bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 3475: Negative impact of evaporation on cervical cancer cells during long term incubation is alleviated by Thermo Scientific Edge plate
Authors: Neeley Cindy , Verna Sarah 
Published: May 2015

Abstract
With more than half a million new cases and 275,000 deaths each year, cervical cancer ranks as the third and the fourth most common cause of cancer incidence and mortality, respectively, in women worldwide. Prophylactics, screening, testing, and treatment options for cervical cancer lead to an increasing need for new and innovative technologies. Microplates are widely engaged in all aspects of cervical cancer research. However, researchers have long struggled with media evaporation from the perimeter wells of their microplates. This condition negatively affects research results and lab productivity. In this study, we demonstrated that human cervical cancer HeLa cells suffered significant reduction in cell viability over 7-day incubation in the perimeter wells of standard 96-well plate. HeLa cells in these wells underwent premature NFκB nuclear translocation suggesting the onset of cell stress during culture. In comparison, study using the Thermo Scientific Edge plate with an innovative design of “build-in” mote showed significantly less evaporation from the perimeter wells. The variations between perimeter wells and center wells were minimal in Edge plate, indicating uniformed performance across the entire plate. Advantages of Edge plate were further demonstrated by the improvement in HeLa cell viability in perimeter wells when compared to standard 96-well plate. HeLa cells cultured in Edge plate were in a much healthier state and only demonstrated NFκB nuclear translocation when stress-inducing agent TNF-α was applied to the culture. In summary, Edge plate allows the use of all 96 wells without the concern of evaporation, resulting in improved consistency in assay models for in vitro research of cervical and other types of cancer.
Citation Format: Cindy Neeley, Sarah Verna. Negative impact of evaporation on cervical cancer cells during long term incubation is alleviated by Thermo Scientific Edge plate. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3475. doi:10.1158/1538-7445.AM2014-3475
Abstract 3479: The cellular thermal shift assay as a tool for setting indivual treatment schemes
Authors: Molina Daniel M. , Nordlund Pär 
Published: May 2015

Abstract
Many cancers respond insufficiently to existing therapies and acquired drug resistance often develops. To address this challenge, a range of different therapeutic strategies is currently in development. Many of these are based on the concept of targeted therapies, where target proteins are drivers of cancer processes or synthetic vulnerabilities of cancer cells. In this project we have used the newly developed CETSA method to monitor levels of drug binding to specific target proteins in tumors and primary cells from breast cancer patients. CETSA is a generic method for evaluating drug binding to target proteins in cells and tissues. The technique is based on the physical phenomenon of ligand-induced thermal stabilization of target proteins. Using this technique, it is possible to look at interactions between a drug and protein of interest without having to label them. Previously, we have validated drug binding in mammalian cancer cell lines for a set of important clinical targets and shown that a range of critical factors that are important for drug development can be identified at the target engagement level, including drug transport and activation, off-target effects, drug resistance as well as drug distribution in animal tissues.
By using different drugs and amounts we now have preliminary data suggesting that CETSA could be used as a tool for optimizing treatment schemes for individual care and for detecting resistance development at an early stage.
Citation Format: Daniel M. Molina, Pär Nordlund. The cellular thermal shift assay as a tool for setting indivual treatment schemes. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3479. doi:10.1158/1538-7445.AM2014-3479
Abstract 3481: Genetically-engineered mice as a cell line isolating tool
Authors: Kamiyama Hirohiko , Rauenzahn Sherri , Maitra Anirban , Eshleman James R. 
Published: May 2015

Abstract
BACKGROUND
Isolation of cell lines from patients’ tumors is difficult, due in large part, to contaminating fibroblasts that often overgrow the malignant cells. The same is true of xenografted tumors. To overcome this problem, we developed biochemically selectable mouse cells by using genetically-engineered mice.
METHODS
We constructed a series of hypoxanthine phosphoribosyl transferase (hprt) null immunodeficient mice. These include nude hprt-null, SCID hprt-null and NOD-SCID hprt-null mice.
Tumors from patients were implanted into these mice for growth. During growth of xenografted human cancers, hprt-null murine stromal cells replace their human counterparts to facilitate the growth of human cancer cells. Explanted tumors were then grown in tissue culture flasks with selection media (hypoxanthine, aminopterin, thymine; HAT media) to eliminate the mouse biochemically-defective fibroblasts and produce pure human cancer cell lines.
RESULTS
We successfully established several pancreatic cancer cell lines and an ovarian cancer cell line from patients using the hprt null immunodeficient mice.
CONCLUSIONS
The new cell line isolating system using genetically-engineered mice provides a greater chance to isolate pure cancer cell lines from patients’ tumors. This may allow personalized chemotherapy selection.
Citation Format: Hirohiko Kamiyama, Sherri Rauenzahn, Anirban Maitra, James R. Eshleman. Genetically-engineered mice as a cell line isolating tool. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3481. doi:10.1158/1538-7445.AM2014-3481
Abstract 3488: HPV detection by PCR in real time in peruvian women
Authors: Manrique Javier , Sarria Gustavo , Arias Abelardo , Mora Pamela , Limache Abel , Nuñez Maria del Carmen , Sullcahuaman Yasser , Vidaurre Tatiana 
Published: May 2015

Abstract
Background. In Perú Cervical cancer is a significant public health problem, according Globocan, it is the most frequent cancer among women in Peru, the incidence of this cancer is 34.5 and the mortality 16.3. In 2004, cervical cancer was responsible of 66,771 DALYs in Peru, 18.2% of the total. The human papillomavirus (HPV) is a well-known cause of cervical cancer. HPV tests are used as an adjunct test to decrease the false-negative rate of cytological screening. The HPV test will permit to separate the population in two groups, women with high risk to cancer cervical (HPV+) and women with low risk to cancer cervical (HPV-).
Objective. To identify the prevalence of the genotypes of Human Papillomavirus (HPV) in Peruvian women from marginal urban area of Lima according age.
Methodology. Samples of 5460 women aged 18 to 63 years were studied for analysis by the automated Roche Cobas 4800 system that detects genotypes 16 and 18 specifically and 12 other genotypes (31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 66) considered high risk HPV, for this purpose the system uses specific primers for the L1 region of the viral genome and control the system using B globin gene.
Results and Conclusions. According PCR screening the total samples were 5,460 (100%), 855 (15.62%) were positive by PCR, of the PCR positive 319 were positive by CBL (5.84%), 16 of them were LIE-AG (0.29%) and 0 carcinomas. The genotypes of PVH more frequent was 16 (16%), genotype 16 plus others high risk virus was 69 (8%), PVH 18 was 8 (3%). Of the 853 women that were positive for PCR, 149 of them had the highest risk HPV genotype 16 and the age group that most often present for this genotype was 30 to 39 years, this group is consider as high risk population. In general, PCR have been demonstrated an adequate prevalence rate of women in high risk according of other literature and we consider as an important test to cervical cancer control.
Ilustración 1. Frequency of HPV in Peruvian women.
Illustration 2. HPV Genotypes in peruvian women
Illustration 3. Distribution of CBL (+)
Ilustración 3. Genotipos de PVH y distribución por grupo etáreo. / HPV genotype distribution per age group.
Citation Format: Javier Manrique, Gustavo Sarria, Abelardo Arias, Pamela Mora, Abel Limache, Maria del Carmen Nuñez, Yasser Sullcahuaman, Tatiana Vidaurre. HPV detection by PCR in real time in peruvian women. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3488. doi:10.1158/1538-7445.AM2014-3488
Abstract 3495: A nucleolus-predominant piggyBac transposase increases transposition efficiency in human cancer cells
Authors: Hong Jin-Bon , Chou Fu-Ju , Ku Amy T. , Fan Hsiang-Hsuan , Lee Tung-Lung , Huang Yung-Hsin , Su I-Chang , Chen You-Tzung 
Published: May 2015

Abstract
PiggyBac is a prevalent transposon system used to deliver transgenes into and to functionally explore the mammalian untouched genomic territory. Efforts to increase its transposition efficiency in mammals through engineering the corresponding transposase (PBase) codon usage to improve its expression level is reported. The hyperactive PBase developed through screening for mutant variants are also established. To increase the safety for its potential use in regenerative medicine applications, site-specific transposition using engineered Zn finger-, Gal4- fused PBase, and an excision-prone PBase variant are also successfully developed. Here we report the construction of a nucleolus predominant PBase, NP-mPB, by adding a nucleolus predominant (NP) signal peptide from HIV-1 TAT protein to a mammalian codon optimized PBase (mPB). Although there is a predominant fraction of the NP-mPB-tGFP fusion proteins concentrated in the nucleoli, an insertion site preference toward nuleolar organizer regions (NORs) is not detected. Instead a 3-fold increase in piggyBac transposition efficiency is found in human cancer cell line.
Citation Format: Jin-Bon Hong, Fu-Ju Chou, Amy T. Ku, Hsiang-Hsuan Fan, Tung-Lung Lee, Yung-Hsin Huang, I-Chang Su, You-Tzung Chen. A nucleolus-predominant piggyBac transposase increases transposition efficiency in human cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3495. doi:10.1158/1538-7445.AM2014-3495
Abstract 3500: NCI's Provocative Questions Initiative
Authors: Berny-Lang Michelle A. , Greenspan Emily J. 
Published: May 2015

Abstract
In 2011, the NCI Director, Dr. Harold Varmus, created the Provocative Questions (PQ) initiative to encourage imaginative, bold approaches designed to tackle perplexing and previously neglected areas of cancer research. Based upon workshops and discussions with the extramural cancer research community and NCI program directors, a set of 24 questions and accompanying requests for applications (RFAs) were developed, addressing diverse topics in cancer risk and prevention, tumor development, and cancer detection, diagnosis, and treatment. In order to stimulate innovative hypotheses and approaches, the “power of the ideas” was heavily weighted with a de-emphasis on preliminary data. In the first year of the initiative, the NCI awarded 56 unique proposals, totaling $21.5 million of research support via the R01 and R21 mechanisms. Building upon the 2011 RFAs and adjusting to changes in the research landscape, 24 revised questions were developed for the 2012 RFAs with a commitment of up to $30 million in support. The NCI released the 2013 RFAs in September 2013 with a revised set of 20 questions, including new questions related to clinical effectiveness. Several PQ-supported research projects funded in the first year of the initiative will be highlighted in order to demonstrate the breadth of topics and high level of innovation supported by the initiative. Projects will be selected from the four main PQ thematic areas to provide a sense of the many diverse approaches being used to answer the selected PQ. In addition, trends and criteria from awarded proposals will be presented to provide insight to potential applicants regarding the outcomes of the program to date. Through engagement of the cancer research community, the PQ initiative seeks to continually leverage scientific advances to address currently unsolved, understudied questions in cancer, which may influence the future directions of NCI-sponsored research.
Citation Format: Michelle A. Berny-Lang, Emily J. Greenspan. NCI's Provocative Questions Initiative. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3500. doi:10.1158/1538-7445.AM2014-3500
Abstract 3501: Aspirin modulates oncogene expression in hct 116 colon cancer cells
Authors: Dachineni Rakesh , Ai Goqiang , Gunaje Jayarama B. 
Published: May 2015

Abstract
Aspirin is a 100 year old Non-steroidal anti-inflammatory drug (NSAID). Beside its use a cardio-protective agent, it is also used for treatment of headache, fever, and inflammation. Many studies have shown that regular intake of aspirin for 5 years or more reduces the risk of colon, breast, prostate, lung and skin cancers. However, mechanism for such actions is not very well understood. Since transformation of a normal cell to cancer cell often involves mutation and activation of proto-oncogene, we initiated this research to understand if aspirin modulates the level of oncogene products. In this study we focused on three different oncogenes; c-FOS, c-JUN and c-RAF. c-FOS and c-JUN are transcription factors, they form a heterodimer called Activator protein (AP-1) transcription factor and regulate the expression of other genes. We observed that, in serum starved HCT-116 colon cancer cells Aspirin and Salicylic acid inhibited serum induced c-FOS protein expression, however, levels of c-JUN protein were not inhibited. In fact Aspirin and Salicylic acid increased c-JUN levels marginally over the serum induced levels at all time points examined. Exposure of cells to Aspirin and Salicylic acid inhibited c-RAF levels in a concentration dependent fashion. Inhibition was observed at physiologically achieved concentration of 250 -500 micro molar Salicylic acid suggesting that Aspirin may mediate its effects through the formation of Salicylic acid. We are currently investigating how inhibition of c-RAF levels by Aspirin and Salicylic acid affects downstream signaling molecules such as p42/p44 MAP kinases. Modulation of proto oncogenes by Aspirin may represent an important pathway by which Aspirin may mediate its anti-cancer effects.
Citation Format: Rakesh Dachineni, Goqiang Ai, Jayarama B. Gunaje. Aspirin modulates oncogene expression in hct 116 colon cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3501. doi:10.1158/1538-7445.AM2014-3501
Abstract 3507: STAT3beta suppresses tumorigenesis via modulating the phosphorylation dynamics and transcription activity of STAT3alpha in esophageal squamous cell carcinoma
Authors: Zhang Haifeng , Lai Raymond , Li Enmin , Xu Liyan 
Published: May 2015

Abstract
While the oncogenic role of STAT3 is well-documented, a number of studies have described that STAT3 carries tumor suppressor functions. We hypothesized that the relative abundance of STAT3α and STAT3β, the two STAT3 isoforms, dictate its exact functional roles in cancer cells. Using Western blots and a cohort of esophageal squamous cell carcinoma (ESCC)(n=91), we found that STAT3β significantly correlated with a shorter survival (P=0.030), whereas phospho-STAT3α-Tyr705 and total STAT3 did not carry significant prognostic value. Correlating with these observations, STAT3β significantly suppressed the oncogenic effects of STAT3α in ESCC cell lines in a soft-agar clonogenic assay. Interestingly, while STAT3β suppressed the transcriptional activity of STAT3α, it enhanced the phosphorylation of STAT3α-Tyr705 and its nuclear translocation. STAT3β also prolonged the phosphorylation of STAT3α-Tyr705 and increased its cytoplasmic localization following cytokine stimulation. Furthermore, the substantial increase in phospho-STAT3α-Tyr705 in this setting was related to STAT3β-mediated inhibition of dephosphorylation. Taken together, our findings have highlighted the tumor suppressor roles of STAT3β via its interactions with STAT3α at different levels. Our data also strongly suggests that, an accurate interpretation of the oncogenic activity of STAT3α in tumors based on the detection of nuclear STAT3 or phospho-STAT3-Tyr705 requires the knowledge of the STAT3β expression status.
Citation Format: Haifeng Zhang, Raymond Lai, Enmin Li, Liyan Xu. STAT3beta suppresses tumorigenesis via modulating the phosphorylation dynamics and transcription activity of STAT3alpha in esophageal squamous cell carcinoma. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3507. doi:10.1158/1538-7445.AM2014-3507
Abstract 3512: MYCN and survivin cooperatively contribute to malignant transformation of fibroblasts
Authors: Hipp Nora , Christner Lisa , Wirth Thomas , Mueller-Klieser Wolfgang , Walenta Stefan , Schröck Evelin , Debatin Klaus-Michael , Beltinger Christian 
Published: May 2015

Abstract
The oncogenes MYCN and survivin (BIRC5) maintain aggressiveness of diverse cancers including sarcomas. To investigate whether these oncogenes cooperate in initial malignant transformation, we transduced them into Rat-1 fibroblasts. Indeed, survivin enhanced MYCN-driven contact-uninhibited and anchorage-independent growth in vitro. Importantly, upon subcutaneous transplantation into mice, cells overexpressing both instead of either one of the oncogenes generated tumors with shortened latency, marked anaplasia and an increased proliferation-to-apoptosis ratio resulting in accelerated growth. Mechanistically, the increased tumorigenicity was associated with an enhanced Warburg effect and HIF1α-linked vascular remodeling. This cooperation between MYCN and survivin may be important in the genesis of several cancers.
Citation Format: Nora Hipp, Lisa Christner, Thomas Wirth, Wolfgang Mueller-Klieser, Stefan Walenta, Evelin Schröck, Klaus-Michael Debatin, Christian Beltinger. MYCN and survivin cooperatively contribute to malignant transformation of fibroblasts. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3512. doi:10.1158/1538-7445.AM2014-3512
Abstract 3516: The mitochondrial sirtuin SIRT3 promotes survival of human melanoma cells in vitro
Authors: George Jasmine , Nihal Minakshi , Singh Chandra K. , Zhong Weixiong , Ahmad Nihal 
Published: May 2015

Abstract
Melanoma, a potentially lethal form of skin cancer, is the fifth most common type of new cancer diagnosis in American men and the sixth most common type in American women. Alarmingly, the annual incidence of melanoma among whites has increased steadily (&gt;60% over the past 30 years). Despite new developments in therapy, the overall survival of patients with advance-stage melanoma has not significantly improved. Therefore, concerted mechanism-based efforts are needed for prevention, diagnosis and treatment of this deadly neoplasm. A better understanding of molecular mechanisms contributing to melanoma development and progression can be useful in crafting new strategies for melanoma management. We are studying the role of sirtuin family of proteins in melanoma development and progression. Mammalian sirtuins (SIRT 1-7) are nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases, which have been shown to regulate metabolism, stress responses, and longevity, in model organisms. The role of sirtuins in cancer is fairly complex with dichotomous functions (tumor promoter versus tumor suppressor) depending on cell contexts. SIRT3 is a mitochondrial deacetylase that has been shown to be important in maintaining cellular metabolism by regulating mitochondrial functions. We have previously shown that SIRT3 was overexpressed in human melanoma cells and tissues and its inhibition resulted in an antiproliferative response in human melanoma cells (In: AACR Annual Meeting: Proceedings; 2013 April 6-April 10, Washington, DC; Abstract # 13-LB-9391). In this study, we found that short hairpin RNA (shRNA)-mediated knockdown of SIRT3 in SK-MEL-28 melanoma cells resulted in 1) G1-phase arrest of cell cycle, 2) induction of senescence as assessed by increase in senescence-associated β-galactosidase (SA-β-gal) activity, 3) senescence associated hetrochromatin formation (SAHF), 4) decrease in cell migration, and 5) increase in protein levels of p53, phospho-p53 (Ser15), p21Waf1, pRb and p16INK4a. Further, a stable exogenous overexpression of SIRT3 resulted in an increase in cell growth and clonogenic survival in Hs 294T melanoma cells. Based on our data we suggest that SIRT3 could be a contributing factor in melanoma survival. However, further extensive in-vitro and in- vivo studies are needed to ascertain the functional significance of SIRT3 in melanoma development and progression.
Citation Format: Jasmine George, Minakshi Nihal, Chandra K. Singh, Weixiong Zhong, Nihal Ahmad. The mitochondrial sirtuin SIRT3 promotes survival of human melanoma cells in vitro. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3516. doi:10.1158/1538-7445.AM2014-3516