bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 3266: Alpha2 and beta-adrenergic action on human breast cancer cells growing in nude mice
Authors: Piñero Cecilia Pérez , Entschladen Frank , Lüthy Isabel Alicia 
Published: February 2011

Abstract
Breast cancer, the most common cancer amid women in the majority of countries, is among the most stressful of diseases. The principal effectors of the stress system include the catecholamines epinephrine and norepinephrine. The catecholamines bind to α1-, α2- and β-adrenoceptors (AR). Our group has recently described α2-adrenoceptors in human tumor and non-tumor breast cell lines by reverse transcription (RT)-PCR, immunocytochemistry and binding assays. Moreover, the stimulation by α2-adrenoceptor agonists was associated with increased cell proliferation and tumor growth. On the other hand, we observed a reduction in tumor growth when the animals are treated with the pharmacological α2-antagonist RAUWOLSCINE (RAW). The expression of β2-AR has been described in different experimental models for breast cancer. The aims of the present work were: to assess the effect of β-adrenergic compounds in the human breast cancer cell lines growing in nude mice (IBH-4 and IBH-6); to study the migration potential of these cell lines using video microscopy in three dimensional collagen lattices knowing that migration of tumor cells is a prerequisite for invasion and metastasis development. The daily administration of 1,2mg/kg of the SALBUTAMOL (SALB) significantly diminished tumor growth. The same result was seen when using the α2-antagonist RAW (0,5mg/kg). As an example for tumor IBH-4 treated with SALB, on day 20: 444.16 ± 76.59mm3 vs. 843.40 ± 189.41 mm3, p&lt;0.05; RAW on day 24: 775.04 ± 68.12mm3 vs 1237.84 ± 134.97mm3 p&lt;0.01. Tumor IBH-6, on day 21: SALB: 125.40 ± 25.42mm3 vs. 579.40 ± 207.96mm3 p&lt;0.01. The combined treatment of SALB + RAW did not exert any synergic or additive effect compared with each independent treatment. ERK phosphorylation is in agreement with tumor growth results. When analyzing the migration potential of the cells in response to adrenergic stimulation by three dimension video microscopy in collagen lattices, cell migration was decreased when the cells were treated with RAW, SALB and PROP and increased when treated with epinephrine. The migratory activity for each treatment was calculated as the portion of cells which was locomotory active (% locomoting cells). We conclude that both RAW, acting as α2-AR antagonist and SALB, acting through β-AR, inhibit tumor growth. Regarding cell migration, the results are promising and in agreement with the in vivo experiments. These compounds, devoid of serious side-effects, could eventually be employed to inhibit tumor growth. In the future, it might be useful to analyse the metastatic potential of the cells.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3266.
Abstract 3297: CD90/Thy-1-positive cells in the peripheral blood of tumor patients co-express CD44
Authors: Wagner Kathleen , Berndt Alexander , Hochhaus Andreas , Clement Joachim H. 
Published: February 2011

Abstract
Aims: Interactions between epithelial tumor cells and the surrounding milieu are an essential regulatory component of tumor development. Especially the contribution of the crosstalk between epithelial tumor cells and tumor-associated fibroblasts (TAFs) on tumor progression and metastasis formation is of emerging interest. Therefore, we ask whether circulating TAFs could be detected in the peripheral blood of tumor patients and how they could be further characterized.
Methods: CD90/Thy-1 is a putative marker of TAFs. A fluorescence-scanning-cytometer (scanR) was used to detect and quantify vital CD90-positive cells in blood samples from individual tumor patients (e.g. breast, bladder, kidney). For further analysis CD90-positive cells were separated from leukocyte fractions pooled from different tumor patients using an immunomagnetic cell separation technology (ROBOSEP®). The CD90-positive fraction was subsequently analyzed by immunofluorescence and immunohistochemistry. We focused on the expression of other stroma markers like FAP-alpha and cell surface proteins like CD44 which are involved in metastasis formation.
Results: In cell culture experiments we established CD90 as a highly specific marker for fibroblasts. The amount of CD90 positive cells in whole blood samples varied from 0 up to 54,000 cells/ml and changed over time. The CD90-positive cells were enriched immunomagnetically from the leukocyte fraction pooled from tumor patients. By immunofluorescence we approved the cell vitality and verified that the separated cells do not belong to the sub-population of CD34-positive blood stem cells. Blood samples from more than 300 patients with solid tumors were tested for the presence of CD90-positive cells. Immunofluorescence double staining of the separated cells showed the co-expression of CD90 and CD44, which participates in a wide variety of cellular functions like hematopoiesis and tumor metastasis formation. Further immunohistochemical analysis demonstrated the expression of CD29 which is involved in metastasis formation and CD105 a marker for activated fibroblasts in a subset of the CD90-positive cell fraction. Conclusions: We could show that CD90-positive cells circulate in the peripheral blood of tumor patients. The additional expression of other stroma and tumor associated proteins on the cells could argue for their involvement in aspects of tumor progression. Ongoing studies should evaluate their suitability as prognostic factor.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3297.
Abstract 3300: MYC regulation of a “poor prognosis” metastatic cancer cell state
Authors: Wolfer Anita , Wittner Ben S. , Irimia Daniel , Flavin Richard J. , Lupien Mathieu , Gunawardane Ruwanthi N. , Meyer Clifford A. , Lightcap Eric S. , Tamayo Pablo , Mesirov Jill P. , Liu Xiaole S. , Shioda Toshihiro , Toner Mehmet , Loda Massimo , Brown Myles , Brugge Joan S. , Ramaswamy Sridhar 
Published: February 2011

Abstract
Gene expression signatures are used clinically as prognostic tools to determine the risk of individual patients with localized breast tumors developing distant metastasis. However, we lack a clear understanding of whether these correlative biomarkers link to a common biological network that regulates metastasis. METHODS: In order to address this question, we analyzed thirteen different well-described (including two in clinical use) “poor outcome” cancer signatures in a cell line model of estrogen receptor positive breast cancer (MCF7) manipulated by diverse oncogenic stimuli. RESULTS: We find that the c-MYC oncoprotein coordinately regulates the expression of these thirteen different “poor outcome” cancer signatures. In addition, functional inactivation of MYC in human breast cancer cells specifically inhibits their distant metastasis in vivo and invasive behavior in vitro. CONCLUSION: These results suggest that MYC oncogene activity, as reflected by “poor prognosis” signature expression, may be necessary for the translocation of “poor outcome” human breast tumors to distant sites.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3300.
Abstract 3312: Molecular profiling of melanoma primary tumors
Authors: Essner Richard 
Published: February 2011

Abstract
Objectives: A number of pathologic features have been identified from primary melanoma that are useful for determining patient prognosis including tumor thickness, ulceration, mitotic rate and Clark level; and the tumor status of the sentinel nodes (SN). Because none of these factors is useful for evaluating the outcome of individual patients we used a cDNA microarray to determine the relevance of molecular profiling of the primaries to determine the presence of lymph node metastases.
Methods: We obtained intact melanoma primaries and SN from 12 patients and microdissected both for molecular analysis. RNA was extracted and purified by RNeasy (Qiagen, Valencia, CA). GEArray Q series-Human Tumor Metastasis Gene Array Kits (Superarray, Bethesda, MD) were used to evaluate gene expression from biotinylated cDNA and images were acquired on the Molecular Dynamics storm 860 imaging station (Amersham Pharmacia Biotech, United Kingdom, Ltd). The signal intensity which corresponds to the quantity of cDNA bound to the array was analyzed by the ScanAlyze V2.50 image analysis software (Covance, Berkeley, CA).
Results: RNA was evaluated from 12 primary melanoma and matching SN, 7 with metastases. Four genes: caveolin (CAV1), Lim kinase (LIMK), matrix metalloproteinase 15 (MMP15) and vascular endothelial growth factor (VEGF) demonstrated consistent up-regulation in primary melanoma associated with SN metastases identified by H & E and the presence of these genes expressed in SN. Human melanoma cell lines and tumor-negative SN served as controls. Receiver operator curves (ROC) for genes: CAV1, LIMK, MMP15 and VEGF were constructed and the area under the curves (AUC) were determined as: 0.956+0.056, 0.978+0.039, 0.822+0.114 and 0.91+0.08, respectively. The combined concordance of LIMK and VEGF to predict metastases was 0.94
Conclusions: Gene expression profiling of primary melanoma can be used for predicting the presence of SN metastases. Up-regulation of LIMK and VEGF from the primary tumors may be an important first step to understand the early mechanism for patients developing lymph node metastases.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3312.
Abstract 3319: Human triple-negative breast cancer stem cells utilized for drug discovery therapeutics for triple-negative breast cancer patients
Authors: Sharma Cristian V.R , Passarini Jenna D. , Majdoub Mariam W. , DiMaggio Christina M. , Sobhy Omar M. , Punzalan Rubio R. , Sharma Michael V.R. , Harris-White Marni E. , Warden Michael W. , Sharma Sherven P. , Sharma Jay P. 
Published: February 2011

Abstract
Breast cancer is the most common malignancy among women in developed countries, affecting more than a million women per year worldwide. Of these, triple negative breast carcinoma represents 10-17 %. Triple negative breast carcinomas, characterized by estrogen, progesterone and HER2 receptor negativity are very aggressive tumors with poor prognosis. Breast Cancer Stem derived from triple negative parental Breast Cancer tumors, are a subpopulation of cells within the parental breast cancer population within the individual which are positive for the following markers: CD133+CD44+CD24+ESA+SSEA-1+TRA-1-61+& TRA1-81+ and Oct ¾ these Breast Cancer Stem cells are highly tumorigenic and possess the stem cell-like properties of self-renewal and the ability to produce differentiated progeny. Breast Cancer Stem cells also demonstrate up regulation of SSEA3+, SSEA4+ upon differentiation into parental cancer phenotype. Individualized treatment (tailored therapy) based on molecular biology markers of tumor and patient is the trend in clinical practice these days. However, molecular targets and predictors for the treatment of triple negative breast carcinoma do not currently exist. With the identification and characterization of Breast Cancer Stem Cells from parental triple negative tumors, enables one to screen novel drug candidates for potential development of therapeutics for triple negative Breast Cancer Patients. In this study we have utilized Breast Cancer Stem Cells from triple negative Tumors to screen potential drug candidates. The Breast Cancer Stem Cell based assay system may provide novel therapeutic approaches into treatment of triple negative breast cancer patients, which are resistant to standard chemotherapy and radiation.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3319.
Abstract 333: FISH markers in oral tongue squamous cell carcinoma
Authors: Wangsa Darawalee , Ryott Michael , Elmberger Göran , Schäffer Alejandro A. , Auer Gert , Lundqvist Elisabeth Åvall , Munck-Wikland Eva , Ried Thomas , Heselmeyer-Haddad Kerstin 
Published: February 2011

Abstract
Oral tongue squamous cell carcinoma (OTSCC) is a continued health problem worldwide, and is associated with poor prognosis. Genetic alterations in head and neck cancers have frequently been shown, however, reports about alterations in OTSCC and their correlation with clinical and histopathological parameters are limited. We investigated OTSCC by analyzing five probe markers (TERC, CCND1, EGFR, P53 and CEP®4) by means of fluorescence in situ hybridization (FISH) in sixty-five patients (Stage I, n=15; Stage II, n=30; Stage III, n=7; Stage IV, n=13). Higher copy number gains in all five markers was found to be significantly (P=0.002) correlated to non-smoking habits while low-level copy number gains corresponded to smokers in OTSCC patients. Of the five markers, CCND1 was found to have the highest mean copy number gain in comparison to all other markers used in this study. The percentage of cells with elevated (&gt;3 signals) CCND1 copy number gain increased with stage. In Stage II OTSCC, CCND1 copy number gain correlated significantly (P=0.03) with a better prognosis in patients. Of the patients with increased CCND1 copy number gains (&gt;3 signals in at least 5% of cells), all were non-smokers. In conclusion, high copy number gain using FISH correlated with non-smoking habits, making it particularly interesting to explore the mechanism of how these patients develop cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 333.
Abstract 3333: Therapeutic efficacy and safety of TRAIL-producing human adipose tissue-derived mesenchymal stem cells against experimental brainstem glioma
Authors: Kim Seung-Ki , Choi Seung Ah , Hwang Sung-Kyun , Wang Kyu-Chang , Cho Byung-Kyu , Phi Ji Hoon , Lee Ji Yeoun , Jung Hee Won , Lee Do-Hun 
Published: February 2011

Abstract
Mesenchymal stem cells (MSCs) have an extensive migratory capacity for gliomas, which is comparable to that of neural stem cells. Among the various types of MSCs, human adipose tissue-derived MSCs (hAT-MSC) emerge as one of the most attractive vehicles for gene therapy because of their high throughput, lack of ethical concerns, and availability and ease of isolation. We evaluated the therapeutic potential and safety of genetically engineered hAT-MSCs encoding the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) against brainstem gliomas.
hAT-MSCs were isolated from human fat tissue, characterized, and transfected with TRAIL using nucleofector. The therapeutic potential of TRAIL-producing hAT-MSCs (hAT-MSC.TRAIL) was confirmed using in vitro and in vivo studies. The final fate of injected hAT-MSCs was traced in long-survival animals. The characterization of hAT-MSCs revealed the expression of MSC-specific cell-type markers and their differentiation potential into neuronal lineage. Short-term outcomes included a 56.3% reduction of tumor volume (P &lt; 0.001) with increased apoptosis (3.03-fold, P &lt; 0.05) in animals treated with hAT-MSC.TRAIL compared with the control groups. Long-term outcomes included a significant survival benefit in the hAT-MSC.TRAIL-treated group (26 days of median survival in the control group vs 84 days in the hAT-MSC.TRAIL-treated group, P &lt; 0.0001), without any evidence of mesenchymal differentiation in vivo. Our study demonstrated the therapeutic efficacy and safety of nonvirally engineered hAT-MSCs against brainstem gliomas.
Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3333.
Abstract 3339: Elimination of cancer stem cells in pancreatic cancer cell lines by a combinatorial therapy
Authors: Visús Carmen , Lozano-Leon Antonio , Wang YangYang , Chang YooJung , Whitcomb David C. , Brand Randall E. , DeLeo Albert B. 
Published: February 2011

Abstract
Cancer stem cells (CSC) are tumor initiating cells and considered resistant to current conventional chemo and radio therapies. Consequently, novel strategies are needed to target these cells. Tumor cells expressing elevated levels of aldehyde dehydrogenase 1 family member A1 activity (ALDHbright cells) have been shown to have many properties attributed to CSC, including tumorigenicity in immunodeficient mice. We used FACS analysis to identify and sort ALDHbright cells from several human pancreatic cell lines using ALDEFLUOR (Stem Cell Technologies, Vancouver Canada). We show that ALDHbright but not ALDHnegative cells sorted from the human MiaPaCa-2 pancreatic adenocarcinoma cell are highly tumorigenic at low inoculum of 500 cells in immunodeficient NOD.SCID mice, a critical property of CSC. Previously, we identified the ALDH1A188–96 peptide as an HLA-A2-restricted, cytotoxic T cell (CTL)-defined tumor antigen. Using a flow cytometry-based assay, ALDHbright cells in the HLA-A2+ MiaPaCa-2 cell line were selectively eliminated in vitro by ALDH1A188–96 peptide-specific CTL. The Hedgehog (Hh) stem cell signaling pathway has been shown to play a critical role in invasion and metastasis in pancreatic cancer. Treatment of the MiaPaCa-2 cell line with the Hg inhibitor, cyclopamine, significantly eliminated ALDH+ MiaPaCA-2 cells compared to treatment with conventional chemotherapeutic agents. The efficacy of a combinatorial therapy consisting of adoptive transfer of ALDH1A1-specific CTL combined with systemic administration of cyclopamine in vitro and in vivo on ALDHbright cells and in vivo growth inhibition of MIA PaCa-2-derived xenografts is detailed.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3339.
Abstract 3355: Comparison of CD133, uPAR, and CXCR4 expression in lung cancer cell lines under normal and spheroid culture conditions
Authors: Lee Alan J. , Sarfaraz Sami , Voeller Donna M. , Giaccone Giuseppe 
Published: February 2011

Abstract
Background: Cancer stem cells (CSC) have been identified in several solid tumors including breast, brain, and recently lung cancers, etc. In the CSC model, CSCs are thought to be able to self-renew extensively, grow as spheroids in vitro, and be resistant to conventional cancer therapies. CD133, uPAR and CXCR4 have been reported as putative markers that can be used to mark enriched cancer stem cell populations. Although CD133, uPAR and CXCR4 have been implicated in CSC biology and identification, their application as lung CSC (LCSC) markers have not been fully explored. In this study we examined and compared CD133, uPAR and CXCR4 expression in non-spheroid cells and CSC-like spheroid cells derived from several lung and non-lung cancer cell lines.
Methods: We cultured four classic small cell lung cancer (SCLC) lines, two variant SCLC lines, three non-small cell lung cancer (NSCLC) lines, one primary lung cancer line derived in our lab, three lymphoma cell lines, one thymoma cell line, and one breast cancer cell line. Cell lines were maintained in RPMI or DMEM with 10% fetal calf serum. Spheroids were cultured and maintained in low-attachment flasks in serum free media supplemented with EGF and FGF. CD133, CXCR4, and uPAR expression were evaluated by immunostaining followed by flow cytometry analysis.
Results: Under spheroid culture conditions, CD133 expression tends to remain the same or increases in most of the cell lines tested. SCLC and lymphoma lines tend to express more CD133 than NSCLC and non-lung cancer lines in both normal and spheroid culture conditions. uPAR expression is generally low, however when detectable, it only shows up in cell lines grown in spheroid culture conditions. CXCR4 expression generally increases in spheroid culture conditions with greater expression seen in SCLC lines and lymphoma lines.
Conclusion: Spheroid cells tend to exhibit higher CD133 expression than cells under regular culture conditions. This finding supports the idea that CD133 is enriched in LCSC populations. SCLC and lymphoma lines in normal and spheroid culture conditions express more CD133, uPAR, and CXCR4. This does not appear to be tied to adherent growth properties as two adherent SCLC lines displayed no striking difference in expression compared with other non-adherent SCLC lines. However the tendency for SCLC cells and lymphoma cells to grow in regular culture conditions as clumps may offer some insight into the increased expression of these markers.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3355.