bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 989: Mild ER stress increases human ABC transporter expression and drug transport function in polarized cell monolayers.
Authors: Fung King Leung , Pixley Jessica , Talbert Darrell J. , Kapoor Khyati , Ambudkar Suresh , Gottesman Michael M. 
Published: August 2014

Abstract
Expression of ATP-binding cassette (ABC) transporter genes such as MDR1 (ABCB1/P-gp) is associated with poor outcome in chemotherapy and a multidrug resistant phenotype in cancer. Endoplasmic reticulum (ER) stress has been implicated in tumor growth but its role in drug resistance remains unclear. Here, we hypothesize that ER stress could increase expression of drug efflux transporters. To test this hypothesis, we developed a transient expression system in which human ABC transporters were ectopically expressed in a cell line monolayer by the BacMam baculovirus. The baculovirus is able to infect several mammalian cell lines including LLC-PK1, T-84, and MA104 without affecting the tightness of the host cell monolayers. In LLC-PK1 cells infected by BacMam vectors, induction of mild ER stress by pre-incubation (pre-conditioning) with thapsigargin (0.5 μg/ml) or tunicamycin (1 μg/ml), which are well-characterized ER-stress inducers, increased ABCB1 (P-gp) and ABCG2 (BCRP) levels. Drug transport assays showed that P-gp expressing cells pre-conditioned with thapsigargin showed increased directional transport of [3H] paclitaxel across the cell monolayer. The effect of thapsigargin was inhibited by the presence of the Erk inhibitor PD098059 but not the P38(MAPK) inhibitor SB203580, or the phosphatidylinositol 3-kinase (PI3-kinase) inhibitor LY294002, suggesting that expression of ABC transporter is influenced by mild ER stress response and, at least in part, by the ERK/MAPK signaling pathway. Although pre-conditioning with tunicamycin can increase P-gp expression, it also inhibits N-glycosylation of P-gp. Collectively, our findings indicate that mild ER stress responses up-regulate drug transporters introduced into cells by BacMam vectors.
Citation Format: King Leung Fung, Jessica Pixley, Darrell J. Talbert, Khyati Kapoor, Suresh Ambudkar, Michael M. Gottesman. Mild ER stress increases human ABC transporter expression and drug transport function in polarized cell monolayers. [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 989. doi:10.1158/1538-7445.AM2013-989
Abstract 996: Receptor tyrosine kinase AXL is upregulated in metformin resistant prostate cancer cells.
Authors: Bansal Nitu , Mishra Prasun , Cruz Kathleen , Bertino Joseph 
Published: August 2014

Abstract
Metformin is a biguanine derivative, widely used as an antidiabetic drug. Epidemiological studies on several types of cancers including breast, prostate, ovarian and pancreatic cancer show that patients treated with metformin have a lower incidence of cancer. Mechanistic studies have shown that metformin inhibits cancer cell viability by activating the AMP activated protein kinase (AMPK) pathway and inhibiting mTOR. In this study we developed a metformin resistance LnCap prostate cancer cells by exposing the cells continuously increasing concentrations of metformin. Micro-array data analysis comparing the resistant cells (4-fold) to parental cells showed that genes associated with receptor binding and with cell proliferation are primarily affected. EDIL3 (EGF-like repeats and discoidin I-like domains 3), EREG (eEpiregulin) and AXL (Axl receptor tyrosine kinase) are top three up regulated genes (∼ 35 fold). CALB2 (cCalbindin 2) and TPTE (transmembrane phosphatase with tensin homology) were the top down regulated genes (10 fold down regulated). AXL overexpression has earlier been demonstrated in Imatinib resistant CML cell lines and in CML cells from patients. We are currently investigating the role of Axl receptor tyrosine kinase in metformin resistant prostate cancer cells.
Citation Format: Nitu Bansal, Prasun Mishra, Kathleen Cruz, Joseph Bertino. Receptor tyrosine kinase AXL is upregulated in metformin resistant prostate 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 996. doi:10.1158/1538-7445.AM2013-996
Abstract 998: Poly(ADP-Ribose) polymerase inhibitor overcomes Rad51- mediated prostate cancer cells’ resistance to Topoisomerase I inhibitor under hypoxia.
Authors: Wu Minghui , Zhang Jingsong , Wang Xue 
Published: August 2014

Abstract
Intra-tumoral hypoxia has been proposed to create a “mutator” phenotype through down-regulation of DNA repair, leading to increased genomic instability and drug resistance. There is increasing interest to target hypoxic cancer cells with DNA-damaging agents and inhibitors of DNA repair. Here, we showed that hypoxia did not sensitize castration-resistant prostate cancer cells to the poly(ADP-ribose) polymerase (PARP) inhibitor veliparib or the DNA-damaging topoisomerase I inhibitor: Irinotecan or SN38. Although DNA repair proteins like Rad51 were decreased under hypoxia, up-regulation of Rad51 and Rad51 nuclear foci formation was observed soon after treatment with veliparib and SN-38 under hypoxia. This Rad51 up-regulation occurred at the transcription level and was mediated at least in part by E2F1. Inhibiting Rad51 expression with siRNA overcame prostate cancer cells’ resistance to SN-38 under hypoxia. Combining veliparib with Irinotecan significantly enhanced DNA damage and apoptosis under both hypoxic and normoxic culture conditions. Such enhanced DNA damage and anti-tumor activities were seen in the presence of Rad51 up-regulation and confirmed in vivo with PC3 mouse xenografts. These data illustrate a dynamic regulation of Rad51 by prostate cancer cells in response to hypoxia and DNA damage. The veliparib and Irinotecan combination can be further explored as a treatment for metastatic castration-resistant prostate cancer patients who have progressed through standard treatments.
Citation Format: Minghui Wu, Jingsong Zhang, Xue Wang. Poly(ADP-Ribose) polymerase inhibitor overcomes Rad51- mediated prostate cancer cells’ resistance to Topoisomerase I inhibitor under hypoxia. [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 998. doi:10.1158/1538-7445.AM2013-998
Abstract ADV06: The power of social media in patient advocacy.
Authors: Ciccarella Annemarie 
Published: August 2014

Abstract
Patient advocates are harnessing the power of social media by developing relationships with like-minded advocates from around the globe. Worldwide collaboration is now achieved seamlessly thanks to outlets like twitter with messages appended using a hash tag
Of greatest interest to me is bringing the voice of the patient to every aspect along the research continuum. Our unique perspective as stakeholders whose lives are directly impacted brings invaluable input to the table. From assisting in the writing of lay abstracts for funding applications to the review of grant applications, the voice of the patient is crucial. No longer will content sit on the sidelines, advocates want to be active participants in their treatment and many of us are especially interested in playing a role in the determining what constitutes worthwhile research. If it doesn't matter to the vast majority of the patient population, is it worth pursuing? While each individual story is important, the collective voice of the community is the most important voice of all.
Through social media interaction, a "connected" advocate has their finger on the pulse of what is important within their community. We sit in major conferences, sharing presentations in real time with others who are not in attendance. Active social media advocates are sharing stories as they hit the medical journals, discussing their relevance and oftentimes have doctors participating those discussions. Patients as partners, as collaborators whose voices are making a difference represent a powerful and positive paradigm shift in medical treatment and in the research landscape.
Citation Format: Annemarie Ciccarella. The power of social media in patient advocacy. [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 ADV06. doi:10.1158/1538-7445.AM2013-ADV06
Abstract ADV07: Cancer simplified: A web-based learning system for newly-diagnosed patients.
Authors: Darrow Duncan 
Published: August 2014

Abstract
Mission Statement:
Improving the quality of care for cancer patients on the East End of Long Island by establishing the Nations’ largest free cancer counseling center with a regional focus.
Initiatives:
We provide psycho-social counseling to approximately 300 newly-diagnosed cancer patients each year with a professional staff that includes two oncology social workers, a clinical psychologist with a PhD and a registered nurse. We also author a unique book - Coping with Cancer on the East End - which is a “where-to-find-it” guide to regional cancer care resources.
Poster Description:
It will focus on a relatively new initiative at Fighting Chance which is called “Cancer Simplified.” This is, in essence, a “sister website.” It serves as a web-based learning system about the “ABCs” of cancer, using a PowerPoint platform and is intended for newly-diagnosed patients with a high school reading level.
Cancer simplified aims to demystify the basic concepts of “what is cancer” using depiction instead of jargon-laden explanation. A deck of power point slides is augmented by a set of videos portraying Fighting Chance patients discussing their “cancer journeys.” Finally, a third element, known as “Easy Read,” drills into some of the largest cancer-helpful websites (like the ACS and NCCN) and takes the visitor directly to the most user-friendly pamphlets embedded in that site.
Citation Format: Duncan Darrow. Cancer simplified: A web-based learning system for newly-diagnosed patients. [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 ADV07. doi:10.1158/1538-7445.AM2013-ADV07
Abstract ADV13: Kure It Cancer Research.
Authors: Jones Karen 
Published: August 2014

Abstract
Kure It funds researchers conducting innovative projects in the fields of kidney cancer and other underfunded malignancies. Kure It raises funds inseveral ways: through annual special events; contributions from family and community foundations; and partnerships with the self storage industry, through which we've created tailored programs and events aimed at raising funding and awareness. Since its inception in 2007, Kure It has raised over $1.6 million for research. Our goal is to raise $1 million annually going forward. In 2012, Kure It awarded grants totaling $900,000, including two $250,000 awards given through Kure It's partnership with the AACR. Kure It funds support the work of researchers at major cancer centers across the United States.
Citation Format: Karen Jones. Kure It Cancer Research. [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 ADV13. doi:10.1158/1538-7445.AM2013-ADV13
Abstract ADV14: One advocate's journey: I went from fighting for my life to now fighting for others.
Authors: Keesen Kristen 
Published: August 2014

Abstract
Kristin Keesen, 45 year old colorectal cancer survivor from Colorado, describes her personal journey with colorectal cancer, and how she became inspired to work with Fight Colorectal Cancer to help others.
Fight Colorectal Cancer demands a cure for colon and rectal cancer. We educate and support patients, push for changes in policy that will increase and improve research, and empower survivors to raise their voices against the status quo.
Fight Colorectal Cancer believes that a cure means accessible, accurate population-based screening, and personalized treatment. To that end, we connect with people touched by colorectal cancer, provide information to help them cope with their current situation and then, if they choose, empower them to raise their voices and training advocates around the country. Fight Colorectal Cancer and our advocates educate lawmakers and regulators, pushing them for better policies. Our research advocates serve on research committees and help focus on meaningful outcomes. They also collaborate with a variety of prestigious academic institution on research projects.
In 2013, our One Million Strong initiative will help our advocates engage the general public by asking them to take the pledge to get screened if appropriate, and spread the word without screening.
Our programs include:
- Research Advocacy Training and Support (RATS): training lay advocates to participate effectively in the research process.
- Patient Information Services: providing information in multiple channels.
- Lisa Fund: career development funding for young researchers performing translational research relevant to patients with metastatic colorectal cancer.
Our seminal effort is Call-on-Congress, our annual advocacy training and lobbying event which is based on our regulatory and legislative priorities.
Citation Format: Kristen Keesen. One advocate's journey: I went from fighting for my life to now fighting for others. [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 ADV14. doi:10.1158/1538-7445.AM2013-ADV14
Abstract ADV15: Survivors teaching students: Saving women's lives program.
Authors: Leighton Susan L. 
Published: August 2014

Abstract
Since 2002, the Ovarian Cancer National Alliance has been working to save women's lives by helping health care practitioners learn to diagnose ovarian cancer earlier through the Survivors Teaching Students: Saving Women's Lives® (STS) Program. The program brings ovarian cancer survivors into the classrooms of medical schools, nursing schools, nurse practitioners and physician assistant programs to inform students about real women's experiences with the disease. Each woman who presents has a unique story. These women_many diagnosed at an advanced stage_are in a distinct position to help students become more sensitive to the disease's symptoms and risk factors that, in turn, can result in an earlier diagnosis. The STS program is currently presented in 74 medical schools nationwide, 3 nurse practitioner programs, 12 physician assistant programs, 42 nursing schools and 13 other allied health professional schools across the country. Awareness of symptoms and risk factors is one of the only tools available to women and their physicians which may lead to earlier diagnosis. Evaluation of the Survivors Teaching Students program has revealed that the students who have attended an STS presentation have an increased awareness of the symptoms and risk factors of ovarian cancer and when asked about the program after they entered medical practice, the respondents remembered the information they had learned in these presentations and felt it had impacted the ways in which they treated women presenting with these symptoms.
Citation Format: Susan L. Leighton. Survivors teaching students: Saving women's lives 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 ADV15. doi:10.1158/1538-7445.AM2013-ADV15
Abstract ADV22: Susan G. Komen story map.
Authors: Seago-Coyle Rebecca 
Published: August 2014

Abstract
The Susan G. Komen Foundation began as a promise between two sisters to end breast cancer forever. Susan Goodman Komen was diagnosed with breast cancer at the age of 33 and died three years later. Ms. Komen's younger sister, Nancy Goodman Brinker, created the foundation in 1982. The Komen Puget Sound Affiliate was founded in 1993 to forward the mission of our national organization - to save lives and end breast cancer forever by empowering people, ensuring quality of care for all and energizing science to find the cures. Since its inception, the Komen Puget Sound Affiliate has invested nearly $23 million in local nonprofit, tribal and government agencies that provide breast health and breast cancer services to medically underserved residents of our 16-county service area (Service Area).
The Puget Sound affiliate as a community that identify disparities, gaps in service and barriers to care that prevent women who live in our community from accessing, early detecting and surviving breast cancer.
Citation Format: Rebecca Seago-Coyle. Susan G. Komen story map. [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 ADV22. doi:10.1158/1538-7445.AM2013-ADV22
Abstract LB-104: Gadolinium-based nanoparticles sensitize head and neck carcinoma stem and nonstem cells to low and high LET radiation.
Authors: Aloy Marie-Thérèse , Miladi Imen , Armandy Emma , Billotey Claire , Tillement Olivier , Lux François , Perriat Pascal , Janier Marc , Rodriguez-Lafrasse Claire 
Published: August 2014

Abstract
Head and neck squamous cell carcinoma (HNSCC) is an aggressive and recurrent malignancy owing to intrinsic radioresistance and lack of induction of apoptosis. Several strategies aiming at radiosensitizing these tumors are currently being developed, one of these relying on the use of nanoparticles including high Z elements such as gadolinium (Z=64). Once delivered to the tumor, gadolinium-based nanoparticles (GBNs) should amplify the efficacy of radiotherapy through the generation of electron Auger cascades and secondary electrons.
This study aims at demonstrating the in vitro and in vivo radiosensitizing effect of sub-5 nm GBNs (composed of a core of gadolinium oxide, a shell of polysiloxane, and functionalized by diethylene triaminepentaacetic acid) in a SQ20B radioresistant HNSCC model. Owing to the crucial role of cancer stem cells in tumor initiation, disease recurrence and radioresistance, the radiosensitizing effect of GBNs was also tested in SQ20B stem-like cells.
The association of 0,6 mM GBNs with a photon or a 33.6 keV/µm carbon ion irradiation decrease significantly SQ20B cell survival. Radiosensitization goes through the increase in non-reparable DNA double-strand breaks, the shortening of G2/M phase blockage, the inhibition of cell proliferation, each contributing to the commitment into apoptosis. The combined treatment of GBNs with irradiation can also overcome the resistance of SQ20B stem-like cells.
Using an SQ20B tumor-bearing mouse model, we also demonstrate that GBNs in conjunction with photon irradiation significantly retard tumor growth compared with the radiation alone, with complete remission in some mice. Significantly, an increase in apoptosis and decrease in cell proliferation are also detected inside tumors in the combined treatment group.
These results suggest the interesting potential of GBNs in sensitizing resistant HNSCC tumors to radiotherapy and their possible contribution towards overcoming limitations of current cancer treatment.
This project was conducted under the framework of LANTHARAD (PDC019 CLARA 2010), PRRH-ETOILE and LABEX PRIMES (2012)
Citation Format: Marie-Thérèse Aloy, Imen Miladi, Emma Armandy, Claire Billotey, Olivier Tillement, François Lux, Pascal Perriat, Marc Janier, Claire Rodriguez-Lafrasse. Gadolinium-based nanoparticles sensitize head and neck carcinoma stem and nonstem cells to low and high LET radiation. [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-104. doi:10.1158/1538-7445.AM2013-LB-104
Abstract LB-110: Overexpression of EIF5A2 induced by gene amplification or hypoxia plays a pivotal role in tumor metastasis and angiogenesis.
Authors: CAO Tingting , Li Yan , Fu Li , GUAN Xinyuan 
Published: August 2014

Abstract
Hypoxia is often happened in solid tumors, which activates hypoxia response genes such as hypoxia-inducible transcription factors to keep tumor growth under the stress. Here we report that expression of EIF5A2, a frequently overexpressed oncogene in esophageal squamous cell carcinoma (ESCC), can be induced by hypoxia. Expression of EIF5A2 increased significantly in all five tested ESCC cell lines under hypoxic stress (P&lt;0.05), compared with normaxic condition. Besides induced by hypoxia, overexpression of EIF5A2 can be induced by gene amplification. Amplification of EIF5A2 at 3q26 has been frequently detected in various solid malignancies including ESCC. In the present study, overexpression of EIF5A2 was detected in over 40% of ESCC cases, which was significantly associated with lymph node metastasis (P=0.037), tumor invasion (P=0.044) and poor outcome (P=0.09) of ESCC patients. Functional study found that EIF5A2 promoted tumor metastasis and angiogenesis, two typical phenotypic changes of a tumor under hypoxic stress. Molecular study found that EIF5A2 was able to bind to the promoter region of HIF1α and up-regulate its expression, and subsequently promote tumor invasion and metastasis via epithelial-mesenchymal transition (EMT). EIF5A2 could also promote angiogenesis via up-regulating VEGF in a HIF1α-mediated manner. Both in vitro and in vivo assays showed that silencing EIF5A2 expression by RNAi with shRNA-eIF5A2 could effectively inhibit tumor growth, especially when combined with chemotherapeutic agents. Taken together, these findings demonstrated that overexpression of eIF5A2 induced by gene amplification or hypoxia plays critical roles in cancer metastasis and angiogenesis via HIF1α-mediated signaling pathway under normaxic or hypoxic condition, respectively.
Citation Format: Tingting CAO, Yan Li, Li Fu, Xinyuan GUAN. Overexpression of EIF5A2 induced by gene amplification or hypoxia plays a pivotal role in tumor metastasis and angiogenesis. [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-110. doi:10.1158/1538-7445.AM2013-LB-110