bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 3348: Immunophenotyping, xenotransplantability and molecular cytogenetic features of the sarcomatoid renal carcinoma cell line RCC52: Pathobiological significance
Authors: Hsieh Chin-Hsuan , Weng Wen-Hui , Chuang Kung-Lung , Chen Ying-Tzu , Pang See Tong , Chen Hung-Chang , Chuang Cheng-Keng , Liao Shuen-Kuei 
Published: February 2011

Abstract
The immunobiology of sarcomatoid renal cell carcinoma (RCC) and how it has been transformed or progressed from clear cell-RCC are currently poorly understood. We analyzed a sarcomatoid renal carcinoma cell line (RCC52) derived from a primary clear cell renal carcinoma with intensive sarcomatoid differentiation, with respect to its immunophenotyping, molecular cytogenetic features and xenotransplantability. RCC52 cells grown as monolayers consisted of mostly small-sized epithelioid cells along with a small proportion of spindle/fibroblast-like cells, suggestive of growth of the sarcomatoid, but not clear cell component of the tumor. Cytofluorometric analysis revealed a phenotype of cell surface HLA-I−, E-CDH−, N-CDH−, EpCAM−, CD44+, CD54+, CD58+, URO1+ and URO10+ and cytoplasmic AE1+, E-CDH−, N-CDH+, Vimentin+, S100+ and VEGF+. Spectral karyotyping (SKY) show the chromosomal abnormalities in 22 metaphases examined to be 40-42&lt;2n&gt;,X,-Y[22]; der(2)t(2,3)(q35;q21)[20]; der(14)(14;17)(p11;q12)[22]; −3[11]; +7,+7[14]; −14[9]; −15[14]; −10[10]; −22[16]. Numerical imbalances were also assessed by comparative genomic hybridization, which are found to be consistent with the findings determined by banding and SKY. These results along with the documented genotype have established the identity of the RCC52 cell lines. Nude mouse xenografts resulting from RCC52 cell s.c. injection and the original tumor shared similar histopathology with mostly sarcomatoid elements with occasional clear cell areas, suggesting malignant potential of this cell line and the capability of sarcomatoid RCC cells to undergo transdifferentiation or dedifferentiation. The total HLA class I loss caused by the two distinctive mutations in the β2-microglobulin gene and loss of heterozygosity (LOH) in chromosome 15 observed recently (Cancer ImmunoI Immunother, 58:395-408, 2009) did not prevent sarcomatoid RCC52 cells from undergoing such transdifferentiation. Overall our results is of immunological (evasion of the host immunosurveillance) and pathobiological (progression/differentiation/transdifferentiation) significance, which forms the basis of further investigations with additional cell lines/ clones and tissues of clear cell-RCCs with sarcomatoid differentiation to confirm (i) loss HLA class I expression in most, if not all, sarcomatoid RCCs, and (ii) the proposed sequence of clear cell-RCC → fibroblast-like sarcomatoid RCC → epithelioid sarcomatoid RCC, which could in turn transdifferentiate into clear cell-RCC.
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 3348.
Abstract 3350: Cancer stem cells and lymph node metastasis in early stage breast cancer
Authors: Tiezzi Daniel G. , Valejo Fernando AM , Marana Heitor RC , Clagnan Willian Simões , Benevides Luciana , Carrara Hélio HA , Silva João Santana , Andrade Jurandyr M. 
Published: February 2011

Abstract
Breast cancer is the leading cause of malignancy in women worldwide. Metastatic dissemination is the major cause of death. The mechanisms involved in cancer dissemination are unclear. The identification of tumor initiating cells in solid tumors has been reported. Initiating cells, also referred as cancer stem cells (CSCs), were defined as a CD44+/CD24— in breast carcinomas and have the ability to self-renewal, differentiate into any cell in the tumor and metastasize. The presence of CSCs is a suitable hypothesis for breast cancer metastasis and treatment failure. Nevertheless, there is no evidence of the relationship between CSCs in primary tumor and metastasis. Methods: we prospectively included 20 early-stage (I and II) breast cancer patients (17 invasive ductal carcinoma, 1 invasive lobular carcinoma, 1 metaplastic carcinoma and 1 tubular-lobular invasive carcinoma), and two patients with ductal carcinoma in situ (DCIS) subjected to primary surgery. The proportion of CSCs was analyzed in 22 primary tumors and in three lymph node metastasis by flow cytometry. Anti-human CD326 (EpCam; FITC), anti-human CD227 (MUC-1; FITC), anti-human CD44 (APC) and anti-human CD24 (PE) were used for phenotype analysis. The percentage of CD44+/CD24- cell population in primary invasive tumors was compared with standard prognostic factors. The mean age was 58.3 years (37 - 77), the mean pT was 1.8 cm (0.5 - 3.5), 13 patients (59%) had no axillary lymph node metastasis (NLN group) and 9 had positive axillary metastasis (PLN group) confirmed for standard histological evaluation. The ER, PR and HER2 positive expression rates were 84.2%, 78.9% and 15.7%, respectively. The Wilcoxon or Kruskal-Wallis tests were used for statistical analyses. Results: the percentage of CSCs in primary invasive ductal carcinoma (IDC) was 7.1% (0.2 - 29.4). In two DCIS we found 4.5% and 8.2% of CSCs. In lymph node metastases we observed a mean of 11.9% (1.5 - 31.1). In the other subtypes the mean percentage of CSCs was 12.7% (1.1 - 31.1). There was no association between CSC population in IDC and age (p= 0.8), pT (p= 0.7), tumor grade (p= 0.4), ER (p= 0.1), PR (p= 0.3) and HER2 (p= 0.4). We observed a significant increase in CSC population in PLN group [mean= 12.4% (4.1% - 29.4%)] when compared to patients without lymph node metastasis [mean= 2.4% (0.2% - 4.6%0] (p= 0.0008). Conclusion: this preliminary study indicates that the metastatic dissemination is associated with an increase in CSC population in early-stage breast 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 3350.
Abstract 3351: Cancer stem cell marker CD133 effects on invasion and self-renewing in malignant brain tumors
Authors: Kim Dong-Ok , Kim Jeong-Hoon , Ra Young-Shin 
Published: February 2011

Abstract
Background and Purpose: Patients with malignant brain tumors have been suffering from its recurrence or short median survival with only a few years, despite advanced medical development. Present studies have shown that cancer stem cell marker CD133 is correlated with invasiveness and metastasis in malignant brain tumors. Some researchers have reported that CD133 in brain tumors influenced on survival regardless of grades. Hence, we analyzed the invasion and self-renewal abilities in a variety of brain tumors having the different WHO grades and compared the differences between low and high malignant brain tumors expressing CD133.
Methods and Results: CD133+ cells were stained by immunocytochemistry and followed by counting under fluorescence microscope. We identified cell invasion ability using Matrigel invasion chamber and capacity for self-renew by colony-forming assay, respectively, following CD133 isolation by MACS column. As a result, we found that although the number of CD133+ cells in high malignant brain tumors(HMBTs) was less than those in low malignant brain tumors(LMBTs), the CD133+ cells in HMBTs showed powerful invasion abilities recording the differences of three to six times than in the CD133- cells. In contrast, in LMBTs, the CD133+ cells hardly effected on invasion. We also observed stronger self-renewal potential in CD133+ cells generated from HMBTs than in LMBTs. Conclusions: Taken together, even though various brain tumors expressed CD133 as a cancer stem cell marker, the CD133+ cells functioned as a useful tool in terms of evaluating invasion and self-renewal properties in just HMBTs, but not in LMBTs. Therefore, CD133 will be powerful marker as a poor prognostic factor in brain tumors and this may provide us some strategies to treat HMBTs.
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 3351.
Abstract 3354: Study of glioblastoma stem cell-like cancer stem cells on tumorigenesis and recurrence by multiple imaging modalities
Authors: Lin Liang-Ting , Chiou Shih-Hwa , Yun Zhong , Lee Yi-Jang 
Published: February 2011

Abstract
CD133 (Prominin-1) have been reported as one of CNS cancer stem cell markers, and is used for isolating cancer stem cells via fluorescence-activating cell sorting. However, more and more new evidence showed that CD133 cannot totally indicate to cancer stem cells, and the role of CD133 plays in glioblastoma still remains controversial. Here, we tend to use multiple imaging modalities to investigate CD133-positive and CD133-negative cells on tumorigenesis and recurrence in vivo. We sorted patient tumor-derived GBM cells by FACS with CD133-PE staining, and delivered multicistronic reporter system into each group of cells by lentivirus. The established cells stably expressed green fluorescent protein, firefly luciferase and thymidine kinase, and each of them was assayed in vitro. GFP expression was used for collecting cells with better reporter efficiency. Our in vitro results showed that CD133-positive cells revealed shorter doubling time and better transgene expression than CD133-negative cells. Furthermore, both groups of CD133 expression cells were xenografted orthotropically into left brain of NOD/SCID mice, and the tumorigenesis phenomenon were evaluated by magnetic resonance imaging and bioluminescence. Tumor formation was observed in both groups, suggested that CD133 may not be the key role in tumorigenesis of glioblastoma. Moreover, to demonstrate the relationship between cancer recurrence and cancer stem cells, we also treated the xenografted mice with ganciclovir to generate cytotoxicity by tk gene for 2 weeks, and in vivo imaging was recorded for upcoming 2 weeks. For future work, we plan to figure out whether the CD133 takes the most responsibility in tumor recurrence, and look forward to the other stemness-related markers such as Sox2, that may also provide a novel approach in cancer prognosis.
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 3354.
Abstract 3361: Immunohistochemical analysis of CD133/44 expression in surgical specimens of squamous cell carcinoma of the esophagus after neoadjuvant chemotherapy
Authors: Nakajima Takako Eguchi , Yoshida Hiroshi , Taniguchi Hirokazu , Masutomi Kenkichi , Shimoda Tadakazu , Yamada Yasuhide 
Published: February 2011

Abstract
PURPOSE: Both CD133 and CD44 have been reported as putative markers for cancer-initiating cell in various malignancies such as colon, prostate and pancreatic cancers. No immunohistochemical analysis correlated with clinicopathological outcome have been reported in squamous cell carcinoma of the esophagus. We evaluated the values of CD133/44 as markers for prognosis and chemoresistance in the patients with esophageal cancer.
MATERIALS AND METHODS: The expression of CD133/44 was assessed by immunohistochemistry in a series of 58 surgical specimens of squamous cell carcinoma of the esophagus after neoadjuvant chemotherapy: 2 courses of 5-fluorouracil and cisplatin. Immunopositive cells were counted from 10 fields in the representative section and expressed as a percentage. The specimen with necrosis or disappearance of the tumor cells in more than 1/3 of the whole lesion was determined as positive histological response specimen.
RESULTS: CD133 expression (positive cells: 0% &lt;) was detected in 47 of 58 patients (81%). Overall survival of the CD133 positive patients was significantly poorer than CD133 negative patients (3-year survival: 43% vs 91%, P=0.012). Disease free survival of the CD133 positive patients was also significantly poorer than CD133 negative patients (3-year relapse free survival: 31% vs 73%, P=0.031). Histological response rate in the CD133 positive patients was significantly lower than that in the CD133 negative patients (17% vs 64%, P=0.004). CD44 expression was detected in all patients, and the rate of positive cells in each tumor was 100% in all patients.
CONCLUSION: CD133 expression can be a prognostic marker and also a marker for chemoresistance of 5-fluorouracil and cisplatin in patients with squamous cell carcinoma of the esophagus. CD44 expression is not a marker for any clinicopathological outcome in patients with squamous cell carcinoma of the esophagus.
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 3361.
Abstract 3362: Diethylaminobenzaldehyde (DEAB) is not a specific inhibitor of ALDH1a1 isozyme
Authors: Moreb Jan S. , Chang Lung-Ji , Han Shuhong , Ostmark Blanca 
Published: February 2011

Abstract
With the cancer stem cell theory, there has been an invigorated new interest in finding more markers for stem cells. Aldehdye dehydrogenase (ALDH) is one such marker that became popular since a flow cytometry based assay, Aldeflour staining, has become available. Diethylaminobenzaldehyde (DEAB), used in the Aldeflour assay, has been published many years ago as a specific inhibitor for ALDH1 isoform. The Aldeflour assay is promoted as testing the enzymatic activity of ALDH1. Therefore most researchers believe that the high ALDH activity detected in these early progenitors is mainly due to ALDH1. In this study, we explore the specificity of DEAB as an inhibitor of ALDH activity. We used two cancer cell lines known to have very low baseline ALDH activity, K562 leukemia and H1299 lung cancer cell lines. We prepared lentiviral vectors containing the full length of either ALDH2 or ALDH1a2 cDNA and used them to over express the enzymes in the two cell lines. Successful expression was measured by ALDH activity assay as well as by Western blot analysis and RT-PCR. Aldeflour staining assay was also used. The results show that we created 4 cell lines with successful high expression of each of the two enzymes as confirmed by multiple assays including the Aldeflour assay. In order to study the specificity of two known ALDH activity inhibitors, DEAB and tetraethylthiuram disulfide (disulfiram), we incubated each cell line with either inhibitor at 25 μM concentration for 48 hr and then measured the remaining ALDH enzymatic activity. Our results show that both inhibitors reduced ALDH activity of both overexpressed isozymes, ALDH2 and ALDH1a2, by 70-80%. These results suggest that DEAB is not a specific inhibitor for ALDH1a1 and that aldefluor assay is not specific assay for ALDH1a1 either. Therefore, investigators should be careful in their conclusions when using DEAB in studying candidate stem cells and that studies with more specific inhibitors, such as siRNA, are needed.
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 3362.
Abstract 3363: Identification and characterization of stem-like cells in human esophageal epithelial and adenocarcinoma cells
Authors: Zhao Ronghua , Ulmer Elisabeth , Quaroni Luca , Casson Alan G. 
Published: February 2011

Abstract
The aim of this study was to identify and characterize stem-like cells in human normal esophageal epithelial and adenocarcinoma cell lines.
The immortalized esophageal epithelial cell line, Het-1A, and the primary esophageal adenocarcinoma (EADC) cell line, OE33, were first studied by flow cytometry and immunofluorescence using a panel of antibodies to putative stem cell biomarkers which included CD34, CD44, CD44/CD24, CD117/integrin α6, Musashi I, EpiCam, and Oct 4. Fluorescence activated cell sorting (FACS) was then used to isolate 15% of cells with the highest CD44 staining (CD44high) or reactive oxygen species (ROS) (ROShigh) and 15% of cells with the lowest (including negative) CD44 staining (CD44low) or ROS (ROSlow). Each cell population was further characterized using sphere-forming assays, soft agar clonogenic assays, flow cytometry for ROS, and synchrotron mid-infrared (IR) spectromicroscopy.
CD44 positivity was found in 90% of Het-1A and 75% of OE33 cells overall. For both Het-1A and OE33 cell lines, spheroid formation (mean±SD/5000 cells) was significantly higher in cells expressing high levels of CD44 (Het-1A:138.33±2.08 vs. 97.67±1.53, p&lt;0.01; OE33: 150.00±31.19 vs. 100.67±7.02, p=0.056) and low levels of ROS (Het-1A: 149.33±20.43 vs. 92.00±8.89, p=0.011; OE33: 199.67±31.63 vs. 119.33±14.47, p=0.016). Colony formation (mean±SD/1000 cells) was also found to be significantly higher in CD44high (Het-1A: 15.33±4.51 vs. 8.00±1.00, p=0.051; OE33: 92.67±11.02 vs. 18.00±1.73, p&lt;0.01) and ROSlow (Het-1A: 45.00±1.00 vs. 31.67±3.79, p&lt;0.01; OE33: 33.00±5.29 vs. 14.67±5.03, p=0.012) cell populations. Whereas OE33 CD44high cells were found to express consistently lower levels of ROS compared with OE33 CD44low cells (p&lt;0.01), no differences in ROS expression were found in Het-1A cells sorted by CD44 expression. Spectromicroscopic analysis revealed only small non-significant differences between cell populations sorted by CD44 and ROS expression.
We conclude that the higher rates of spheroid formation and clonogenicity of Het-1A and OE33 cells expressing high levels of CD44 (CD44high) and low levels of ROS (ROSlow) reflect an enrichment of stem-like cell populations in esophageal cell lines. However, the significant differences in ROS levels between CD44high OE33 cells and CD44high Het-1A cells suggests unique and biologically distinct pathways in stem-like cells derived from normal and malignant esophageal epithelia.
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 3363.
Abstract 3366: Significance of a stemness factor, Sox2, in gastric cancer
Authors: Matsuoka Junko , Yashiro Masakazu , Kashiwagi Shinichiro , Kato Yukihiro , Fuyuhiro Yuhiko , Doi Yosuke , Noda Satoru , Kubo Naoshi , Tanaka Hiroaki , Muguruma Kazuya , Inoue Toru , Yamada Nobuya , Sawada Tetsuji , Ohira Masaichi , Ishikawa Tetsuro , Hirakawa Kosei 
Published: February 2011

Abstract
Introduction: Sox genes encode a family of high-mobility group transcription factors that play critical roles in organogenesis. Sox2 is suggested to be one of stemness factors that render the reprogramming capability of adult cells into germ-line-competent induced pluripotent stem cells. Sox2 might be associated with cancer stem cells that are the only cells with unlimited proliferation potential and with the capability of driving tumor progression. Recently, a number of studies have reported the correlation between Sox transcription factors and human cancers. Since little is known about the efficacy of Sox2 as a potential biomarker for gastric cancer, we investigated the significance of Sox2 expression in human gastric cancer.
Material and Methods: A total of 260 patients who had undergone resection of a primary gastric cancer at our institute were enrolled. Sox2 expression was analyzed by immunohistochemistry. Sox2 expression was evaluated by intensity of staining and percentage of stained tumor cells: intensity was given scores 0-3 (0=no,1=weak, 2=moderate 3= intense) and population was given scores 0-5 (0=0%, 1=1-25%, 2=26-35%, 3=36-45%, 4=46-65%, 5=66-100%) The two scores were then added to obtain the final result of 0-8. Expression of Sox2 was considered high expression when scores were ≥5 and low expression when scores were ≤4.
Results: Sox2 expression was positive in 153 (58.8%) of 260 gastric cancers. There was a statistically significant correlation between Sox2 expression and depth of tumor invasion (p=0.002) and lymphatic invasion (p=0.002). The prognosis of patients with Sox2 expression positive tumors was significantly (p=0.046) worse, while a multivariate analysis revealed that Sox2 expression was not an independent prognostic factor.
Conclusion: Sox2 expression might be associated with invasion of gastric cancer. Sox2 expression might be a useful prognosis marker for patients with gastric 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 3366.
Abstract 3368: Characterization of stem cell like cells in kidney cancer
Authors: Boström Anna-Karin , Johansson Martin , Axelson Håkan 
Published: February 2011

Abstract
Contemporary tumor biology challenges the previous belief that all cancer cells are capable of sustaining tumor growth. Instead, data is accumulating in favor of a concept where a small percentage of the total tumor cell number, are believed to have the capacity to drive cancerous growth. These cells are called tumor initiating cells or cancer stem cells (CSCs). The presence of CSCs in the tumor may increase malignancy potential, mediate resistance to conventional therapy and lead to poor survival outcomes. To achieve effective prognostic and therapeutic strategies it is important to identify markers for and CSC-unique properties.
Our study aims at identifying cells with stem cell like properties in renal cell carcinoma (RCC) and specify their role in tumorigenesis.
ALDH activity has been used to isolate hematopoetic and breast stem cells and high expression of ALDH has been identified in breast cancer with poor prognosis.
We have used the ALDEFLUOR assay to isolate stem cell like cells from both primary and established RCC cultures. We found that the ALDH positive cells have a greater colony forming capacity and ability to grow under low attachment conditions, as compared to cells with low ALDH activity. We also found that CD133, another known stem cell marker, was expressed at higher levels in the ALDH positive cells.
The ALDH positive cells were characterized using global gene expression analysis, producing a framework for further characterization. The clinical validity of this population was assessed using gene expression from a data set of 176 primary RCCs and these analysis indicate that the stem cell expression profile is associated with decreased disease specific survival.
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 3368.