tbuckley/cabot-search huggingface dataset:
GFA and S 100 Protein Levels as an Index for Malignancy in Human Gliomas and Neurinomas2
Authors: C. M. Jacque, M. Kujas, A. Poreau, M. Raoul, P. Collier, J. Racadot, N. Baumann
Journal: JNCI Journal of the National Cancer Institute (1979)

Journal Article GFA and S 100 Protein Levels as an Index for Malignancy in Human Gliomas and Neurinomas Get access C. M. Jacque, C. M. Jacque 3Laboratoire de Neurochimie INSERM U.134, Hôpital de la Salpêtrière, 75634 Paris Cédex 13, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar M. Kujas, M. Kujas 4Laboratoire d'Histologie, Clinique Neurochirurgicale, Hôpital de la Pitié, 75634 Paris Cédex 13, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar A. Poreau, A. Poreau 3Laboratoire de Neurochimie INSERM U.134, Hôpital de la Salpêtrière, 75634 Paris Cédex 13, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar M. Raoul, M. Raoul 3Laboratoire de Neurochimie INSERM U.134, Hôpital de la Salpêtrière, 75634 Paris Cédex 13, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar P. Collier, P. Collier 3Laboratoire de Neurochimie INSERM U.134, Hôpital de la Salpêtrière, 75634 Paris Cédex 13, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar J. Racadot, J. Racadot 4Laboratoire d'Histologie, Clinique Neurochirurgicale, Hôpital de la Pitié, 75634 Paris Cédex 13, France. Search for other works by this author on: Oxford Academic PubMed Google Scholar N. Baumann N. Baumann 3Laboratoire de Neurochimie INSERM U.134, Hôpital de la Salpêtrière, 75634 Paris Cédex 13, France. 5We are grateful to Dr. F. Haguenau (Collège de France, Paris) for judicious advice and comments on the text. We are also grateful to Dr. A. Bignami (Veterans Administration Hospital, West Roxbury, Mass.) and Dr. E. Bock (University of Copenhagen, Copenhagen, Denmark) for the anti-GFA sera and to Dr. P. Calissano (Laboratorio di Biologia Cellulare, Rome, Italy) for the anti-S 100 sera with which we could refer our own sera. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 62, Issue 3, March 1979, Pages 479–483, https://doi.org/10.1093/jnci/62.3.479 Published: 01 March 1979 Article history Received: 26 April 1978 Accepted: 20 September 1978 Published: 01 March 1979
Geographic Patterns of Bladder Cancer in the United States
Authors: W J Blot, J F Fraumeni
Journal: JNCI Journal of the National Cancer Institute (1978)

Age-adjusted rates of mortality during 1950–69 from bladder cancer were correlated with demographic and industrial indexes for the 3,056 counties of the contiguous United States. Rates among whites and nonwhites of both sexes rose sharply with urbanization. A small but positive socioeconomic gradient was observed, and mortality was slightly higher among males In counties with high percentages of British and German residents. Even after controlling for demographic variables, the Northeastern excess of bladder cancer among whites was sizable, whereas the regional differences among nonwhites were small. The high rates in the Northeast were seen in both sexes and In rural as well as urban areas, with mortality in small counties in upstate New York and New England equaling or exceeding those in large metropolitan centers elsewhere In the country. Outside the Northeast, high rates were generally limited to urban areas, but clusters of elevated mortality occurred among white males along the Illinois-Wisconsin border, in parts of lower Michigan, and in southern Louisiana. Industrial factors may explain at least part of the geographic clustering, inasmuch as rates among males were significantly higher in U.S. counties where the chemical Industry is heavily concentrated. Increases were also associated with the printing industry, but correlations with 16 other major manufacturing industries were near or below expected levels.
Oligomeric and phosphorylated alpha-synuclein as potential CSF biomarkers for Parkinson’s disease
Authors: Nour K. Majbour, Nishant N. Vaikath, Karin D. van Dijk, Mustafa T. Ardah, Shiji Varghese, Louise B. Vesterager, Liliana P. Montezinho, Stephen Poole, Bared Safieh-Garabedian, Takahiko Tokuda, Charlotte E. Teunissen, Henk W. Berendse, Wilma D. J. van de Berg, Omar M. A. El-Agnaf
Journal: Molecular Neurodegeneration (2016)

Despite decades of intensive research, to date, there is no accepted diagnosis for Parkinson's disease (PD) based on biochemical analysis of blood or CSF. However, neurodegeneration in the brains of PD patients begins several years before the manifestation of the clinical symptoms, pointing to serious flaw/limitations in this approach. To explore the potential use of alpha-synuclein (α-syn) species as candidate biomarkers for PD, we generated specific antibodies directed against wide array of α-syn species, namely total-, oligomeric- and phosphorylated-Ser129-α-syn (t-, o- and p-S129-α-syn). Next we sought to employ our antibodies to develop highly specific ELISA assays to quantify α-syn species in biological samples. Finally we verified the usefulness of our assays in CSF samples from 46 PD patients and 48 age-matched healthy controls. We also assessed the discriminating power of combining multiple CSF α-syn species with classical Alzheimer's disease biomarkers. The combination of CSF o-/t-α-syn, p-S129-α-syn and p-tau provided the best fitting predictive model for discriminating PD patients from controls. Moreover, CSF o-α-syn levels correlated significantly with the severity of PD motor symptoms (r = -0.37). Our new ELISA assays can serve as research tools to address the unmet need for reliable CSF biomarkers for PD and related disorders.
The Role of Whole Genome and Whole Exome Sequencing in Preventive Genomic Sequencing Programs
Authors: Gabrielle Bertier, Ma'n H. Zawati, Yann Joly
Journal: The American Journal of Bioethics (2015)

The target article by Lazaro-Munoz and colleagues (2015) proposes policy recommendations on opt-in/opt-out strategies for the development of population-based preventive genomic sequencing programs ...
Effect of Tumor Removal on the Presence of Lymphocytic Cortisol Metabolism-Enhancing Factor in Plasma of Cancer Patients23
Authors: Ariel Barkan, Elizabeth Barkan, Henriette Hoogervorst Spalter, Haiuta Kaufman, Ami Klein
Journal: JNCI Journal of the National Cancer Institute (1980)

Because lymphocytic cortisol metabolism-enhancing factor (LCMEF) is absent in the plasma of cancer patients (CP), this study was undertaken to determine the influence of tumor removal on this phenomenon. Known concentrations of human iymphocytas were incubated with cortisol in media containing 50% phosphate-buffered saline (PBS) and 50% of one of the following: a) homologic normal plasma (HP), b) plasma from patients with noncancerous diseses (NCO) before surgery, c) plasma from patients with NCO after surgery, d) plasma from CP before tumor removal, e) plasma from CP after tumor removal, f) plasma from long-surviving CP (LSCP), and g) PBS. With the exception of plasma from the LSCP group, all the plasma had the capacity to enhance the lymphocytic cortisol metabolism (LCM) when compared with that of PBS. There was no significant difference between the metabolism obtained with HP and that obtained with plasma from patients with NCO either before or sfter surgery. The plasma from CP led to a significant reduction in activity, with no significant differences in conversion rates before and after tumor removal. The plasma from LSCP failed to enhance LCM, had a conversion rate similar to that of PBS and significantly lower than that of the plasma from CP, and appeared to contain no LCMEF. These findings, which showed that the lack of LCMEF in CP is not influenced by tumor removal, may indicate 1) that the lack of LCMEF preceded the appearance of cancer or 2) irreversibility of a possible anti-LCMEF synthesis effect was induced by the tumor.
The targeted delivery of the c-Src peptide complexed with schizophyllan to macrophages inhibits polymicrobial sepsis and ulcerative colitis in mice
Authors: Ye-Ram Kim, Jangsun Hwang, Hyun-Jung Koh, Kiseok Jang, Jong-Dae Lee, Jonghoon Choi, Chul-Su Yang
Journal: Biomaterials (2016)
Phase-2 study of neoadjuvant chemoradiation in locally advanced rectal adenocarcinoma: The Radio-Xelox study
Authors: M. Salimichokami, M. Vafai, S. Derakhshani, S. Aminian, A. A. Vaheed
Journal: Journal of Clinical Oncology (2006)

13549 Background: Neoadjuvant Radiation treatment has been shown in many studies to decrease the incidence of loco-regional relapse in pts with locally-advanced Rectal Adenocarcinoma. Capecitabine and Oxaliplatin are both effective antineoplastic drugs in Colorectal Adenocarcinoma. They also have radiosensitizing effects. Hence,it is rational to combine these agents in association with radiotherapy,to achieve local controle and prevent systemic spread of the cancer. Methods: Thirty-eight pts with Rectal Adenocarcinoma (T3-T4 and/or N+) received radiation treatment (2.0 Gy, 5days a wk over 5 wks,total dose 50 Gy) plus oral Capecitabine at 600 mg/m 2 twice a day and iv Oxaliplatin at 35 mg/m 2 once weekly × 5wks. Surgery was performed 6wks post completion of XRT. Our end points were safety/feasibility and response/efficacy as demonstrable by the rate of pathologic complete remission (path-CR). Results: Seven pts (20%) acheived path-CR. Diarrhea was the most important severe adverse effect (in 25% of pts). fourteen pts (40%) showed good regression (very few cancer cells in fibronecrotic tissue Dworak grade 3). The remaining 17 pts showed less favorable regression or no significant change. Conclusions: Preoperative Radiation treatment plus chemotherapy with XELOX regimen is feasible, safe and effective with an impressive rate of path-CR in locoregionally advanced Rectal Adenocarcinoma. No significant financial relationships to disclose.
Multiple antigens in a breast cancer vaccine result in a higher immune response rate in breast cancer patients
Authors: J. F. Head, K. Hsu, X. Jiang, R. L. Elliott
Journal: Journal of Clinical Oncology (2004)

2607 Background: We have previously reported that whole cell preparations of breast carcinoma cells from either an autologous or allogeneic source (MCF-7 cells) and tumor antigens (CA 15–3, CEA and CA125) could produce immune responses, increased lymphocyte proliferation in a Lymphocyte Blastogenesis Assay (LBA), in breast cancer patients vaccinated with tumor cells, tumor antigens and two biological adjuvants (IL-2 and GM-CSF). The present study was undertaken to determine if the use of multiple antigens, cells and tumor antigens, in a breast cancer vaccine could increase the proportion of patients demonstrating an immune response to vaccination. Methods: Twenty-four patients were vaccinated 6 times with allogeneic cells, CA 15–3, CEA, and CA 125 antigens. LBAs were done before and after vaccination and the ratio of antigen to the media control was determined for each antigen before and after vaccination (a ratio of 1 means no stimulation by the antigen). The post-vaccine ratios for each patient's antigens were compared to the pre-vaccine ratio and an increase of 2 times was considered a significant immune response. Results: The following immune response rates were found: 25% (6 of 24 patients) for allogeneic MCF-7 cells, 21% (5 of 24 patients) for CA 15–3, 25% (6 of 24 patients) for CEA and 22% (5 of 23 patients) for CA 125. When an immune response to either the whole cell or any one of the tumor antigens was considered an immune response for that patient, then 58% (14 of 24) of the patients had immune responses. Conclusions: Whole cell preparations of allogeneic MCF-7 cells and tumor antigens (CA 15–3, CEA and CA 125) can induce immune responses in breast cancer patients. Each antigen produces an immune response, as measured by a LBA, in approximately 25% of the patients but by using multiple antigens over half of the patients will have an immune response to one or more of the antigens. This suggests that the use of multiple antigens in cancer vaccines may increase the clinical response rate, but a larger study with long-term follow-up will be needed. No significant financial relationships to disclose.
Chemotherapy with gemcitabine and oxaliplatin in 13 malignant pleural mesothelioma (MPM): A monocenter experience
Authors: J.-M. Brechot, J.-F. Morère, G. Des Guetz, K. Chouhania, J.-L. Breau
Journal: Journal of Clinical Oncology (2004)

7250 Background: A wide range of chemotherapic agents used singly or in combination have been evaluated in MPM. Doublets with gemcitabine and a platinum salt emerge as one of the most promising regimen. The combination of gemcitabine and oxaliplatin (GEMOX) has a very good toxicity profile. This chemotherapy has been administered in clinical practice in our department for 2 years. Methods : We have rewieved the data of consecutive non pretreated MPM patients (pts) treated with GEMOX between October 2001 and October 2003 at our department. Results : 13 pts (9 males, 4 females), mean age 62y (50–74), PS 0–1 12 pts, PS 2 1 pt, with a MPM diagnosed by pleuroscopy (9), thoracotomy (1) or blind pleural biopsy (3), with epithelial (4), mixed (4) and unspecified (5) histological subtype, all stage III or IV, received as outpatient treatment an association of gemcitabine 1000mg/m2 D1 and oxaliplatin 100mg/m2 D2 every 2 weeks with a mean of 8 cycles. In 9 evaluable pts, 2 PR, 6 SD and 1PD were observed. Median time to progression (TTP) was 7,5 months. Median survival is 12 months. Seven pts died, all in progressive disease. No grade 3 or 4 hematologic toxicities were observed. In 5 cases, treatment was discontinued because of non hematologic toxicities (allergia grade 3 in 2 pts at the 6th and 7thcycles, peripheral neurotoxicity in 3 pts (at the 6th and 10th cycles). Conclusion : GEMOX is a well tolerated and active chemotherapy regimen in MPM. It could be recommended in clinical practice. No significant financial relationships to disclose.
Conventional cautions regarding online information: Do they predict accuracy of breast cancer websites?
Authors: F. Meric-Bernstam, M. Walji, D. Sagaram, S. Sagaram, C. W. Johnson, E V. Bernstam
Journal: Journal of Clinical Oncology (2006)

6086 Introduction: Cancer patients and oncologists are increasingly using the Internet. Online information is affecting patient decisions regarding treatment. Therefore, multiple organizations published advice on how to screen out problematic information online. In the present study, we sought to determine whether existing quality assessment tools can screen out false or inaccurate breast cancer information online. Methods: Using 15 representative search queries on five popular search engines and only the first page of results, we generated a list of 1,585 Web pages. After eliminating irrelevant, broken and duplicate links 343 unique web pages were downloaded and evaluated for website characteristics, information accuracy and 15 quality criteria: authorship identified, author credentials identified, physician credentials stated, author affiliation stated, sources clear, general disclosures, attribution/references provided, disclosure of ownership, date created displayed, date of last update displayed, date of creation or last updated displayed, editorial process stated, internal search engine present, feedback mechanism provided and copyright notice. Quality criteria were evaluated by an independent evaluator blinded to the accuracy information. Accuracy was determined independently by a pair of clinically trained evaluators. Results: Of 343 pages evaluated, 41 false/misleading statements were displayed on 18 distinct pages. The presence of an internal search engine was correlated most strongly (r = .196, r 2 = .038) with health information accuracy. However, all quality criteria (alone or in combinations tested exhaustively) were linearly associated with less than 7% of the variance in number of inaccuracies per website. Conclusion: Currently available technical quality criteria do not identify false or misleading online information about breast cancer. At this time, directing patients to websites with known content appears to be the only way to ensure patients will not encounter false or misleading online information. No significant financial relationships to disclose.
Antiproliferative effect of mimosine in ovarian cancer
Authors: A. Restivo, L. Brard, C. O. Granai, N. Swamy
Journal: Journal of Clinical Oncology (2005)

3200 Objective: Iron plays a critical role in cell proliferation and survival making it a potential target for cancer therapy. Iron chelators have recently been shown to possess selective anti-neoplastic properties. Mimosine, a plant amino acid, acts as a potent iron chelator, but its use in gynecologic malignancies has yet to be tested. It is a naturally occurring plant amino acid known to arrest cell-cycle progression at the G1-S border in cultured cells. The objective of our study was to evaluate the anti-proliferative and pro-apoptotic effects of mimosine on human and rat ovarian cancer cells. Methods: Human (CaOV-3 & OvCAR) and rat (NuTu 19) ovarian cancer cell lines were treated for 24–72 hours with mimosine at varying doses ranging from 50 to 800 micro-molar concentrations. Untreated cells were used as a control. Cell viability was measured by MTS reduction assay and cell proliferation was determined by BrdU incorporation. Apoptosis was analyzed by DNA fragmentation. Iron challenge studies were performed to determine the role of iron in the cytotoxic effect of mimosine. Results: Mimosine demonstrated dose dependent anti-proliferative effects on all the ovarian cancer cells tested. Cell viability was inhibited over 70% at a dose of 200μM mimosine. Mimosine also inhibited DNA synthesis as revealed by BrdU incorporation assay. Fifty percent inhibition in DNA synthesis was observed at 100 μM dose level of mimosine. Addition of ferric ion effectively reversed the effects of mimosine, indicating that the effect of mimosine is mediated by iron chelation. In addition, mimosine induced apoptosis. DNA fragmentation analysis confirmed apoptosis. Further testing revealed mimosine to have significant dose-dependent antiproliferative effects on vulvar and cervical cancer cell lines and only a minimal effect on endometrial and colorectal cells. Conclusions: Mimosine, an iron chelator, has potent cytotoxic and anti-proliferative effects on a human and rat ovarian cancer cells. Iron challenge studies imply that the anti-proliferative effect of mimosine is mediated by iron chelation. Mimosine induced apoptosis. No significant financial relationships to disclose.
Influence of a novel polymorphism in the 3’ untranslated region of the gene <i>PLK1</i> upon PLK1 mRNA expression and survival of patients with renal cell carcinoma
Authors: J. C. Vogler, K. Riemann, U. H. Frey, H. S. Bachmann, H. Rübben, W. Siffert
Journal: Journal of Clinical Oncology (2008)

22005 Background: Polo-like kinases (PLK) belong to the family of serine/threonine kinases. They regulate the transit from the G2 phase to mitosis during the cell cycle. PLK1 is overexpressed in human tumors which correlates with cancer progression. Novel PLK1-inhibitors were developed to improve the efficacy of standard chemotherapeutics which interfere with the cell cycle. Because genetic polymorphisms can influence the transcription of genes, the importance of an A>G single nucleotide polymorphism (SNP) in the 3’ untranslated region (3’UTR) of PLK1 was examined for PLK1 expression and survival for patients with clear cell renal cell carcinoma (RCC). Methods: The examinedtumor collective comprised 141 patients who were treated for RCC at the Department of Urology of the University Hospital of Essen, Germany. DNA was genotyped using the restriction fragment length polymorphism method (RFLP). Kaplan- Meier plots and the log-rank test for trend were used to detect a potential association of overall survival with the 3’UTR SNP. To determine potential genotype-dependent mRNA expression quantitative real-time PCR (qRT-PCR) was applied. Results were compared using ANOVA. Results: Genotyping of the RCC collective showed that 41.1% of the patients were homozygous for the A-allele, 49.6% were homozygous for the G-allele and 9.3% were heterozygous. Acorrelation between the 3’UTR-polymorphism in PLK1 and overall survival was detected showing reduced overall survival for patients carrying the G allele (p=0.009). qRT-PCR analysis showed an increased mRNA expression of PLK1 associated with the G- allele compared to the A allele in tumor tissue from patients with RCC. Conclusion: It has already been described that PLK1 is overexpressed in human tumors and that the abundance of PLK1 correlates with their malignancy. The results presented here show that the abundance of PLK1 is associated with genotypes of the polymorphic 3’UTR. PLK1 genotypes could be a marker for survival of patients with RCC and could potentially be used to identify responders to PLK1 inhibitors. No significant financial relationships to disclose.
Behavioral Screening and Intervention for Improving Lower-Extremity Arthroplasty Outcomes and Controlling Costs
Authors: Richard L. Brown
Journal: JAMA Surgery (2016)

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SK053 An Inhibitor Of Enzymes Involved In Allosteric Disulfide Bonds Formation Induces Differentiation Of Human AML Cells
Authors: Justyna Chlebowska, Malgorzata Firczuk, Karolina Furs, Angelika Muchowicz, Radoslaw Sadowski, Adam D. Staruch, Szymon Klossowski, Ryszard Ostaszewski, Anna Paulina Dabrowska-Iwanicka, Jakub Golab, Dominika Nowis
Journal: Blood (2013)
P-137 Clinical feature of 53 patients with biliary neuroendocrine tumors: Retrospective study for Korean neuroendocrine tumor of gallbladder, extrahepatic biliary tract, and ampulla of Vater
Authors: J.H. Cho, W.J. Lee, S.H. Lee, K.H. Lee, K.J. Lee, K.B. Park, J.K. Lee, H.Y. Jeong, C.H. Yang
Journal: Annals of Oncology (2015)