bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract LB-428: Upregulation of serum amyloid A1 (SAA 1) gene is associated with ulcerative colitis-related colon cancer
Authors: Schaffer Michael W. , Smith Joan C. , Roy Tanusri Ghosh , Moses Harold L. , Adunyah Samuel E. , M'Koma Amosy E. 
Published: July 2012

Abstract
Purpose: Ulcerative colitis (UC)-associated colon cancer is frequently diagnosed in an advanced stage. SAA1 is a secreted protein made in the liver and circulates in low levels in blood. SAA1 gene is expressed in colon carcinomas and is a chemoattractant with induction of migration, adhesion, and tissue infiltration of monocytes and Polymorphnuclear-leucocytes (PMN-L).
Methods: Laser capture microdissection of colonic submucosa from UC (n=8), Crohn's colitis (CC) (n=8)), and normal (NL, n=8) samples was performed. The submucosal mRNA was extracted using the PicoPure(TM) RNA Isolation Kit. Comprehensive gene expression analysis of the pooled mRNA from each group was then performed using the Affymetrix GeneChip® Gene 1.0 ST Array System. Statistical comparisons of UC vs. CC and NL as well as CC versus UC and NL were performed (Wilcoxon Rank Test). To detect changes for UC, we compared UC to CC and UC to NL; and for CC, we compared CC to UC and CC to NL.
Results: Analysis of all UC vs. CC and NL controls showed 28,869 genes which were represented on the array by 26 probes spread across the full length of each gene. When compared UC vs. CC and NL SAA1 remained the most upregulated gene showing a 56.8-folds and 91.3-folds (p&lt; 0.0001) over expression.
Conclusion: Microarray assessments show significantly overexpression of SAA1 in UC specimens. SAA1 has a role in local inflammation in the microenvironment of malignant tissue and is expressed in colon carcinomas. Our finding may potentially facilitate and validate the SAA1 as a new early predictive clinical marker and a unique target for designing novel selective inhibitors for therapeutic intervention of UC-associated CRC.
Acknowledgement: 3U54CA091408–09S1 (MMC-VICC partnership)
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-428. doi:10.1158/1538-7445.AM2011-LB-428
Abstract LB-432: Effect of chronic nicotine consumption on NNK-induced lung tumors in the A/J mouse
Authors: Murphy Sharon E. , von Weymarn Linda B. , Schutten Melissa M. , Lewellen Mitzi , Kassie Fekadu , Modiano Jaime F. 
Published: July 2012

Abstract
Nicotine replacement therapy (NRT) is often used to maintain smoking cessation. Some individuals continue to use NRT for years after smoking cessation, and some NRT users continue to smoke. It is important to understand the impact of chronic nicotine use on lung cancer risk. Therefore, we determined the effect of nicotine administration on NNK-induced lung tumors in the A/J mice. P450 2A enzymes are key catalysts in NNK bioactivation, and nicotine is both an inhibitor and a mechanism based inactivator of P450 2A-catalyzed nicotine metabolism. These data suggest nicotine might protect from NNK-induced tumorigenesis. However, several investigators have reported that nicotine inhibits apoptosis, enhances angiogenesis and enhances proliferation. We hypothesized that nicotine would prevent or delay initiation of NNK-induced tumors, but accelerate tumor growth by reducing apoptosis and promoting inflammation. To test this, female A/J mice were administered a single dose of NNK (100 mg/kg i.p) and 200 ug/ml nicotine in the drinking water. Nicotine was administered 2 weeks prior to NNK, 44 weeks after NNK, throughout the experiment, or without NNK treatment. There were several key outcomes of this study: Chronic nicotine consumption did not affect P450 2A5-catalyzed metabolism in the lung of liver. Nicotine administration alone for 44 weeks did not increase lung tumor multiplicity. Nicotine given before or after NNK administration did not increase, or decrease, tumor number or tumor size. There was also no difference in the number of carcinomas per mouse or the number of adenomas with dysplasia. In conclusion, nicotine consumption in the drinking water had no effect on the tumorigenicity of NNK in the A/J mouse.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-432. doi:10.1158/1538-7445.AM2011-LB-432
Abstract LB-436: Rectal aberrant crypt foci for estimate of colorectal tumor recurrence: 3-year follow up study
Authors: Uchiyama Takashi , Takahashi Hirokazu , Sakai Eiji , Hosono Kunihiro , Endo Hiroki , Nakajima Atsushi 
Published: July 2012

Abstract
Background and Aims: Endoscopic screening and removal of colorectal tumor can reduce colorectal cancer, although surveillance colonoscopy is currently recommended after the initial screening and removal of colorectal tumor due to the possibility of newly developing tumor. Aberrant crypt foci (ACF) serve as surrogate biomarkers of human colorectal carcinogenesis. In this study we aimed to investigate the relationship between ACF and the recurrence of colorectal tumor after endoscopic polypectomy.
Methods: We performed high-magnification chromoscopic colonoscopy to identify lower rectal ACF on 82 subjects who underwent endoscopic polypectomy, and surveillance colonoscopy 3 years after baseline polypectomy at Yokohama City University Hospital.
Results: Marked elevation of the ACF number at baseline findings was observed in the tumor recurrence patients in comparison with the non recurrence patients (p &lt; 0.01). ROC analysis showed high specificity of the number of ACF for diagnosis of any tumor recurrence.
Conclusion: This is the first study to investigate relation between ACF and the recurrence of colorectal tumor after endoscopic polypectomy. These results suggested that ACF is useful for predictive factors for the recurrence of tumor.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-436. doi:10.1158/1538-7445.AM2011-LB-436
Abstract LB-462: Chemopreventive effects of freeze-dried strawberries in inflammation-associated mouse colon tumorigenesis
Authors: Yan Fei , Guan Huaji , Wang Yongquan , Huang Xin , Nines Ronald G. , Stoner Gary D. , Chen Tong 
Published: July 2012

Abstract
Colorectal cancer (CRC) is one of the most common malignant neoplasms in the United States. The risk for CRC is associated with extent and duration of inflammatory bowel disease (IBD). Patients with IBD are at increased risk of developing CRC when compared to the general population. Therefore, primary cancer chemoprevention is an important strategy to reduce the risk of CRC in IBD patients and thus, this approach has recently received more attention. Our laboratory has conducted extensive research on cancer chemoprevention in GI tract. In our previous study, we found that dietary freeze-dried black raspberries significantly inhibited adenoma and adenocarcinoma formation and decreased the level of oxidative stress in an azoxymethane (AOM)-induced rat CRC model. In a carcinogen-induced rat esophageal cancer model, we found that dietary freeze-dried strawberries significantly inhibited tumor development. However, the effects of strawberries in inflammation-associated CRC have not been investigated as yet. The principal objective of this study is to investigate the inhibitory effects of dietary freeze-dried strawberries in AOM/Dextran Sodium Sulfate (DSS)-induced mouse colon carcinogenesis. At 4–5 weeks of age, male Crj: CD-1 mice were given a single intraperitoneal injection of AOM (10mg/kg body weight), followed by 2% DSS in their drinking water for seven days, starting one week after the AOM injection. After 3 weeks, animals were fed AIN-76A diet or AIN-76A diet containing 10% freeze-dried strawberries. At week 20, mice were sacrificed for histopathological examination. We found that strawberries significantly decreased tumor incidence from 100% in mice treated with AOM/DSS only to 44.4% in mice treated with AOM/DSS plus strawberries (55.6% reduction, P = 0.02). We also found that the average animal body weight was significantly higher (P = 0.036) in animals fed strawberries (41.9 ± 5.3 g) when compared to animals fed control diet (38.7 ± 3.7 g). A large-scale investigation of the inhibitory effects of strawberries on biomarkers associated with colon carcinogenesis is under way. (Supported by California Strawberry Commissions)
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-462. doi:10.1158/1538-7445.AM2011-LB-462
Abstract LB-49: The endoplasmic reticulum chaperone protein GRP94 is required for maintaining hematopoietic stem cell interactions with the adult bone marrow niche
Authors: Luo Biquan , Lam Ben S. , Lee Sung Hyung , Wey Shiuan , Zhou Hui , Wang Miao , Chen Si-Yi , Adams Gregor B. , Lee Amy S. 
Published: July 2012

Abstract
Hematopoietic stem cell (HSC) homeostasis in the adult bone marrow is regulated by both intrinsic gene expression products and interactions with extrinsic factors in the HSC niche. GRP94, an endoplasmic reticulum chaperone, has been reported to be essential for the expression of specific integrins and selectively regulates early T and B lymphopoiesis. Interestingly, multipotent hematopoietic progenitors persisted and even increased in GRP94 deficient bone marrow chimeras, however, the mechanism is not well understood. Here we employed a conditional knockout strategy to acutely eliminate GRP94 in the hematopoietic system. Cell cycle analysis revealed that a loss of quiescence and an increase in proliferation led to an increase in Grp94 knockout (KO) HSCs. This expansion of the HSC pool can be attributed to the impaired interaction of HSCs with the niche, evidenced by enhanced HSC mobilization and severely compromised homing and lodging ability of primitive hematopoietic cells. Transplanting wild-type (WT) hematopoietic cells into a GRP94 null microenvironment yielded a normal hematology profile and comparable numbers of HSCs as compared with WT control, suggesting a cell autonomous effect. Investigating this, we further determined that there was a near complete loss of integrin α4 expression on the cell surface of Grp94 KO HSCs, which showed impaired binding with fibronectin, an extracellular matrix molecule known to play a role in mediating HSC-niche interactions. Collectively, our studies establish GRP94 as a novel cell intrinsic factor required to maintain the interaction of HSCs with their niche, and thus regulate their physiology.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-49. doi:10.1158/1538-7445.AM2011-LB-49
Abstract LB-5: The dominant-negative effect of an insulin-like growth factor-1 mutant that is defective in binding to integrins (αvβ3 and α6β4)
Authors: Fujita Masaaki , Ieguchi Katsuaki , Cardiff Robert , Borowsky Alexander D. , Takada Yoshikazu 
Published: July 2012

Abstract
Insulin-like growth factor-1 (IGF1) is a major therapeutic target for cancer. Integrin αvβ3 plays a critical role in regulating IGF1 signaling, while the specifics are unclear. We recently reported that IGF1 directly binds to αvβ3. The integrin-binding defective IGF1 mutant (R36E/R37E) is defective in inducing IGF signaling and a ternary complex (αvβ3, IGF1R, and IGF1) formation, although the mutant still binds to the type 1 IGF receptor (IGF1R). These findings suggest that direct binding of IGF1 to αvβ3 is required for intracellular signaling (J. Saegusa, S. Yamaji, K. Ieguchi, C.Y. Wu, K.S. Lam, F.T. Liu, Y.K. Takada, and Y. Takada, The direct binding of insulin-like growth factor-1 (IGF-1) to integrin αvβ3 is involved in IGF-1 signaling. J Biol Chem, 2009. 284: 24106–14). Here we describe that R36E/R37E suppressed proliferation and intracellular signaling induced by WT IGF1 in NIH3T3 fibroblasts, C2C12 myoblasts, and MCF-7 breast cancer cells (a dominant negative effect). R36E/R37E suppressed anchorage-independent growth of MCF-7 cells, while WT IGF1 enhanced it. Also, R36E/R37E suppressed the tumorigenesis of MCF-7 cells in SCID mice, while wt IGF-1 markedly enhanced it. Since MCF-7 cells express little or no αvβ3, we studied which integrins are involved in IGF signaling. We discovered that α6β4, which is over-expressed in cancer and implicated in tumor progression, directly binds to WT IGF1 (but not to R36E/R37E) in MCF-7. Interestingly, WT IGF1 induced a ternary complex formation (α6β4, IGF1, and IGF1R) but R36E/R37E did not. These results suggest that α6β4 in addition to αvβ3 plays a role in IGF signaling through direct binding to IGF1, and that R36E/R37E acts as an inhibitor of IGF signaling. We propose that R36E/R37E has potential as a therapeutic agent in cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-5. doi:10.1158/1538-7445.AM2011-LB-5
Abstract LB-50: Ionizing radiation can enhance TGFß induced EMT: Investigation of signatures of cross-talk with the ATM pathway
Authors: Wang Minli , Hada Megumi , Pluth Janice , Anderson Jennifer , O'Neill Peter , Cucinotta Francis 
Published: July 2012

Abstract
Epithelial-mesenchymal transition (EMT), a process whereby epithelial cells undergo transition to a mesenchymal phenotype, has long been known to play a role in cellular differentiation during development and tumor invasion. EMT can be viewed as an extreme form of cell plasticity characterized by loss of epithelial markers, cytoskeletal reorganization, and transition to a spindle-shaped morphology concurrent with acquisition of mesenchymal markers. Whereas EMT can be induced by a wide array of stimuli and cytokines, TGFβ is considered to be a key player of the process. Ionizing radiation (IR), both a carcinogen and a therapeutic agent, induces TGFβ activation in vivo, and also sensitizes human epithelial cells to undergo TGFβ-mediated EMT. In order to understand the likelihood of EMT following space radiation exposures to astronauts, we investigated possible interactions between the TGFβ and ATM pathway following radiation using hTERT immortalized human esophageal epithelial cells (EPC-hTERT), and mink lung epithelial cells (Mv1Lu). The identification of EMT can be shown in changes to morphology, related gene over expression or down regulation, which can be detected by RT-PCR, immunostaining and western blotting. Our study shows EMT can be induced by TGFβ alone, and a combination of heavy ion or proton radiation and TGFβ treatment in non-transformed Mv1Lu and EPC-hTERT cells can enhance the induction of EMT, with a dose as low as 0.1Gy. Pretreatment with TGFβRI inhibitor (SD208) can efficiently attenuate the Smad signaling pathway as detected by the phosphorylation of Smad2, as well as EMT. Serum deprival can also induce EMT-like phenotype in epithelial cells, which can be minimized by the TGFβRI inhibitor. In order to detail the role of the DNA damage response in EMT, we are studying inhibition of ATM or p53 in relation to TGFβ induced EMT. Results for cells irradiated in the presence of TGFβ, and the resulting function of ATM or p53 in the TGFβ mediated EMT process will be reported.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-50. doi:10.1158/1538-7445.AM2011-LB-50
Abstract LB-65: Advocating for Cancer Patients
Authors: Cowan Belita 
Published: July 2012

Abstract
The Lymphoma Foundation of America (LFA) is a national, nonprofit charity dedicated to helping cancer patients and their families. The organization provides support and counseling services, research, grants, a patient hotline, referrals, second opinions, information about patients' rights, and financial assistance to low-income families.
LFA in comprised of a scientific panel of experts with backgrounds in epidemiology, genetic, and biomedical research. Peer-reviewed research reports are published by the Foundation. LFA's report entitled, “Do Pesticides Cause Lymphoma”, is a meta-analysis of the scientific literature on the association between pesticide exposures and nonhodgkin lymphoma. “Lymphoma and Solvents” is another well-known LFA-published report on the relationship between benzene and lymphoma.
Each year, LFA selects promising, young university-based researchers for their outstanding work in cancer epidemiology to receive the “Young Scientist Award”. As part of the Foundation's education and outreach, it produces webcasts and partners with Patient Power to broadcast radio talk shows. These resources help patients gain the information needed to make appropriate decisions about their treatment options.
The Foundation also takes an active role in national health policy. LFA served as the lead amicus organization in the Agent Orange case argued before the U.S. Supreme Court. Lymphoma Foundation of America also filed a precedent-setting Freedom of Information Act request with the National Cancer Institute (NCI). This FOIA request established the right of cancer patients to receive copies of their experimental treatment protocols in all federally-funded cancer clinical trials. LFA has testified at multiple congressional hearings on the environmental causes of cancer.
Lymphoma Foundation of America is an independent nonprofit organization and does not accept drug company or medical industry funding. LFA is entirely supported by individuals and charitable foundations. The Lymphoma Foundation of America was founded in 1986 by lymphoma patients who came together to help each other recover from cancer. Today, LFA serves as a leading voice for the lymphoma patient community.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-65. doi:10.1158/1538-7445.AM2011-LB-65
Abstract LB-77: The Closing of the Every Woman Counts Program in California and Our Efforts to Reopen It
Authors: McDonald Sammantha 
Published: July 2012

Abstract
The California Collaborative of Susan G. Komen for the Cure includes the seven California affiliates located in Sacramento, San Francisco, Fresno, Los Angeles, Inland Empire, Orange County and San Diego. The Collaborative was originally formed to share best practices and synergies, but has since included public policy issues in its initiatives.
The ‘Every Woman Counts’ program was administered by California's Department of Public Health and provided breast and cervical cancer testing, diagnosis and treatment to uninsured women 40 years and older. The Public Policy Committee of the Collaborative worked very hard with the state's elected officials to help helped draft new legislation, propose an audit of the program, and lobby Capitol Hill. Advocates worked with the governor's health staff to ask for the capitol building to be lit pink to help raise breast cancer awareness. Supporters also spoke with anyone who would listen about the importance of this program for the insured and the lives that could potentially be lost if breast cancer went undetected. As a result of their efforts, the Collaborative found several supportive members in the state's legislature. The organization's representatives managed to pass legislation in late August to reinstate the ‘Every Woman Counts’ program.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-77. doi:10.1158/1538-7445.AM2011-LB-77
Abstract LB-84: The Importance of Consumer Involvement in Design, Implemenation and Dissemination of Breast Cancer Research
Authors: Werner Kathleen 
Published: July 2012

Abstract
There is a growing recognition among researchers and clinicians to include consumers and patients in all stages of cancer research. Various advocacy groups and individuals are designing programs to educate and equip survivors and consumers on various aspects of the cancer research and advocacy processes. It is crucial to make these consumers valued members of the dialogue on developing research that may one day directly impact them. The consumer voice is a valued aspect of research that has been consistently overlooked by many researchers and clinicians in the past. By including consumer perspective, these researchers and clinicians are now finding it can greatly enrich the scope, design, impact and outcomes of their research. This poster follows the path of one such consumer advocate_a young, pre-menopausal breast cancer survivor_and how other such consumers can impact the research process to maximize consumer benefit. Researchers will be able to explore how they may better engage consumers for enrichment of their research impact and stated aims.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-84. doi:10.1158/1538-7445.AM2011-LB-84