bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 2226: Intraoperative harvesting of human fallopian tubes for cytodiagnostic and pathobiological studies
Authors: Esposito Nicole N. , Kruk Patricia A. , Hoffman Mitchell , Glazerman Larry R. , Nicosia Santo V. 
Published: June 2012

Abstract
Background: Fallopian tube intraepithelial cancer is a potential precursor of high-grade, sporadic and familial, pelvic carcinomas. Materials and Methods: Using a protocol for rapid intraoperative cytology (IC), fallopian tube fimbrial epithelium (FTFE) was harvested from 24 women (age: 40-80) undergoing surgery for non-neoplastic (N = 14, leiomyomas, adenomyosis, ovarian and paraovarian serous cysts, endometriosis) and neoplastic (N = 10, serous and endometrioid carcinomas with tubal involvement) lesions. Under IRB-approved protocol, eight cytological imprints were obtained from each fimbria and stained intraoperatively by Diff-Quik® and Papanicolaou for general morphology, by Trypan blue to assess cell viability and by rapid immunohistochemistry for evaluation of cytokeratin (CAM 5.2), Ki67 (MIB-1) p53 and high motility group protein (HMGA2) expression. Results: Tubal imprints yielded 0.5-1 x106, cytokeratin-positive and &gt; 85% viable cells/patient with a 2:1 distribution of ciliated: mucous cells dispersed within a proteinaceous material of variable density with rare microcalcifications; reactive fibroblasts and mesothelial cells represented &lt; 3% of cell harvests with the highest percentage seen in endometriosis and malignancies. Malignant fimbrial imprints (8 serous and 2 endometrioid carcinomas) exhibited diffuse accumulation of p53 and HMGA2, a Ki67 proliferation index of 50-70% and displayed diagnostic malignant criteria in all cases. Conclusions: Tubal harvest and intraoperative cytology of fallopian tubes allows for: a) rapid evaluation of tubal cancer, currently viewed as the main source of high-grade serous ovarian carcinomas; and b) triaging of cellular material for basic and translational studies including molecular cancer pathobiology and biomarker discovery. The technique will also provide a useful diagnostic adjunct to emerging in vivo high-resolution optical technologies. (Supported by Ovarian Cancer Research Fund).
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2226. doi:10.1158/1538-7445.AM2011-2226
Abstract 2229: Detection of somatic mutations in KRAS gene in Chilean patients with advanced colorectal cancer
Authors: Hurtado Claudia , Zárate Alejandro J. , Kronberg Udo , Lévican Jorge , Contreras Luis , López-Köstner Francisco 
Published: June 2012

Abstract
Introduction: At present, the application of tailored oncologic therapies requires previous performance of mutational analysis of certain genes. In patients with advanced colorectal cancer (CRC), it is essential to detect the presence of activating mutations in the KRAS gene to predict the effectiveness of certain treatments.
Purpose: To determine the presence of KRAS mutations in Chilean patients with advanced CRC, and correlate the mutational status with clinical-pathological data.
Methods: Between October 2009 and August 2010, we prospectively studied the presence of somatic mutations in the KRAS gene in codons 12 and 13 in biopsies of patients with advanced colorectal cancer by allele specific and real time PCR kit. The results were registered in a database, along with the pathology results and clinical data of the patients. Statistical analysis was performed by Student T test and Chi-square test. A p&gt;0.05 was no significant.
Results: A total of 123 patients were analyzed, with a mean age of 61 years and male predominance (60%). Mutations were detected in 47 (39%) of them and only in 2 cases the study was inconclusive. The distribution of the different mutations was as follows: 12Asp (32%), 12Val (26%), 13Asp (19%), 12Cys (11%), 12Ala (6%) and 12Ser (6%). Separated by gender, the detection rate was higher in male patients (45% vs 30%) (p=0.59). Analyzing the data by location of tumor, we found that mutations in right colon tumors was present in 26% (6/23), whereas tumors of the left colon and sigmoid were 43% (16/37) (p=0.1). Mutations detected in patients with lymph node metastasis was 42% comparing to node-negative patients (32%) (p=0.3). In patients with poorly differentiated tumors we found 50% mutations compared to well differentiated (18%) (p=0.08). Finally, the mortality was similar when we compared between WT and mutations patients.
Conclusions: In Chile, 39% of patients with advanced CRC carry mutations in KRAS gene. This result is similar to that described in other populations. There is a tendency to a higher mutation rate in males, patients with left colon cancer, poorly differentiated tumors and patients with lymph nodal involvement.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2229. doi:10.1158/1538-7445.AM2011-2229
Abstract 2245: Fever-range whole-body thermochemotherapy (FR-WB-TT + chemo-biotherapy) can induce long-duration response in both metastatic small-cell lung cancer (SCLCA) and other chemotherapy resistant neuroendocrine cancers
Authors: Bull Joan Marie C , Dancsak Theresa , Su Young , Li Shuang , Redwine Michael D. , King Terri M. , Brown Robert E. 
Published: June 2012

Abstract
Introduction: Metastatic small-cell lung cancer (SCLCA) often relapses quickly after chemotherapy and survival thereafter is short. Resistant neuroendocrine cancers of other origins also have a poor prognosis. Methods: A schedule-optimized Phase I-II thermochemotherapy regimen combining FR-WB-TT with cisplatin (CIS), gemcitabine (GEM), and metronomic interferon-α (IFN) was tested. The treatment regimen used an explicitly sequenced combination of CIS (60 mg/m2) given day 1 with weekly IFN (100 mcg. peginterferon-α-2). On day 3, thirty-six hours later, FR-WB-TT (6h at 40°C) was administered with GEM (600 mg/m2). GM-CSF was administered daily for 10 days beginning 1 week after GEM. The cycle was repeated every 28 days. Results: We have treated 14 patients with metastatic neuroendocrine cancer; 3 with SCLCA and 11 with other neuroendocrine cancers (4 large-cell neuroendocrine of lung, 3 pancreas, 2 prostate, 1 H&N, & 1 adrenal). Thirteen (93%) received prior chemotherapy. The number of treatments ranged from 1-6 (median 4). Response: Using RECIST criteria, we documented: 2 complete responses [CR; 14 %; both SCLCA, durations 45+ months (m), 52 m], 6 partial responses (PR; 43%; &gt;90% tumor response; mean duration 25 m, range 8-37 m; 2 prostate, 2 pancreas, 1 H&N, 1 adrenal). Three patients had stable disease (SD; 21%; all &gt; 4 m duration; 2 large-cell of lung, 1 pancreas). Three patients had progressive disease (PD; 21%; 2 large-cell neuroendocrine of lung, 1 SCLCA). In summary, we observed a 57% overall response (CR + PR). Toxicity: We documented grade 2 leucopenia in twelve patients (86%), grade 2 thrombocytopenia in eight patients (57%), and grade 1 thrombocytopenia in six patients (43%). All patients developed grade 2 anemia. One patient (7%) had a small, grade 2, skin burn. We observed no neuropathy or ototoxicity. Although not formally documented, responding patients experienced increased quality of life with greatly decreased/elimination of pain, weight gain, and resumption of normal activity. Conclusion: This multimodality FR-WB-TT regimen appears to be well tolerated, and demonstrates good clinical activity of relatively long duration in metastatic SCLCA and other resistant stage IV neuroendocrine cancers.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2245. doi:10.1158/1538-7445.AM2011-2245
Abstract 2252: ALDH7A1 expression is associated with recurrence in patients with resected non-small cell lung carcinoma
Authors: Giacalone Nicholas J. , Eisenberg Rosana , Chen Heidi , Olsen Sandra , Massion Pierre , Carbone David P. , Dang Thao P. , Lu Bo 
Published: June 2012

Abstract
The aldehyde dehydrogenase (ALDH) enzymes are important for detoxification of endogenous and exogenous aldehydes. Expression of ALDH family members has recently been described as a potential marker for tumor-initiating cancer stem cells in a variety of human malignancies, including lung cancer. We were interested to determine whether expression of ALDH7A1, a member of the ALDH family, has prognostic significance in resected non-small cell lung carcinoma (NSCLC). Tumor specimens were obtained for 107 patients with completely resected stage I through stage III NSCLC from paraffin-embedded tissue microarrays and stained with an antibody specific for ALDH7A1. Staining patterns were graded by a pathologist based on the intensity of staining and the percentage of cells stained. A staining score index was calculated by multiplying intensity score by the percentage area with positive staining. An index of ≥100 was considered positive, while an index &lt;100 was deemed negative, as determined by visually determining a clear positive stain supported by histograms of the range of scores. Staining index was subsequently correlated with clinical data. Positive ALDH7A1 staining was identified in 46 patients, and negative staining was noted in 48 patients, with 13 tumor sections missing. Multivariate analysis demonstrated that NSCLC patients with positive ALDH7A1 expression had decreased overall survival relative to ALDH7A1-negative tumors, although this did not reach significance (hazard ratio 1.42, 95% confidence interval 0.84 to 2.389; p=0.192). However, patients with ALDH7A1-expressing NSCLC tumors had a significantly higher incidence of lung cancer recurrence compared to patients with ALDH7A1-negative tumors (hazard ratio 6.24, 95% confidence interval 2.06 to 18.86; p=0.001). These data indicate that ALDH7A1 staining is present in a substantial number of NSCLC tumors and may be a biomarker predictive for increased incidence of cancer recurrence in patients with surgically resected NSCLC.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2252. doi:10.1158/1538-7445.AM2011-2252
Abstract 2255: Diagnostic and prognostic value of oncogenic human papillomavirus in patients with carcinoma of unknown primary of the neck
Authors: Speel Ernst-Jan M. , Straetmans Jos M.J.A.A. , Vent Julia , Mujagic Zlatan , Henfling Mieke , Haesevoets Annick , Haidl B , Huebbers Christian U. , Ramaekers Frans CS , Kremer Bernd , Klussmann Jens P. 
Published: June 2012

Abstract
Objective. To date, there is no consensus on the optimal diagnostic and therapeutic strategy for patients with carcinoma of unknown primary (CUP) of the neck. These tumors are heterogeneous in their clinical and biological characteristics, and a pre-operative prognostic marker is desirable to optimize therapy and improve outcome and survival. Human papillomavirus (HPV) is an etiologic factor in a subgroup of head and neck squamous cell carcinomas and has been identified as a significant prognostic biomarker. We sought to determine if HPV also may add relevant information on the origin and prognosis of these tumors.
Material and method. 47 patients (mean age 58.7 years; 40 men, 7 women) presenting with CUP of the neck between 1994 and 2008 in Cologne were examined by standard diagnostic procedures including radiological imaging of the head, neck, thorax and abdomen, positron emission tomography (PET), panendoscopy, curettage of the nasopharynx, bilateral tonsillectomy and blind probes of the base of tongue. All patients were surgically treated with neck dissection of the diseased neck as well as adjuvant chemoradiation. The mean follow up time was 34 months.
Formaldehyde-fixed, paraffin-embedded tissue specimens of the 47 metastases were examined retrospectively by means of p16INK4A immunohistochemistry, HPV-specific PCR and fluorescence in situ hybridization. Results were correlated with clinical follow-up data.
Results. Oncogenic HPV was present in 12/47 (26%) metastases (10 with HPV 16), which showed also p16INK4A overexpression. In 42% of CUP patients the primary tumor was discovered during follow-up. A significant correlation between HPV positivity and later detection of the primary tumor in the oropharynx was found (p=0.038). Moreover, patients with a p16INK4A- (13/47) or HPV-positive tumor had a more favorable overall 5-year survival rate then p16INK4A- and HPV-negative tumors (69% vs 33%, p=0.05; 65% vs 37%, p=0.093; respectively).
Conclusion. HPV is present in a quarter of neck metastases of CUP patients and the presence of oncogenic HPV and p16INK4A expression can serve to locate the primary tumor in the oropharynx. In addition, both biomarkers are indicators of a favorable prognosis.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2255. doi:10.1158/1538-7445.AM2011-2255
Abstract 226: Transcriptional control of the BRCA1 expression by a metabolic switch
Authors: Di Lijun , Fernandez Alfonso , Gardner Kevin 
Published: June 2012

Abstract
Deletion or loss of BRCA1 function is the major cause of most familial forms of breast cancer, decreased expression of non-mutated BRCA1 alleles is often found in sporadic breast cancer, suggesting that alterations in BRCA1 transcriptional regulation may contribute to non-inherited forms of breast cancer. BRCA1 plays a central role in maintenance of genome stability and cell cycle control and therefore, often recognized as both a “care taker” and “gate keeper” of the genome. In this study, we show that BRCA1 expression is controlled by a tightly regulated dynamic balance between the association of transcriptional co-activators and co-repressors that regulate histone acetylation and chromatin accessibility at the BRCA1 promoter during the transcriptional response to estrogen stimulation. A central regulatory step in the control of the BRCA1 promoter is the eviction of the co-repressor and metabolic sensor C-terminal-binding protein1 (CtBP1). Loss of CtBP1 from the BRCA1 promoter either by estrogen induction, CtBP1 RNAi depletion or increasing NAD+/NADH ratio results in elevated histone acetylation, HDAC1 dismissal from the BRCA1 promoter and increased BRCA1 transcription. These findings indicate that BRCA1 expression is controlled by a metabolic switch that dynamically influences the localized deposition of epigenetic marks and chromatin structure at the BRCA1 promoter and suggests that caloric intake may influence the levels of this critical tumor suppressor in mammary tissues. Strikingly extended observation of other DNA damage response genes indicate that they are also under direct regulation by CtBP and CtBP complex. These data suggest a global molecular linkage between cellular metabolic status and the capacity to maintaining the genome free from damage or mistakes.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 226. doi:10.1158/1538-7445.AM2011-226
Abstract 2263: Prognostic significance of miR-215 in colon cancer
Authors: Karaayvaz Mihriban , Pal Timothy , Song Bo , Zhang Cecilia , Georgakopoulos Penelope , Mehmood Saira , Burke Stephanie , Shroyer Kenneth , Ju Jingfang 
Published: June 2012

Abstract
Background: We have previously shown that miR-215 suppressed the expression of key targets such as thymidylate synthase (TS), dihydrofolate reductase (DHFR), and denticleless protein homolog (DTL) in colon cancer. miR-215 is a tumor suppressor candidate due to the up-regulation of p53 and p21 by targeting DTL. However, high levels of miR-215 conferred chemoresistance due to cell cycle arrest and reduced cell proliferation by suppressing DTL. In this study, the clinical significance of miR-215 was further investigated as a potential prognostic biomarker in colon cancer patients.
Methods: Total RNAs were extracted from 34 paired normal and colon (stage II and III) tumor specimens using Trizol based approach. The levels of miR-215 and a closely related miR-192 were quantified using real time qRT-PCR expression analysis. The expression of DTL mRNA and protein were quantified by real time qRT-PCR and immunohistochemistry.
Results: The expression levels of miR-192 (p=0.0008) and miR-215 (p&lt;0.0001) were significantly decreased in colon tumors compared to normal tissues. DTL was significantly over-expressed and was inversely correlated with miR-215, further suggesting an in vivo physiological relevance of miR-215 mediated DTL suppression. Kaplan-Meier survival analysis revealed that high levels of miR-215 expression (hazard ratio, 0.36; log rank test, p=0.04) are closely associated with poor patient's overall survival. Furthermore, an elevated expression of a miR-215 target protein DTL was detected in colon cancer tissues while no expression was present in normal tissues.
Conclusion: miR-215 has a unique potential as a prognostic and diagnostic biomarker in stage II and III colon cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2263. doi:10.1158/1538-7445.AM2011-2263
Abstract 2271: Single nucleotide polymorphisms in p53 codon 72 is associated with grade III tumors in African Americans with breast carcinoma
Authors: Shanmugam Chandrakumar , Salih Chura , Katkoori Venkat R. , Bovell Liselle L. , Callens Tom , Messiaen Ludwine M. , Hameed Omar , Grizzle William E. , Manne Upender 
Published: June 2012

Abstract
Background: Breast carcinomas (BCs) are more aggressive in African Americans (AAs) than in non-Hispanic Caucasian Americans (NHCAs); the reasons for this difference have not been fully elucidated. We recently demonstrated that single nucleotide polymorphisms (SNPs) at codon 72 of the p53 gene are significantly associated with a worse outcome in AAs with colorectal carcinomas. Therefore, we determined the prevalence of such SNPs in BCs and its possible association with adverse clinical or pathological features of BCs in AAs as well as NHCAs.
Methods: To determine the phenotypic status at codon 72, DNA samples, extracted from 137 BCs and their matching benign tissues (from 47 AAs and 90 NHCAs), were analyzed for genotypes by direct sequencing of exon 4. Also, these samples were evaluated for microsatellite (MS) instability by use of the ABI 3100 system. The results obtained were correlated with the demographic and clinicopathological features of the BCs.
Results: Overall, SNPs leading to either Arg/Pro or Pro/Pro at codon 72 were observed in 102 of 137 (74%) BCs, with a slightly higher prevalence in AAs compared to NHCAs (39 of 47; 83% vs. 63 of 90; 70%). The most frequent phenotype was Arg/Pro (84 of 137; 61%), followed by Arg/Arg (35 of 137; 26%) and Pro/Pro (18 of 137; 13%). The prevalence of the homozygous Pro/Pro phenotype, known to be associated with aggressive tumor behavior, was higher in AAs compared to NHCAs (19% vs. 10%). BCs with Pro/Pro or Arg/Pro SNPs were significantly more prevalent in grade III tumors (84%) than in grade I and II tumors (60%) (P=0.005); specifically, this distribution was highly significant in AAs (100% vs. 53%; χ2P=0.0001) as compared to NHCAs (72% vs. 62%; χ2P=0.451). Also, in AAs, BCs with the Pro/Pro phenotype were more frequently associated with MS stable status compared to the other phenotypes (63% vs. 18%; χ2P=0.011). Furthermore, Pro/Pro phenotype was associated with a shorter median survival in AAs (39.9 months) compared to NHCAs (112.2 months).
Conclusions: These preliminary findings suggest that SNPs at codon 72 of p53 gene are associated with aggressive tumor behavior in AAs. Additionally, the Pro/Pro phenotype is associated with MS stable disease and with a shorter median survival in AAs but not in NHCAs. These studies were supported by the UAB-SPORE grant (a pilot study and a supplement) from NCI/NIH (5P50CA089019) and by the Susan G. Komen Breast Cancer Foundation (POP0601383).
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2271. doi:10.1158/1538-7445.AM2011-2271
Abstract 2274: The association of preoperative serum level of lipocalin2 with breast cancer prognosis
Authors: Sung Hyuna , Lee Sang-Ah , Lee Kyoung-Mu , Lee Ji-Young , Oh Jungmin , Lee Yunhee , Li Lian , Park Sue K. , Yoo Keun-Young , Noh Dong-Young , Ahn Sei-Hyun , Kang Daehee 
Published: June 2012

Abstract
Purpose: The association between the expression level of lipocalin2 with cancer progression has already been reported in several tumors such as lung, colon, and breast cancer. However, no previous study has examined the relationship between the circulating level of lipocalin2 and its effect on the prognosis of breast cancer. Thus, this study aimed at assessing whether the preoperative serum level of lipocalin2 is related to the risk of recurrence and death in patients who have undergone curative surgical treatment for breast cancer.
Design: A total of 370 histologically proven breast cancer patients who had undergone curative resections of the tumor between Mar 2004 and Jan 2007 were included in this study. The median follow-up time of survivors was 4.35 years. The preoperative serum level of lipocalin2 was assayed by using enzyme-linked immunosorbent assay. Disease-free survival was defined as the time from surgery to the date of the first locoregional recurrence, first distant metastasis, or death from any cause. Univariate survival analysis was performed using the Kaplan-Meier method, and log-rank tests were employed for comparison of survival curves. Multivariate analyses were conducted using Cox's proportional hazard regression model adjusted for age, tumor size, lymph node metastasis, hormone receptor status, adjuvant chemotherapy and hormone therapy.
Results: The Kaplan-Meier curve showed that patients with upper three-quarters of lipocalin2 concentration combined had lower survival rates than the patients with lowest quarter concentration (P=0.014). In multivariate analysis, lipocalin2 remained an independent prognostic marker for disease-free survival after adjusting for known prognostic factors. The hazard ratio comparing the uppermost quartile to the lowest quartile of lipocalin2 was 2.33 (95% confidence interval, 1.19-4.56; P=0.015).
Conclusions: The results revealed that patients with higher level of lipocalin2 showed significantly lower disease-free survival than patients with lower level. Our study suggests that the higher preoperative level of lipocalin2 may be closely linked to poor prognosis in breast cancer. Further validation is required and functional studies are warranted to elucidate the underlying biological mechanisms for the association.
Key words: Lipocalin2 (LCN), serum biomarker, breast cancer, prognosis
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2274. doi:10.1158/1538-7445.AM2011-2274