasey D. , Handshoe John , Skelton Rachel , Chatfield Lindsay , Xue Liquan , Morris Stephan W. , Hout David R. 
Published: August 2014

Abstract
Lung cancer is the main cause of cancer mortality worldwide. Approximately ∼80% of lung cancer cases are non-small cell lung cancer (NSCLC) in type and &gt;50% of NSCLC are adenocarcinoma in histopathology. A shifting paradigm in the field of pulmonary oncology is the identification of molecular markers that are therapeutic targets and/or provide prognostic information. The recent recognition of the role biomarkers such as EGFR, KRAS, and ALK play in NSCLC adenocarcinoma patients demonstrates this trend. Although these three highly characterized molecular markers make up one-quarter to two-thirds of NSCLC adenocarcinoma patients, the remaining population, termed “Triple-Negative Lung Cancer” (TNLC), has yet to be fully defined. The complete absence of therapeutic targets for triple-negative lung cancer patients undeniably supports the need to identify up-regulated and mutated genes that better define this poor prognostic cohort. Recent genome-wide expression profiles subdivided TNLC patients into a poor prognostic group based on the overexpression of the DEP domain containing 1 gene (DEPDC1) (Okayama et al., 2011). We hypothesized that overexpression of DEPDC1 correlates with a specific sub-population of adenocarcinoma patients. Our initial studies indicate that DEPDC1 is constitutively expressed in both normal lung as well as lung cancer specimens. DEPDC1 transcripts are present as two variants (V1 and V2), with constitutive expression of the V1 variant in normal lung. We hypothesized that expression of the V2 transcript could be unique to NSCLC adenocarcinomas. Screening of FFPE NSCLC adenocarcinoma specimens using a proprietary qPCR approach demonstrated the presence of the DEPDC1 V2 variant but at levels that were not sufficient to serve as a sole biomarker. We therefore investigated whether the ratio of DEPDC1 V2 expression relative to V1 could serve as a biomarker in TNLC. Our preliminary data suggest that the ratio of V2 to V1 expression of DEPDC1 does in fact segregate TNLC into specific sub-populations. These studies have exciting diagnostic as well as therapeutic implications as Phase I/II studies using novel peptide vaccines derived against DEPDC1 have proven tolerable and efficacious for patients with bladder cancer and could potentially be extended to target these newly identified TNLC sub-populations.
Citation Format: Brock L. Schweitzer, Kasey D. Lawrence, John Handshoe, Rachel Skelton, Lindsay Chatfield, Liquan Xue, Stephan W. Morris, David R. Hout. The unknown piece of the pie: Molecular markers in triple-negative lung 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 1930. doi:10.1158/1538-7445.AM2013-1930
Abstract 1931: Development of a functional assay for the determination of BRCA1 carrier status.
Authors: Bathurst Lauren , Uy Paolo , Feilotter Harriet , Davey Scott 
Published: August 2014

Abstract
Germline mutations in the breast cancer susceptibility gene BRCA1 confer an overall lifetime risk of developing breast cancer of up to 80%. Given the high risk of cancer development associated with BRCA1 mutation carriers, it is important that they be identified early and accurately. However, identification is impeded by the number of Variants of Unknown Significance (VUS), therefore there is compelling rationale for a functional assay that will identify pathogenic mutations. Previous work in our lab developed a novel functional assay to predict BRCA1 status based on gene expression profiles. That study analyzed EBV-transformed lymphoblastoid cell lines (LCLs) of BRCA1 mutation carriers (BRCA1+/−) and controls (BRCA1+/+) and found that lymphocytes from BRCA1 carriers could be distinguished with high fidelity (∼90% accuracy) from individuals with two wild type copies of the gene. Interestingly, carriers were recognized through their basal gene expression profiles. Global gene expression level changes following ionizing radiation (IR) to induce the DNA damage response (DDR) did not support the development of an accurate class predictor.
The final predictor included a set of 43 genes. Many of these genes were also markers of differentiation in blood cells. A subset of these genes have now been validated in LCLs using qRT-PCR and protein-based methods including single reaction monitoring mass spec (SRM-MS) and flow cytometry. These assays were able to distinguish BRCA1 mutation carriers from controls based on the expression levels of specific markers, including genes with known roles in lymphocyte differentiation. Using these techniques, ongoing work is being done to test the ability of these markers to discriminate BRCA1 mutation carriers from controls using lymphocytes isolated from fresh blood samples.
Citation Format: Lauren Bathurst, Paolo Uy, Harriet Feilotter, Scott Davey. Development of a functional assay for the determination of BRCA1 carrier status. [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 1931. doi:10.1158/1538-7445.AM2013-1931
Abstract 1932: Association of genetic variants with prostate cancer risk.
Authors: Andavolu Radhika G. , Cardenas Jean-Luc , Shore Ross , Rubin Zach , MacMurray James , Chiravuri Krishna Kanth , Andavolu Murthy VS , Rubakovic Svetlana 
Published: August 2014

Abstract
Background: Genetic alterations can contribute to the malignant transformation and progression of prostate cancer. We have previously shown a strong association between specific leptin gene alleles, elevated serum leptin level, and body mass index in subjects with prostate and breast cancer. These studies showing association with leptin suggest a strong link with obesity as an increased risk factor. Studies have shown that adipose tissue TNFa and leptin, which are both overexpressed in obesity, induces the production of acute phase reactants through their autocrine or endocrine role. When GSTP1 is inactivated, prostate cells appear to become more vulnerable to somatic alterations upon chronic exposure to genome-damaging stresses such as oxidants and electrophiles that are contributed by environment and lifestyle. Studies also show that the methylation status of glutathione S-transferase p1 (GSTP1) could individually distinguish prostate cancer from benign prostatic hyperplasia. Based on prior studies, it is possible that multi gene analysis can provide better diagnostic or prognostic values for prostate cancer. Methods: In this study, we screened leptin gene markers, TNFa, GSTP1 and BCCIP(TOK-1A) in 126 prostate cancer and normal healthy age & sex matched controls (Prostate cases: Age range 45-94, Mean age 73.3 Control males: Age range 65-98, Mean age 73.5). Polymerase chain reaction was used to amplify Leptin, TNF-308 and GSTP1 genes and the products are analyzed using 3130 Genetic analyzer and PCR-RFLP methods. Statistical analysis was performed using the SPSS/PC statistical program (version 10.0 for Windows; SPSS, Inc.,Chicago, IL). Relationships between two groups and genotype variables were assessed by Pearson's correlation coefficient.
Conclusions: Prostate cancer is a complex, heterogeneous disease and there a variety of gene-based biomarkers that have been associated with prostate cancer. Our results show strong association of leptin (p&lt;0.006), GSTP1 (p&lt;0.023) with prostate cancer. Individually TNF and BCCIP showed a modest association but TNF/BCCIP gene interaction had a significant effect on prostate cancer risk and disease progression suggesting a multigene model for prostate cancer screening.
Citation Format: Radhika G. Andavolu, Jean-Luc Cardenas, Ross Shore, Zach Rubin, James MacMurray, Krishna Kanth Chiravuri, Murthy VS Andavolu, Svetlana Rubakovic. Association of genetic variants with prostate cancer risk. [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 1932. doi:10.1158/1538-7445.AM2013-1932
Abstract 1933: Visfatin promotes malignant breast cancer behavior through activation of STAT3.
Authors: Yuan Shyng-Shiou F. , Chen Yun-Ju , Lee Yi-Chen , Hou Ming-Feng 
Published: August 2014

Abstract
Background. Obesity-associated adipocyte dysfunction and adipocytokine imbalance has become a major focus in breast cancer research. In this study, the role of circulating visfatin, a recently discovered adipocytokine, in breast cancer was explored.
Methods. Serum visfatin was analyzed by enzyme-linked immunosorbent assay and correlated with clinicopathological characteristics and survival, while the expression of phosphorylated and activated STAT3 in breast cancer tissue was analyzed by immunohistochemistry. The biologic activity of visfatin as well as the underlying mechanisms was analyzed by using XTT cell proliferation assay, flow cytometry and immunoblotting analysis in human breast cancer cells.
Results. Serum visfatin was substantially elevated in breast cancer patients. It was positively associated with tumor stage and lymph node metastasis, but negatively associated with estrogen receptor (ER) and progesterone receptor (PR) status. Breast cancer patients with high serum visfatin, especially in combination with ER− and PR− status, had a poor patient survival. On the other hand, patients with high serum visfatin had a lower incidence of disease recurrence and a better patient survival after adjuvant hormone therapy. Serum visfatin was positively associated with STAT3 tyrosine phosphorylation in breast cancer tissues. In agreement with the clinical observation, visfatin treatment in breast cancer cells activated JAK1 and SRC as well as their downstream molecule STAT3, followed by an enhanced G1/S progression and cell proliferation.
Conclusion. Serum visfatin, through activation of STAT3, leads to a malignant cancer behavior and poor survival in breast cancer patients.
Key words: visfatin, adipocytokine, breast cancer, STAT3
Citation Format: Shyng-Shiou F. Yuan, Yun-Ju Chen, Yi-Chen Lee, Ming-Feng Hou. Visfatin promotes malignant breast cancer behavior through activation of STAT3. [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 1933. doi:10.1158/1538-7445.AM2013-1933
Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Abstract 1937: Development of microRNA-based prediction model of Trastuzumab treatment response for HER2-positive breast cancer using FFPE specimens.
Authors: Sato Fumiaki , Wang Zhipeng , Ueno Takayuki , Myomoto Akira , Takizawa Satoko , Pu Feng Ling , Masuda Norikazu , Mikami Yoshiki , Mikami Yoshiki , Shimizu Kazuharu , Saji Shigehira , Toi Masakazu 
Published: August 2014

Abstract
[Background and Aim] Although Trastuzumab has been used for HER2(+) breast cancer, the treatment response of Trastuzumab therapy depends on unknown mechanisms among individual cases. In order to avoid unnecessary adverse events and to lighten financial burden, pre-treatment prediction of trastuzumab treatment response would be beneficial for patients. Thus, in this study, we develop a prediction algorithm using microRNA expression profile using formalin-fixed paraffin-embedded (FFPE) specimens of HER2(+) breast cancer. [Materials and Methods] Eighty-three breast cancer patients who underwent trastuzumab-chemo combined therapy before operations were enrolled with written informed consent. FFPE specimens of pre-treatment core needle biopsy samples were collected, and regions containing cancer and adjacent stromal cells were laser-microdissected. Total RNA samples extracted from the microdissected specimens were subjected for microRNA microarray (3D-Gene®, Toray, Japan) analysis. Among these 83 patients, 39 cases had pCR (definition: complete response in IDC regions regardless presence of DCIS without lymph node metastasis), and the other 44 cases did not. According to the pCR/non-pCR information, we develop a prediction model using 35 signature microRNAs by a SVM technique. Prediction accuracy assessed by Leave-one-out validation was AUROC=0.889. The 35 signature microRNAs for trastuzumab treatment response included 7 out of 8 let-7 family members and miR-125a-5p/b-5p, which were downregulated in pCR specimens. [Conclusion] microRNA profile could predict treatment response of trastuzumab-chemo combined therapy for HER2(+) breast cancer, and the developed prediction algorithm might be a useful tool for clinical decision making.
Prediction Accuracy Outcome: non-pCR Outcome: pCR total Prediction: non-sensitive 35 6 41 Prediction: sensitive 9 33 42 total 44 39 83
Citation Format: Fumiaki Sato, Zhipeng Wang, Takayuki Ueno, Akira Myomoto, Satoko Takizawa, Feng Ling Pu, Norikazu Masuda, Yoshiki Mikami, Yoshiki Mikami, Kazuharu Shimizu, Shigehira Saji, Masakazu Toi. Development of microRNA-based prediction model of Trastuzumab treatment response for HER2-positive breast cancer using FFPE specimens. [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 1937. doi:10.1158/1538-7445.AM2013-1937