bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract ADV04: Wisconsin Breast Cancer and the Environment Research Program.
Authors: Berry Mary Pat 
Published: August 2014

Abstract
The Breast Cancer and Environmental Research Program was established by the NIH to better understand if and how a women's risk of developing breast cancer, is increased by impacted environmental carcinogens during key periods of her development. These periods are referred to as “Windows of Susceptibility.” UW-Madison is one of the eleven project collaborators. The UW-Madison Principal Investigators are Michael Gould and Amy Trentham-Dietz. Dr. Gould is focusing on genetics of supectibilty and resistance to breast cancer during periods of mammary development. His work is focused on areas of the DNA that may be associated with breast cancer. Dr. Trentham-Dietz is looking at environmental exposures that may be associated with breast cancer risk. The joint role of genetics and environmental factors research utilizes data on over 7,000 Wisconsin women. Once the Gould lab identifies genes that confer resistance of susceptibility, the Trentham-Dietz lab will use human DNA to actively identify similar genes in women.
The Wisconsin project includes a particularly strong community partnership whose roles include giving input on the interests of women in the state. These community partners represent diverse organizations whose missions relate to breast cancer. The partners are: Wisconsin Cancer Council, the Breast Cancer Task Force of the WI Cancer Control Plan, Wisconsin Breast Cancer Coalition, Susan G. Komen- South Central Wisconsin Affiliate and the UW-Milwaukee Institute for Urban Health Partnerships. Together and with their distinct constituencies (health organizations, survivors, underserved populations, culturally diverse women, real women and advocates), these community partners do outreach for education relating to the program as well as for dissemination of the work being done at other sites as well as the UW-Madison.
Citation Format: Mary Pat Berry. Wisconsin Breast Cancer and the Environment Research Program. [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 ADV04. doi:10.1158/1538-7445.AM2013-ADV04
Abstract ADV16: Working together to advance research, support patients and create hope.
Authors: Nelson Scott 
Published: August 2014

Abstract
The Pancreatic cancer Action Network (PanCan) is a nationwide network of people dedicated to working together to advance research, support patients and create hope for those affected by pancreatic cancer. Our comprehensive approach included: 1) funding research, 2) demanding more aggressive federal research funding, 3) providing patients and caregivers with reliable information to make informed decisions with their healthcare teams, and 4) helping individuals and communities work together to raise awareness and fund for pancreatic cancer. We have over 500 mostly volunteer team members working in 70 affiliate locations around the country. We have more than 4000,000 constituents. We support the development of a comprehensive pancreatic cancer research community. We recruit, develop and retain the most adept investigators. We provide resources and tools and foster collaborations to advance scientific progress.
Citation Format: Scott Nelson. Working together to advance research, support patients and create hope. [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 ADV16. doi:10.1158/1538-7445.AM2013-ADV16
Abstract ADV23: Bridging the gap: An advocate's breast cancer journey.
Authors: Walker Desiree 
Published: August 2014

Abstract
The poster will prtray the various steps an advocate can take in the world of breast cancer. It will also define the journey through self-advocacy, local advocacy, patient advocacy and legislatie advocacy. These actions support bridging the gap trhough education and empowerment.
Citation Format: Desiree Walker. Bridging the gap: An advocate's breast cancer journey. [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 ADV23. doi:10.1158/1538-7445.AM2013-ADV23
Abstract LB-101: Targeting pancreatic cancer stroma with Palmatine, a novel compound from herbal supplement.
Authors: Chakravarthy Divya , Gong Jingjing , Hwang Rosa F. , Kumar Addanki Pratap 
Published: August 2014

Abstract
Pancreatic ductal adenocarcinoma is the fourth leading cause of cancer related deaths with 5-year survival rates less than 6%. Survival periods with gemcitabine in combination with various agents average over 6 months. Desmoplasia is a striking feature of pancreatic cancer. It is characterized by formation of dense stroma surrounding the tumor. This dense stroma serves as a therapeutic barrier for many chemotherapeutic drugs, in turn decreasing their efficacy. Pancreatic stellate cells (PSCs) have been reported to be involved in the observed desmoplastic reaction. Therefore targeting this stroma can be an alternate approach to pancreatic cancer. Previous studies from our laboratory showed that Nexrutine, a herbal supplement inhibits proliferation of multiple pancreatic cancer cells through modulation of Stat3/NFκB/Cox-2 signaling and reduced the number of animals developing fibrosis in vivo. To the best of our knowledge, the effect of Nexrutine or its active components on pancreatic stroma has not been studied. In this study we evaluated the effect of Nexrutine and Palmatine, an active component of Nexrutine, for its ability to target the stroma. Our studies show for the first time that Palmatine (i) inhibits proliferation of PSCs as well as the tumor cells; (ii) inhibits hedgehog signaling as evidenced by GLI expression and reporter activity; (iii) modulates expression and activity of downstream targets of GLI including Patched1, IKKB-ε and anti-apoptotic protein Survivin. Remarkably Palmatine treatment inhibits invasive ability of PSCs that is associated with reduced levels of COL1A1. Overall this is the first study reporting the ability of Palmatine to modulate Hh signaling and may have utility either alone or in conjunction with Gemcitabine for treatment of pancreatic ductal adenocarcinoma. Supported by NCCAM (AT 005513-01A1 and AT 007448l; APK).
Citation Format: Divya Chakravarthy, Jingjing Gong, Rosa F. Hwang, Addanki Pratap Kumar. Targeting pancreatic cancer stroma with Palmatine, a novel compound from herbal supplement. [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 LB-101. doi:10.1158/1538-7445.AM2013-LB-101
Abstract LB-107: Mitochondrial DNA mutations are diagnostic markers of renal oncocytomas.
Authors: Lang Martin , Vocke Cathy D. , Merino Maria J. , Schmidt Laura S. , Linehan Marston W. 
Published: August 2014

Abstract
Oncocytomas are mostly benign tumors of epithelial origin, characterized by dense accumulation of defective mitochondria. To date, no nuclear gene has been found to be responsible for these tumors, but a correlation of the oncocytic phenotype with the occurrence of disruptive mitochondrial DNA (mtDNA) mutations, mostly affecting genes encoding for proteins of Complex I of the respiratory chain (NADH dehydrogenase), has been shown in sporadic oncocytomas of different organs, including renal oncocytomas (RO).
Kidney cancer is made up of a number of tumors that present with a different histology and clinical course. They are caused by different genes, and therefore therapy needs to be adapted for each type of renal tumor. Imaging techniques are usually not sufficient to distinguish between benign and malignant forms of renal cell cancer (RCC). In addition, it is difficult to differentiate benign ROs from malignant forms of RCCs in samples from biopsies, because they share ultrastructural appearances, including abnormal mitochondria with altered cristae. Therefore, a reliable diagnostic tool would be invaluable to guide clinicians in the management of patients with RCC of unclear phenotype.
In our current work we tested whether mtDNA mutations can be used as diagnostic tools to distinguish between benign ROs and more aggressive forms of RCC. We sequenced the entire mtDNA in 36 samples that included sporadic, bilateral and multifocal as well as familial ROs and 30 non-oncocytic RCCs of different histologies. Moreover, the mitochondrial copy number was determined in all samples by real-time PCR. Furthermore, we sequenced the mtDNA from biopsies and compared it to the mtDNA sequence of the resected tumor.
We found a strong correlation between the presence of disruptive mtDNA mutations affecting complex I genes and the oncocytic phenotype in renal tumors. Additionally, oncocytomas showed significantly higher mtDNA copy number when compared to other RCCs. We also show that the mtDNA sequences from the biopsies correspond to the sequence of the tumor itself and are predictive of the phenotype. Hence, we propose that sequencing of the mitochondrial genome, supported by the analysis of the mtDNA copy number, may be used as a diagnostic tool to distinguish between benign and aggressive forms of RCCs to guide physicians in choosing the appropriate treatment for patients.
Citation Format: Martin Lang, Cathy D. Vocke, Maria J. Merino, Laura S. Schmidt, Marston W. Linehan. Mitochondrial DNA mutations are diagnostic markers of renal oncocytomas. [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 LB-107. doi:10.1158/1538-7445.AM2013-LB-107
Abstract LB-109: Identification of novel keratin fusion in squamous cell carcinomas.
Authors: Cheng Jack , Lai Ming-Tsung , Lee Shan-Chih , Chao Chun-Chin , Chen Chih-Mei , Ng Ka-Lok , Sheu Jim Jinn-Chyuan 
Published: August 2014

Abstract
Genetic instability is a hallmark during cancer development, such that gene fusions frequently occur when chromosomal translocation joins different genes. A variety of gene fusions have been identified in cancer, some of them are well known biomarkers for cancer diagnostic or chemotherapy targets. Our preliminary study uncovered novel gene fusions joining type I and II keratins in oral squamous cell carcinoma (OSCC) by pair-end RNA-seq transcriptome study. This finding was further validated by dual-color FISH and Sanger sequencing following nested PCR. Keratins form imtermediate filaments in a cell with equal-molar pairing of type I and II keratins, which maintain cell integrity under mechanical stresses and regulate adhesion and migration activity. Although keratins have been known as biomarkers in different types of squamous cell carcinoma (SCC), their functions in cancer development remain controversial. Interestingly, we detected the presence of keratin fusion in early-stage cancer specimens, suggesting the involvement of keratin fusion in carcinogenesis. Although sample size was limited, we found the presence of some keratin fusion variants exclusive to late-stage cancer specimens, which suggest the correlation of keratin fusion with cancer development. Besides OSCC, we also identified keratin fusion in esophageal, nasopharyngeal and cervical carcinoma in our preliminary study, which may suggest keratin fusion as a common driving mechanism among SCCs.
Citation Format: Jack Cheng, Ming-Tsung Lai, Shan-Chih Lee, Chun-Chin Chao, Chih-Mei Chen, Ka-Lok Ng, Jim Jinn-Chyuan Sheu. Identification of novel keratin fusion in squamous cell carcinomas. [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 LB-109. doi:10.1158/1538-7445.AM2013-LB-109
Abstract LB-119: Nucleolin promotes leukemogenesis through DNA hypermethylation.
Authors: Shen Na , Yan Fei , Pang Jiuxia , Liu shujun 
Published: August 2014

Abstract
Nucleolin (NCL), an abundant multifunctional phosphoprotein, is upregulated in numerous cancers. While NCL overexpression is implicated in tumor growth and angiogenesis, how NCL over-function contributes to tumorigenesis is poorly understood. Aberrant activity of DNA methyltransferase (DNMT) has been well documented in cancers and higher DNMT expression predicts worse prognosis, but how DNMT gene is regulated remains elusive. Given that NCL deregulation disrupts NFκB pathway, a DNMT1 gene transactivator, we speculated that NCL might promote cancer via DNA hypermethylation. To test this, initially we statistically analyzed 5 datasets from Gene Expression Omnibus. We found that NCL expression is elevated (n=121) and positively correlated with DNMT1/3a/3b in leukemia patients (n=242), indicative of their functional interaction in leukemogenesis. When Kasumi-1 and MV4-11 cells were transfected with NCL siRNA for 48 hours, by Western blot and PCR, we observed that NCL knockdown caused DNMT downregulation. Similar results were obtained when Kasumi-1 and MV4-11 cells were exposed to 1µM or 3µM of AS1411, a quadruplex DNA aptamer binding to NCL, for 48 hours. In contrast, ectopic expression of NCL in 293T cells upregulated DNMT, arguing for the positive role of NCL in DNMT transcription. Mechanistically, NCL-driven DNMT upregulation occurred via NFκB signaling, as NCL dysfunction (by siRNA and AS1411) dephosphorylated NFκBp65 (Ser536), and siRNA-mediated NFκB depletion abolished its phosphorylation leading to DNMT suppression. We then extracted genomic DNA from the above treated cells and subjected to Dotblot using 5mC antibody. We evidenced that NCL inactivation induced global DNA hypomethylation, whereas NCL overexpression resulted in DNA hypermethylation. Functionally, NCL inhibition by siRNA and AS1411 activated caspase-3 and caspase-8 and significantly abrogated leukemia cell clonogenic potential. Further, when MV4-11 cells were transfected with NCL siRNA, at 6 hours after transfection when the cells were not apoptotic, 2X106 cells were injected subcutaneously into nude mice for tumorigenesis (n=6). Compared to scramble control, we found that NCL knockdown dramatically decreased tumor volume and weight. H&E and IHC staining by Ki-67 or 5mC indicated the excessive reduction of tumor-forming rate and the significant decrease of DNA methylation. Thus, our collective findings highlight the interactive features between DNMT machinery and NCL oncogenic pathway providing a rationale for targeting NCL as a general approach to treat cancers unresponsive to current DNA methylation inhibitor therapy.
Citation Format: Na Shen, Fei Yan, Jiuxia Pang, shujun Liu. Nucleolin promotes leukemogenesis through DNA hypermethylation. [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 LB-119. doi:10.1158/1538-7445.AM2013-LB-119
Abstract LB-121: Tumor suppressor p53 is involved in a CHAMP-dependent spindle assembly checkpoint pathway.
Authors: Zhang Piyan , Ungewitter Erica , Appella Ettore , Scrable Heidi 
Published: August 2014

Abstract
A p53-dependent mouse spindle checkpoint has been reported since 1995. However the underlying mechanism is still unknown. Here, we found that p53 formed complexes with CHAMP and MAD2L2. Immunofluorescence analysis revealed that p53, CHAMP and MAD2L2 colocalized at spindle fibres from pro-metaphase to anaphase. CHAMP binds MAD2L2 and antagonizes its inhibition function on APC/C. We discovered that p53 enhanced the inhibition of MAD2L2 by CHAMP. P53 knock-down decreased M-phase index. Exogenous expression of p53 increased M-phase index and extended remarkable length of time in M phase. Notably, the regulation of p53 on M phase index was completely abrogated by either CHAMP or MAD2l2 knock-down, suggesting that the regulation of p53 on spindle assembly checkpoint pathway is dependent on CHAMP and MAD2L2. These results demonstrate that p53 participates in a mitotic checkpoint that ensures the maintenance of genetic fidelity during development.
Citation Format: Piyan Zhang, Erica Ungewitter, Ettore Appella, Heidi Scrable. Tumor suppressor p53 is involved in a CHAMP-dependent spindle assembly checkpoint pathway. [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 LB-121. doi:10.1158/1538-7445.AM2013-LB-121
Abstract LB-122: LY2835219, a selective inhibitor of CDK4 and CDK6, inhibits growth in preclinical models of human cancer.
Authors: Dempsey Jack A. , Chan Edward M. , Burke Teresa F. , Beckmann Richard P. 
Published: August 2014

Abstract
Cell growth is regulated by the activity of certain cyclin-dependent kinases (CDKs), including CDK4 and CDK6 (hereafter CDK4/6), which specifically regulate cell cycle progression through the G1 restriction point. These CDKs act with the D-type cyclins to phosphorylate and inactivate the retinoblastoma (Rb) tumor suppressor protein, which in turn enables cell cycle progression from G1 to S phase. LY2835219 is a selective inhibitor of CDK4/6 with IC50 of 2 and 10 nM for CDK4 and CDK6, respectively. The current study evaluates the activity of LY2835219 in preclinical models of human cancer including non-small cell lung cancer (NSCLC), melanoma, mantle cell lymphoma (MCL), and ovarian cancer. A secondary focus of this study is to identify potential predictive biomarkers for response to LY2835219 in NSCLC, melanoma, and other cancers. For NSCLC, increased sensitivity to LY2835219 is associated both in vitro and in vivo with KRAS mutations. For established melanoma cell lines, similar levels of in vitro sensitivity are observed in different genetic subtypes. Accordingly, LY2835219 shows single-agent activity in the A375 melanoma xenograft model with daily oral dosing at 45 or 90 mg/kg. For MCL, durable growth inhibition of subcutaneously implanted xenografts is achieved with daily oral dosing at 50mg/kg. Finally, in an intra-peritoneal model that recapitulates clinical features of human ovarian cancer, LY2835219 not only inhibits tumor growth but also increases survival. These studies suggest that LY2835219 may have potential therapeutic application in the treatment of human cancers with specific molecular alterations.
Citation Format: Jack A. Dempsey, Edward M. Chan, Teresa F. Burke, Richard P. Beckmann. LY2835219, a selective inhibitor of CDK4 and CDK6, inhibits growth in preclinical models of human 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 LB-122. doi:10.1158/1538-7445.AM2013-LB-122
Abstract LB-165: Safety and pharmacokinetics of liposomal curcumin in healthy subjects:A randomized placebo-controlled double blind first-in human study.
Authors: Storka Angela , Wolzt Michael , Vcelar Brigitta , Bolger Gordon , Majeed Muhammed , Helson Lawrence 
Published: August 2014

Abstract
Purpose: Curcumin exerts anti-proliferative and pro-apoptotic effects against various tumors in vitro and in vivo, and it has been found to suppress carcinogenesis in various organs. A liposomal curcumin formulation was developed enabling intravenous application.
Methods: 50 healthy male or female subjects between 18 and 45 years were allocated to receive single ascending doses of liposomal curcumin as a continuous infusion over 120 min. Dose levels ranged from 10 to 400 mg/m2. Within each dose group one subject was randomized to receive placebo. A premedication of intravenous diphenhydramine and dexamethasone or diphenhydramine alone was administered to prevent hypersensitivity reactions. Pharmacokinetic assessments included plasma and urine levels of Curcumin and tetrahydrocurcumin (THC), the active metabolite of Curcumin and were analyzed by a validated LC/MS/MS method. Safety assessments included monitoring for adverse events, laboratory safety parameters with special focus on hemolysis, vital signs and ECG.
Results and Conclusions: Liposomal curcumin infusions were tolerated without clinical symptoms. At the maximum tolerated dose of 400 mg/m2 of liposomal curcumin, transient increases in erythrocyte mean cell volume, echinocyte formation, and increased plasma lactate were observed. Markers of hemolysis (HBDH, potassium, haptoglobin, LDH, erythrocytes, Hb) did not change significantly, however, a tendency of erythrocyte loss (-0.5 T/l) was observed.
At a dose of 120 mg/m2 intermittent echinocyte formation of some erythrocytes was evident. Curcumin and THC levels were established rapidly forming a plateau during infusion with Cmax for curcumin ranging between 42 ± 22 and 2359 ± 412 ng/mL for doses of 10 to 400mg/m2, respectively. Cmax for THC was 7.1 - 15.8-fold lower than Cmax of curcumin. Upon termination of infusion Curcumin and THC were rapidly cleared from plasma with a mean residence time of 0.62 hr for curcumin and 1.69 hr for THC. Urinary curcumin levels accounted for &lt;0.12% of total systemic clearance.Conclusions: Relevant plasma levels of Curcumin were achieved by infusion of liposomal curcumin over 120 min. A continuous infusion (eg 24h) seems appropriate to achieve sustained exposure to curcumin. 120 mg liposomal curcumin/m2 is proposed as safe starting dose for phase I studies in patients with solid tumors.
Citation Format: Angela Storka, Michael Wolzt, Brigitta Vcelar, Gordon Bolger, Muhammed Majeed, Lawrence Helson. Safety and pharmacokinetics of liposomal curcumin in healthy subjects:A randomized placebo-controlled double blind first-in human study. [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 LB-165. doi:10.1158/1538-7445.AM2013-LB-165