bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 827: Proximity-based c-MET activation assay development in formalin-fixed paraffin-embedded (FFPE) samples and profiling c-MET/HGF axis in human cancer-derived tumors
Authors: Rajiv Dua , Zhang Jianhuan , Parry Gordon , Winslow John , Penuel Elicia 
Published: February 2011

Abstract
Aberrant activation of membrane receptors frequently occurs in human carcinomas. Measurement of receptor phosphorylation is commonly used as an indicator of receptor activation in formalin-fixed paraffin embedded (FFPE) sections. This format is used to preserve human tissue samples and is the most common format for readily-available tissues from clinical trials and patient disease management. However, preservation of the labile phosphorylation signal is often inconsistent and consequently, results can be ambiguous. Here, we describe an alternative, novel approach to detect and quantify both receptor and ligand expression, as well as, activation status in FFPE samples. Specifically, we describe the development and validation of VeraTag based assays to measure total c-Met, total HGF and HGF/c-Met interactions. Using, the VeraTag technology, proximity-based assays, were used to detect and quantify c-MET, HGF, and HGF/c-MET interactions resulting from both exogenous and endogenous ligand stimulation in FFPE-prepared cell line pellets. The developed assays were subsequently used to profile human carcinomas including non-small cell lung, stomach, and head and neck tumors. Our data demonstrate a novel approach to detect and quantify c-Met activation which enables profiling and characterization of the c-Met activation status in FFPE human tissue samples. Furthermore, these data also demonstrate a basic approach to detect and quantify ligand-receptor interactions by VeraTag proximity-based assays that can be widely applied to measure activation of receptors in archived FFPE human tissue samples.
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 827.
Abstract 830: Clinical significance of measuring serum p53 antibodies in synchronous multiple colorectal cancer and double cancer patients
Authors: Kawamata Mayumi , Ota Mitsuyoshi , Fujii Shoichi , Ichikawa Yasushi , Suwa Hirokazu , Tatsumi Kenji , Watanabe Kazuteru , Yamagishi Shigeru , Akiyama, Hirotoshi , Ishikawa Takashi , Chishima Takashi , Shimizu Daisuke , Hasegawa Satoshi , Endo Itaru 
Published: February 2011

Abstract
Aims: The clinical significance of measuring serum p53 antibodies in colorectal cancer patients was evaluated.
Patients and Methods: Preoperative serum tumor markers including CEA, CA19-9 and p53 antibody were examined in 264 patients (stage I: 68, II: 73, III; 81) who were given diagnoses of colon and/or rectal cancer in Yokohama City University Hospital from 2007 to 2008. Correlativity of tumor markers to clinical findings was investigated.
Results: In the overall patients, range, median and positive ratio of each tumor marker are shown in Table 1. Positive ratio of CEA and CA19-9 gradually increased according to clinical stage of the tumor, however, those of p53 showed almost the same concentration in any stage. Then, in stage I patients, positive ratio of p53 was higher than CEA and CA19-9 (p=0.0005).
Thirty five cases (13.3%) of patients had synchronous or metachronous double or triple colorectal cancers. In that group, positive ratio of p53 was 48.3%, and median serum concentration of p53 was 0.915U/ml (0.15-295). Positive ratio and serum concentration of p53 of double or triple colorectal cancer patients were significantly higher than that of single cancer patients (p=0.0375).
Conclusions: Serum concentration of p53 is sensitive, especially in early stage of colorectal cancer compared with other tumor markers. Colorectal cancer patients who showed high concentration of p53 have to be carefully checked for occult 2nd gastrointestinal tumor.1 nnCEA(ng/ml)CA19-9(ng/ml)p53 antibody(U/ml)Range (median)overall2640.3-3371(2.95)1-18927(12)0.15-443(0.53) Stage0180.3-5.7(1.45)1-44(9)0.15-2.36(0.28) StageI680.3-18.3(1.7)1-161(10)0.15-233(0.45) StageII730.5-148.1(3.9)1-1353(13)0.15-435.5(0.775) StageIII810.7-124.4(3.5)1-345(14)0.15-136.2(0.645) StageIV251.8-3371(23.9)1-18927(31)0.15-443(0.58) nCEA(%)CA19-9(%)p53 antibody(%)Positive ratiooverall26432.214.835.2 Stage0185.65.616.7 StageI687.45.929.4 StageII7337.012.341.1 StageIII8137.016.038.3 StaIV2588.048.036.0
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 830.
Abstract 833: Effects of ERCC2 and ERCC4 genetic polymorphisms on survival of patients with esophageal cancer
Authors: Lee Jang-Ming , Yang Shi-Yi , Yang Pei-Wen , Chuang Tzu-Hsuen , Chen Jin-Shing , Hsu Hsao-Hsun , Huang Pei-Ming , Lee Yung-Chie 
Published: February 2011

Abstract
Effects of ERCC2 and ERCC4 genetic polymorphisms on survival of patients with esophageal cancer
Jang-Ming Lee1; Shi-Yi Yang2; Pei-Wen Yang1; Tzu-Hsuen Chuang 1; Jin-Shing Chen1; Hsao-Hsun Hsu1; Pei-Ming Huang1; and Yung-Chie Lee1. 1Department of Surgery, National Taiwan University Hospital; 2Graduate Institute of Epidemiology, National Taiwan University, Taipei
Background: XPD/ERCC2 (ERCC2) and XPF/ERCC4 (ERCC4) are the genes involved in nucleotide excision repair (NER). The clinical roles of the genetic polymorphism of ERCC2 on R156R (rs238406) and rs3136038 within ERCC4 promoter region in esophageal cancer are unknown.
Methods: We evaluated 400 patients with esophageal cancer collected from 1996 to 2009 at National Taiwan University Hospital. The genotypes of ERCC2 on R156R and ERCC4 on rs3136038 within promoter region were analyzed with the TaqMan assay from the genomic DNA of peripheral leukocytes. The results of the genotyping were correlated to the survival of the patients.
Results: There is no significant difference in clinical characteristics among the enrolled patients among different genotypes of ERCC2 and 4. The C/C genotype of ERCC2 R156R shows an insignificant unfavorable progression-free survival (PFS) compared to other genotypes (A/A or C/A) (adjusted [HR] = 1.17, 95% CI=0.90-1.51, P=0.236). The ERCC4 rs3136038 G/A genotype displays significant association with worse PFS compared to other genotypes (A/A or G/G) (adjusted [HR] = 1.29, 95% CI=1.02-1.62, P=0.033). Combining these two polymorphisms, these two unfavorable genotypes (C/C on ERCC2 R156R and G/A on ERCC4 rs3136038) display dose-dependently to associate a worse overall and progression free survival with a significant HR of death and disease progression in the patients with both of the unfavorable genotypes comparing with those who without (adjusted [HR] = 1.49, 95% CI=1.04-2.15, P=0.031 for overall survival[OS]; adjusted [HR] = 1.57, 95% CI=1.09-2.26, P=0.015 for progression free survival [PFS]). Kaplan-Meier survival curves demonstrated a significant different distribution of OS and PFS between all patients by the number of unfavorable genotypes of ERCC2 and 4. (P=0.049 for OS and P=0.040 for PFS).
Conclusion: Our study demonstrated that the genetic variants of ERCC2 and ERCC4 may play a role for the clinical outcome in ECa patients. The patients of esophageal cancer with both C/C on ERCC2 R156R and G/A on ERCC4 rs3136038 may require closer follow-up after treatment.
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 833.
Abstract 834: IGF-II promoter specific methylation patterns are associated with its expression and disease progression in epithelial ovarian cancer
Authors: Lu Lingeng , Katsaros Dionyssios , Qian Biyun , Preti Mario , Menato Guido , Beeghly Alicia , Yu Herbert 
Published: February 2011

Abstract
Purpose: High insulin-like growth factor-II (IGF-II) expression in epithelial ovarian cancer is associated with aggressive disease and poor prognosis. IGF-II expression is regulated by promoter methylation; aberrant methylation is common in cancer. The effect of promoter methylation on IGF-II expression and the role of methylation in ovarian cancer are investigated in a clinical study.
Patients and Methods: The study enrolled 211 epithelial ovarian cancer patients who were followed after surgery for disease outcomes. Fresh tumor samples were collected from the patients and were analyzed for IGF-II promoter methylation using methylation-specific PCR, as well as for IGF-II mRNA expression with qRT-PCR. IGF-II peptide concentrations were measured with an ELISA kit in tumor tissues.
Results: The study found different levels of methylation in 3 IGF-II promoters (P2-P4) which are located in a large CpG island, high methylation in P2 (64.2%) and P3 (52.1%) and low in P4 (9.8%). Promoter-specific mRNA expression was lower in methylated than in unmethylated tumors. P3 methylation and expression appeared to play a major role for IGF-II in ovarian cancer. While methylation in individual promoter was not related to the disease, a methylation pattern between P2 and P3 was significantly associated with clinical and pathological features of ovarian cancer, including tumor grade, debulking results, residual tumor size and treatment response. The methylation pattern was also linked to disease progression, but not overall survival.
Conclusions: Our findings suggest that IGF-II expression affects tumor progression and the expression is regulated by methylation which may have clinical implications in disease management.
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 834.
Abstract 837: Genetic alterations in PIK3CA, AKT2 and PTEN gene associated with poor clinical outcome in oral squamous cell carcinoma
Authors: Huang Shiang-Fu , Chen I-How , Liao Chun-Ta , Wang Hung-Ming , Hsieh Ling-Ling 
Published: February 2011

Abstract
The PI3K/AKT pathway plays a fundamental role in the regulation of cell growth, division, survival, and, when disarranged, tumorigenesis. Phosphatase and tensin homolog deleted from chromosome 10 (PTEN) negatively regulates this pathway by acting as a lipid phosphatase. Genetic alterations in the PIK3CA, AKT2 and PTEN gene are common in the PI3K/AKT pathway in human cancers and associated with the aggressiveness of the disease. Thus, drug discovery activities have been directed over the past few years to identify compounds that effectively and specifically disrupt this pathway in tumor cells. To appraise the possible contribution of genetic alterations in the PIK3CA, AKT2 and PTEN genes in activating PI3K/AKT pathway in areca-quid (AQ) associated oral cavity squamous cell carcinomas (OSCCs), PIK3CA mutations, PIK3CA and AKT2 amplifications, and inactivation of PTEN via loss of heterozygosity (LOH), homozygous deletion (HD) and promoter methylation were examined in 153 OSCCs. The frequency of PIK3CA mutations, PIK3CA and AKT2 amplifications, and inactivation of PTEN was 3.21%, 40.52%, 15.69% and 15.03%, respectively. Increased number of gene alterations in the PIK3CA, AKT2 and PTEN gene (χ2 trend test: P = 0.003 and P = 0.027, respectively) was positively associated with lymph node metastasis and tumor differentiation. Based on the status of gene alterations in the PIK3CA, AKT2 and PTEN gene, a gene dosage effect on disease-free and overall survival was observed in patients who had undergone radiotherapy after surgery; however, this gene dosage effect was not significant in patients who had been treated with surgery alone. In the subset of patients received radiotherapy after surgery, patients who had one alteration in PIK3CA/PTEN/AKT2 gene had a poorer disease-free and overall survival, as compared to those with normal PIK3CA/PTEN/AKT2; and those had at least 2 alterations in PIK3CA/PTEN/AKT2 gene would further worsen the condition. Our study provides a rational for exploring treatment strategies that include radiotherapy combined with compounds blocking PI3K/AKT pathway.
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 837.
Abstract 84: The L-ferritin receptor, Scara5, is expressed on breast cancer and glioma cells: A potential functional significance for cancer-associated high serum/CSF levels
Authors: Alkhateeb Ahmed , Webb Becky , Connor James 
Published: February 2011

Abstract
Elevated levels of circulating ferritin have been associated with several neoplasms, including neuroblastoma, glioblastoma, Hodgkin's lymphoma, and breast cancer. Despite the prognostic value of serum ferritin levels, its role in cancer biology is not understood. Ferritin has long been considered exclusively as an intracellular iron storage protein. However, several lines of evidence have suggested a role for ferritin beyond iron storage, such as angiogenesis, iron delivery, and modulation of the immune response. Recently, a receptor for L-ferritin (the predominant ferritin subunit in the serum and cerebrospinal fluid) has been identified as scavenger receptor class A, member 5 (Scara5). Our preliminary data show Scara5 to be expressed in glioma, neuroblastoma, and breast cancer cells. This novel observation led us to hypothesize that Scara5 internalizes L-ferritin, and serves as a non-transferrin iron delivery mechanism in cancer cells. In support of this hypothesis, we report here that both human liver and human heart ferritins increased cellular survival of the breast cancer cell line MCF-7 in serum free conditions. Taken together, these observations suggest an active functional role for circulating ferritin in tumor biology. The elevated levels of circulating ferritin observed in some cancers may enhance tumor metabolism and growth.
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 84.
Abstract 845: Vascular cell adhesion molecule-1 (VCAM-1) expression in patients with ovarian tumors of low malignant potential
Authors: Henretta Melissa , Scalici Jennifer M. , Duska Linda , Slack-Davis Jill , Atkins Kristen 
Published: February 2011

Abstract
The molecular basis for gynecologic tumor dissemination into the peritoneum is not well understood, however it is the primary mechanism of death in advanced stage ovarian cancers. Although serous borderline and serous invasive ovarian cancers are similar, they differ in their ability to implant and invade peritoneal structures. Vascular cell adhesion molecule-1 (VCAM-1), a cell surface receptor expressed on activated endothelial and mesothelial cells, regulates leukocyte attachment and extravasation at sites of inflammation. Recent studies by our group demonstrated the ability of ovarian carcinoma to induce the expression of VCAM-1 on mesothelial cells, and correlated the presence of VCAM-1 with peritoneal dissemination of the tumor. We undertook the current study to determine whether VCAM-1 is expressed on the mesothelium of patients with borderline ovarian tumors. After IRB approval was obtained, cell blocks containing peritoneum and omentum from 10 patients with borderline tumors were processed and stained using antibodies to VCAM-1. Mesothelial expression of VCAM-1 was determined by a single pathologist blinded to tumor type and stage. Samples were determined to be positive if mesothelial cells demonstrated membrane staining. Cytoplasmic staining for VCAM-1 was not considered positive, nor was staining of non-mesothelial cells. Of the 10 patients, four were stage 1a and six were stage 1c serous borderline tumors. Nine of 10 had peritoneal or omental biopsies that did not stain for VCAM-1. The one sample which did stain positively was micropapillary type, which is an invasive sub-type of borderline ovarian cancers. Together, these observations support the hypothesis that VCAM-1 expression correlates with ovarian cancer peritoneal invasion and offers a possible explanation for the inability of borderline tumors to invade peritoneal structures.
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 845.
Abstract 86: Role of autophagy in lymphoma treatment: Autophagy manipulation in lymphoma therapeutic cell killing
Authors: Gump Jacob M. 
Published: February 2011

Abstract
Manipulation of autophagy to augment cancer treatment is an area of active research. We sought to determine the role of autophagy in lymphoma treatment with cytotoxic chemotherapeutics alone and in combination with both genetic and pharmacologic manipulation (activation and inhibition) of autophagy. We found that cellular responses to certain chemotherapeutic agents are altered by autophagic manipulation whereas others are not. Using single cell microscopic assays and flow cytometry we have found that manipulation of autophagy has an effect on a subset of lymphoma cells in culture altering their response to cell death stimuli. The overall magnitude, kinetics and mechanistic aspects of apoptosis are altered in this subset of cells. This finding that there are differences in the response to autophagy manipulation between cancer cells in a population has implications for the treatment of lymphoma and other cancers.
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 86.
Abstract 871: Dermatofibrosarcoma protuberans in a black African population: A clinicopathologic study with emphasis on the predictors of recurrence and outcome
Authors: Ogun Gabriel O. , Ogunbiyi Adebola O. 
Published: February 2011

Abstract
Background: Dermatofibrosarcoma protuberans are relatively rare in our environment. Detailed studies on the subject in homogenous black African population are rare in literature. The aim of the study was to retrospectively analyze the clinical and histopathologic features of the tumor and identify the factors that directly influence recurrence, outcome and prognosis in the setting of a developing country with limited resources.
Materials and Methods: All cases of Dermatofibrosarcoma protuberans histopathologically diagnosed and available from the files and records of Department of Pathology, University College Hospital, Ibadan, Nigeria between January 1989 and December 2007 were identified, reviewed and included in the study. The detailed clinical parameters like age at presentation, gender, size and site of tumor, stage at presentation, treatment modalities, recurrence and follow up details; also details of histopathologic features like mitotic count and presence of tumor at the resection margins were analyzed.
Results: A total of 58 cases were identified and are presented. All the patients were Nigerians. Patient's age ranged from 5-74 years (median, 35years) with a modal age group of 30-39 years. The male/ female ratio had a male preponderance of 2.2:1. Tumor site distribution was trunk (39.5%), lower limb (27%), Upper limb (21%) and head and neck (12.5%). Tumor size ranged from 1.5 to 21cm. Seventy four percent presented with pT2 (TNM) stage tumor. Size of tumor larger than 7cm, mitotic count of greater than 7 per 10hpf and involvement of the subcutaneous tissue were strong indicators of the likelihood of recurrence. Forty five percent of our patients had recurrence with a patient having eight recurrences. The cost implications significantly delayed adjuvant therapy after surgical resection in our patients. This is because the cost of management is borne directly by patients in our environment. About 50% of our patients especially those with pT1 stage tumors were lost to follow up in less than 6 months. Two of our patients had features with fibrosarcoma-like transformation.
Conclusion: The trunk and the lower limb accounted for 66.5% of location of tumor. The follow up data was poor in patients with small sized tumors. Large tumor size and high mitotic count increased the rate of recurrence. The cost implication of care, which is directly borne by patients due to out-of pocket payment lead to poor follow up and outcome.
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 871.