bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4294: Addressing the limitations of thyroid biopsies: Using elastic scattering spectroscopy to improve the assessment of indeterminate nodules
Authors: Rosen Jennifer E. , Giordano Nicholas J. , Rodriguez-Diaz Eladio , A'Amar Ousama M. , Bigio Irving J. , Lee Stephanie L. 
Published: May 2015

Abstract
Thyroid cancer is the most common endocrine tumor. The gold standard, fine-needle aspiration biopsy, yields 10-25% indeterminate results necessitating diagnostic surgery. Using the real-time imaging technique of elastic scattering spectroscopy (ESS), a pair of fiber optics are inserted through the lumen of a biopsy needle and placed in contact with the thyroid nodule moments before cell collection occurs. Our research focuses on utilizing this optical-biopsy technique to measure tissue in vivo with broadband light during biopsy. In this study we demonstrate the potential our novel ESS-integrated optical biopsy syringe can have on cancer diagnostics. Spectra from 148 patients were collected. Additional time during biopsy to perform ESS measurements was less than 20 seconds. Cytology results for enrolled patients were as follows: 37 indeterminate, 6 insufficient, 5 malignant and 100 benign. Correlating ESS measurements with cytology, we identified changes in spectra when fiber optics were placed in contact with malignant versus benign tissue. From our enrolled benign and malignant patients, we trained an algorithm to diagnose indeterminate nodules based off of ESS spectra and compared to pathology. Preliminary analysis of spectra show ESS has a NPV of 0.99, a sensitivity of 0.92 and a specificity of 0.85. This data suggests that elastic scattering spectroscopy may improve the reliability, speed, and cost of cancer diagnostics.
Citation Format: Jennifer E. Rosen, Nicholas J. Giordano, Eladio Rodriguez-Diaz, Ousama M. A'Amar, Irving J. Bigio, Stephanie L. Lee. Addressing the limitations of thyroid biopsies: Using elastic scattering spectroscopy to improve the assessment of indeterminate nodules. [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 4294. doi:10.1158/1538-7445.AM2014-4294
Abstract 4301: Detection and characterization of regions of hypoxia within orthotopic pancreatic tumors using multispectral optoacoustic tomography
Authors: Hudson Shanice V. , Kimbrough Charles , Egger Michael , Khanal Anil , Smith Michelle E. , Grizzle William E. , McNally Lacey R. 
Published: May 2015

Abstract
Optical imaging is a vital tool in cancer research for visualization of tumors in preclinical models. However, resolution for bioluminescence and fluorescence modalities is restricted to a depth of five millimeters, as light is attenuated at increased depth and autofluorescence can create background noise. Light propagation becomes diffuse at only a few millimeters, resulting in light scattering and absorption. To improve imaging resolution and acquisition in real-time, multispectral optoacoustic tomography (MSOT) was utilized to visualize molecular phenomena such as the tissue oxygenation of characteristically hypoxic aggressive pancreatic tumors. SCID mice were orthotopically implanted with S2VP10L and MIA PaCa-2 pancreatic cancer cells that highly express the epidermal growth factor receptor (EGFR), which exhibits extracellular domain binding of the epidermal growth factor (EGF) ligand.
Cohorts were then intravenously injected with fluorescent EGF ligand probes and imaged semiweekly to follow tumor growth and morphology. Medical Grade Air levels were set to 0.9 L and oxygen at 0.1 L to assess the correlation of increased hypoxia with tumor growth and progression. Pancreatic tumor cells were imaged concurrently with evaluating levels of oxygenated and deoxygenated hemoglobin, providing a distinct picture of the tumor and its vascularization. Use of MSOT to detect regions of hypoxia within tumor was validated using pimonidazole immunohistochemical staining of tumor tissue. For the first time, our data demonstrate regions of tumor hypoxia in living subjects, at depth, and noninvasively, via optoacoustic tomography. Dynamic assessment of tumor microenvironment, especially regions of tumor hypoxia, is essential to effectively target and treat tumors that are otherwise resistant to treatment.
Citation Format: Shanice V. Hudson, Charles Kimbrough, Michael Egger, Anil Khanal, Michelle E. Smith, William E. Grizzle, Lacey R. McNally. Detection and characterization of regions of hypoxia within orthotopic pancreatic tumors using multispectral optoacoustic tomography. [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 4301. doi:10.1158/1538-7445.AM2014-4301
Abstract 4308: 3D nuclear telomeric signatures define circulating tumor cells (CTCs) and characterize CTC subpopulations in intermediate risk prostate cancer patients
Authors: Julius Awe A. , Yan Adam , Shah Nidhi , Ludger Klewes , Kuzyk Alexandra , Xu Michael , Boles Ramy , Saranchuk Jeff , Drachenberg Darrel , Mai Sabine 
Published: May 2015

Abstract
Intermediate risk prostate cancer is a current medical challenge since the patients in this group can either be stable or progress, and there is no predictor for individual risk. Stratifying these patients would spare the patients unnecessary treatment or indicate the start of treatment immediately without losing precious time. Currently, prostate specific antigen (PSA) is used as evidence for biochemical progression. A more sensitive biomarker is needed to detect disease progression earlier and more reliably.
We have isolated circulating tumor cells (CTCs) using a filtration-based device (ScreenCell). We subsequently performed the genetic characterization of the captured CTCs on a single cell basis. Using three-dimensional (3D) nuclear telomere imaging and quantitative analysis of 3D telomeric signatures of CTCs, we have characterized CTCs in the blood of the patients and have identified patient subgroups with one or more groups of CTCs. 380 samples of intermediate risk prostate cancer all revealed the presence of CTCs. However, the CTCs found were not genetically identical. Marked heterogeneity was seen, and three main groups of CTC profiles were defined based on TeloView software our group developed earlier. Repeat samples taken 6 months intervals define stable, mildly changing and significantly altered 3D profiles indicative of disease stability vs. progression.
Citation Format: Awe A. Julius, Adam Yan, Nidhi Shah, Klewes Ludger, Alexandra Kuzyk, Michael Xu, Ramy Boles, Jeff Saranchuk, Darrel Drachenberg, Sabine Mai. 3D nuclear telomeric signatures define circulating tumor cells (CTCs) and characterize CTC subpopulations in intermediate risk prostate cancer patients. [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 4308. doi:10.1158/1538-7445.AM2014-4308
Abstract 4318: Mycoplasma arginini infection shifts the energy catabolism ratio of metastatic macrophages towards fermentation and is associated with an increase in primary tumor size, metastasis and malignancy
Authors: Flores Roberto , Brown Ashley K. , Akgoc Zeynep , Seyfried Thomas N. 
Published: May 2015

Abstract
Mycoplasma are the smallest self-replicating prokaryotes and are burdened by their notoriety. It is widely unknown that mycoplasma are readily detected in many primary human cancer tissues and can influence tumorigenesis. Some mycoplasma species such as M. fermentans and M. hyorhinis can transform normal murine and human cell lines into tumorigenic cells. Mycoplasma infection can inactivate tumor suppressor genes and activate oncogenes. These observations suggest that mycoplasma can be both carcinogenic and or onco-modulators. We found that M. arginini was present in the metastatic macrophage cell line VM-M3 (referred to as M3myco+). Antibiotic was used to eradicate M. arginini (verified by mycoplasmal 16S rDNA PCR amplification) from the M3 cells (M3myco- cells). Oxygen consumption rate was higher in the than the M3myco- cells than in the M3myco+ cells, whereas lactate production was similar in both the M3myco+ and M3myco- cells. Glucose suppressed oxygen consumption in both cell lines indicating a Crabtree effect. The in-vitro proliferation rate was similar in both cell lines when seeded at low density, but was higher in the M3myco+ cells than in the M3myco- cells at higher cell densities. Tumor size at the primary inoculation site in flank was notably smaller and systemic metastasis in the syngeneic inbred VM mouse host was qualitatively less for the M3myco- cells than for the M3myco + cells, respectively. Survival was also longer in VM mice inoculated with the M3myco- cells compared to the M3myco+ cells. Our data indicate that M. arginini is an onco-modulator that might influence tumor growth through an effect tumor cell energy metabolism. (Supported by Boston College Research Expense fund).
Citation Format: Roberto Flores, Ashley K. Brown, Zeynep Akgoc, Thomas N. Seyfried. Mycoplasma arginini infection shifts the energy catabolism ratio of metastatic macrophages towards fermentation and is associated with an increase in primary tumor size, metastasis and malignancy. [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 4318. doi:10.1158/1538-7445.AM2014-4318
Abstract 432: BIN3 is a novel 8p21 tumor suppressor gene that regulates the attachment checkpoint in epithelial cells
Authors: Marshall Netonia , Sanchez Felix , Llobet David , Barrueco Ruth Rodriguez , Castro Veronica , Kotlia Dylan , Pires Maira , Villagrasa Patricia , Putcha Preeti , Parsons Ramon , Pe'er Dana , Silva Jose 
Published: May 2015

Abstract
An important characteristic of multicellular organisms is the control that the tissue architecture exerts on the fate of individual cells. Epithelial cells sense their location through interactions with the extracellular matrix (ECM) and remove themselves by programmed cell death (anoikis) when those interactions are disturbed. Importantly, anoikis is a line of defense that has to be circumvented by cancerous epithelial cells to be able to leave their home environment and establish long distance metastases. Here, by combining a genome-wide RNAi screen and a novel algorithm to study copy number alterations (ISAR-DEL), we identify the Bridging Integrator-3 (BIN3) as a novel 8p21 tumor suppressor gene whose inactivation promotes escape from anoikis in epithelial cancers. Mechanistically, we link the tumor suppression function of BIN3 to its ability to relocate to the cell membrane after cell detachment and to induce a proapoptotic cascade. This death signaling is mediated by CDC42 activation of the P38-α stress pathway and the consequent accumulation of the apoptotic facilitator BimEL. Our results identify BIN3 as a novel epithelial tumor suppressor gene, provide novel insights on the mechanisms of attachment tumor suppressor checkpoint and highlight the importance of anoikis escape in driving cell transformation and metastasis in human cancer.
Note: This abstract was not presented at the meeting.
Citation Format: Netonia Marshall, Felix Sanchez, David Llobet, Ruth Rodriguez Barrueco, Veronica Castro, Dylan Kotlia, Maira Pires, Patricia Villagrasa, Preeti Putcha, Ramon Parsons, Dana Pe'er, Jose Silva. BIN3 is a novel 8p21 tumor suppressor gene that regulates the attachment checkpoint in epithelial 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 432. doi:10.1158/1538-7445.AM2014-432
Abstract 4327: Mitochondrial reprogramming in triple negative breast cancer progression
Authors: Park Junhyoung , Arora Kavisha , Vithayathil Sajna A. , Donti Taraka R. , Creighton Chad , Lewis Michael T. , Sreekumar Arun , Wong Lee-Jun , Kaipparettu Benny A. 
Published: May 2015

Abstract
Unlike other subgroups of patients with breast cancer (BCa), for triple negative (TN) BCa, there is a current lack of understanding of driver pathways and hence are often managed using more generic therapies. Thus, it is important to identify the underlying mechanisms of triple negative breast cancer progression and its racial disparity. Mitochondria-nuclear crosstalk is a bidirectional pathway of communication between mitochondria and nucleus that influences many cellular and organismal activities. This crosstalk can regulate several oncogenic pathways that regulate cellular tumor characteristics. With the advent of transmitochondrial cybrid (cybrid) technology, it is now possible to examine the specific contribution of tumor-associated mitochondria in neoplastic growth and development under a defined common nuclear background. We used this model system to identify mitochondria regulated pathways in TN BCa. Among different oncogenic pathways, Src pathway is frequently over-expressed in TN BCa and Src inhibitors are proposed as one of their current treatments of choice. However, single drug therapy with Src inhibitors failed to control metastatic TN BCa in recent Phase-II trials. These highlight an important question on the mechanism behind the regulation of Src oncogenic signature in TN BCa. Using cybrid technology, we have discovered critical role of cancer mitochondria in the post-translational modification of Src oncogenic pathway. Interestingly we discovered that the Src autophosphorylation, which activate Src-mediated oncogenic pathway, depends on mitochondrial tumor characteristics. Specifically, our strong preliminary data suggest that mitochondrial reprogramming is a critical step in the autophosphorylation and activation of Src pathway in metastatic TN BCa cells. Our findings suggest mitochondria targeted drugs as promising combination therapy for the management of Src positive TN BCa.
Citation Format: Junhyoung Park, Kavisha Arora, Sajna A. Vithayathil, Taraka R. Donti, Chad Creighton, Michael T. Lewis, Arun Sreekumar, Lee-Jun Wong, Benny A. Kaipparettu. Mitochondrial reprogramming in triple negative breast cancer progression. [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 4327. doi:10.1158/1538-7445.AM2014-4327
Abstract 4338: The lipogenic phenotype of HER2/neu-positive breast cancer cells
Authors: Baumann Jan M. , Conklin Douglas S. 
Published: May 2015

Abstract
15 - 30 % of all breast cancer cases are classified as HER2/neu-positive, a very aggressive form of breast cancer that correlates with a poor prognosis, reduced survival time and increased incidence of metastasis. We have shown that the HER2-positive breast cancer cell line BT474 relies on a unique Warburg-like metabolism for survival and aggressive behavior. These cells are dependent on fatty acid synthesis, presumably as a means to regenerate NAD+ for aerobic glycolysis. The cells show markedly increased levels of stored fats compared to other breast cancer cell lines and disruption of the synthetic process results in apoptosis.
This metabolic phenotype is operating at its limits in HER2-positive cells, as addition of exogenous palmitate results in cell death, whereas HER2-normal cells are not affected by this treatment. Microarray analysis of palmitate-treated HER2/neu-positive SKBR3 cells and HER2-normal MCF7 cells suggests that palmitate induces an ER-stress response in the HER2-positive cells. This is congruent with protein markers for stress-related translational stalling, which ultimately result in CHOP-dependent cell death. Palmitate distinctly reduces the expression of the HER3 protein and combination treatments with palmitate and HER2-targeted therapeutic compounds show synergistic effects and markedly increase the cytotoxic effects of either compound alone.
In addition to these translational changes, palmitate treatment of HER2/neu-positive SKBR3 cells results in AMPK activation and subsequent inhibition of fatty acid synthesis. Transcriptome and global metabolite profiling analyses of the effect of increased palmitate on these cells indicate that palmitate alters the metabolic phenotype by re-routing the glucose carbon flux in the cells.
Supported by CDMRP Award W81XWH-11-1-0094 to Jan Baumann and NCI Award 5R01CA136658-03 to Douglas Conklin.
Citation Format: Jan M. Baumann, Douglas S. Conklin. The lipogenic phenotype of HER2/neu-positive breast 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 4338. doi:10.1158/1538-7445.AM2014-4338
Abstract 4348: TGF-β enhances mir-455-5p expression that regulates tumorigenesis through UBE2B in betel quid-associated oral cancer
Authors: Cheng Chao-Min , Shiah Shine-Gwo , Chen Ya-Wen , Chang Jang-Yang 
Published: May 2015

Abstract
Oral cancer is the fourth foremost case of death from cancer, and the major causes of death are local recurrence and distant metastasis. The strong associations between oral squamous cell carcinoma (OSCC) and dietary habits such as alcohol consumption (A), betel quid chewing (B) and cigarette smoking (C) and its predominance in men have been well documented. Evidences have shown that miRNAs are involved in tumorigenesis of various cancers through regulating their downstream targets. In order to identify changes in miRNAs specific for betel quid-associated oral squamous cell carcinoma (OSCC), we investigated the expression profiles of miRNAs in a panel of 40 pairs of OSCC specimens and their matched non-tumorous epithelial counterparts. Our data showed that the expression levels of mir-455-5p are significantly (P&lt;0.0001) higher in tumor tissue than in their counterpart normal tissue. In addition, the expression levels of mir-455-5p in oral cancer cell lines are also higher than normal oral epithelial cell line. Knockdown of mir-455-5p reduces both anchorage-independent growth and proliferative ability in two head and neck cancer cells, and vice versa in mir-455-5p overexpressing cells. Collectively, these evidences showed that mir-455-5p serves as an oncomir in betel quid-associated oral cancer. Furthermore, by analyzing both the array data from cancer patients and cell lines, and then intersected with the results from website tools, we have identified ubiquitin-conjugating enzyme E2B (UBE2B) to be the target of mir-455-5p, which was further validated by 3′-UTR luciferase reporter assay and Western blot analysis. We also revealed that UBE2B suppression actually rescued both cell transformation and growth ability in mir-455-5p knockdown cells. Our data further demonstrated that the expression level of mir-455-5p is regulated by transforming growth factor-β (TGF-β) pathway. Moreover, mir-455-5p expression was suppressed by the treatment of TGF-β downstream regulators. In conclusion, our results showed that the expression of mir-455-5p is regulated by TGF-β-dependent pathway, which subsequently leads to alteration the expression of UBE2B and contribute to the tumorigenesis of betel quid-associated oral cancer. (This work was supported by following grants: National Health Research Institutes CA-101-PP-22, National Research Program for Biopharmaceuticals 100CAP015-5 and National Science Council 102-2325-B-400-007)
Citation Format: Chao-Min Cheng, Shine-Gwo Shiah, Ya-Wen Chen, Jang-Yang Chang. TGF-β enhances mir-455-5p expression that regulates tumorigenesis through UBE2B in betel quid-associated oral cancer. [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 4348. doi:10.1158/1538-7445.AM2014-4348
Abstract 4349: Regulation of proliferation and platelet-derived growth factor expression in desmoid tumors by microRNA-29
Authors: Al-Jazrawe Mushriq , Poon Raymond , Liu Jessica , Alman Benjamin 
Published: May 2015

Abstract
Desmoid tumors (DT), also called aggressive fibromatosis, are a rare, locally invasive soft tissue tumors. While DTs harbor mutations that activate β-catenin, a major effector molecule of canonical Wnt signaling, they also display elevated levels of both Platelet-Derived Growth Factor Receptor Beta (PDGFRβ) and its PDGF-B ligand. We hypothesize that active PDGFRβ signaling maintains DT progression.
We studied the effect of PDGFRβ inhibition on DT growth. Primary cultures of DTs treated with the PDGFRβ inhibitor Sunitinib show a decrease in proliferation rate as measured by bromodeoxyuridine (BrdU) incorporation assay. In vivo, Sunitinib treatment of Apc1638N/+ mice, a mouse model of DT, also decreased the number and size of tumors. To investigate the relationship of β-catenin activation and PDGFRβ activation, we treated human skin fibroblasts with Wnt3a to activate canonical Wnt signaling, and utilized transgenic murine skin fibroblasts harboring an activated form of β-catenin. In both systems, PDGF-B ligand expression increased both at the mRNA and protein level. However, this increase was not observed immediately, suggesting an indirect mode of regulation. The PDGF-B gene contains a conserved microRNA-29 (miR29) binding site in its 3′ untranslated region. In silico miRacts analysis of five independent DT microarray studies predicted miR29 family deregulation. As such, we studied whether miR29 deregulation in DT leads to PDGF-B overexpression and tumor proliferation. By performing quantitative PCR on human DT samples, we observed that the levels of mature forms of all miR29 family members (MIR29A, B, and C) are significantly down-regulated. Overexpressing miR29 in DT cells decreases PDGF-B ligand levels as well as BrdU incorporation rate. Finally, β-catenin-induced modulation of the PDGF-B ligand is abrogated upon inhibiting miR29.
Taken together, these data suggest that PDGFRβ signaling is a potentially important pathway in DT progression. PDGFRβ may be linked to β-catenin by the novel discovery of microRNA-29 down-regulation in DT tumors. This work will offer new perspectives on the molecular biology underlying DT development and help identify novel targets for therapy.
Citation Format: Mushriq Al-Jazrawe, Raymond Poon, Jessica Liu, Benjamin Alman. Regulation of proliferation and platelet-derived growth factor expression in desmoid tumors by microRNA-29. [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 4349. doi:10.1158/1538-7445.AM2014-4349