tbuckley/cabot-search huggingface dataset:
Abstract 4635: FK506 binding protein 51 is a possible novel tumoral marker
Authors: Maria Fiammetta Romano, Simona Romano, Anna D'Angelillo, Elvira De Luna, Stefania Staibano, Massimo Mascolo, Rita Bisogni
Journal: Cancer Research (2010)

Abstract Very recently, we have identified FK506 binding protein 51 (FKBP51), an immunophilin phisiologically expressed in lymphocytes, as a protein associated with malignant melanoma. Its expression correlates with tumor aggressiveness and is maximal in metastatic lesions. We have also demonstrated that FKBP51 is a factor of resistance to genotoxic agents, including anthracyclins and ionizing radiations, because it promotes NF-kB activation. Aim of the present study was to investigate FKBP51 expression in solid tumors. Overall 60 samples, stored in our Patology section, of the following tumors: breast, colon, lung, pancreas, ovary and prostate (10 for each tumor), and a comparable number of normal tissue samples, were analysed for FKBP51 expression by immunohistochemistry. An intense signal was observed in all prostatic and ovarian adenocarcinomas analyzed, but only in a proportion of pancreatic cancer samples analyzed (mostly, esocrine pancreas tumors). Furthermore, an intense nuclear signal was observed in colon and lung adenocarcinomas. Immunohistochemistry was negative in breast cancer. Normal tissues of the same histotype showed very low or undetectable levels of FKBP51. We also measured FKBP51 mRNA levels in deparaffinized tissues from breast, pancreas, prostate and lung samples, both normal and tumoral, by Realtime PCR. All normal tissues analyzed, except for prostate, displayed mRNA levels lower than those of peripheral blood mononuclear cells (PBL). FKBP51 levels in prostate and PBL were similar. Increases in mRNA levels, from 3 to 30 folds, were found in prostate, esocrine pancreas and lung cancers, compared to normal tissue of the same histotype. Very low FKBP51 mRNA levels were found in breast cancer. In conclusion, our preliminary results show that FKBP51 expression increases in different solid tumors, including ovary, prostate, lung, colon, and esocrine pancreas, in comparison with the normal tissue counterpart. This study support the conclusion that deregulated FKBP51 can play a role in malignant transformation. 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 4635.
Optimizing resection of sessile serrated polyps
Authors: Seth Sweetser, Todd Baron
Journal: Endoscopy (2014)

Removal of precancerous lesions during colonoscopy reduces colorectal cancer (CRC) incidence and mortality [1]. Recent data have highlighted that interval CRC occurs despite previous colonoscopy. Incomplete removal of polyps is one of the factors leading to interval CRCs [2]. Incomplete polypectomy of sessile serrated polyps (SSPs) is four-fold higher than that of conventional adenomas [3] and may contribute to a higher risk of interval CRCs.
Abstract 2999: Targeted depletion of all somatically mutated genes in lung cancer cells facilitates identification of mutationally activated novel drivers of lung cancer.
Authors: Shameem Fawdar, Eleanor W. Trotter, Yaoyong Li, Sara Ientile, Crispin Miller, John Brognard
Journal: Cancer Research (2013)

Abstract Approximately 70% of all NSCLC patients present with late stage disease (stage III-IV) and there is a pressing need to develop better therapies for these patients. This remains a major challenge as the underlying genetic causes of nearly half of all NSCLCs remain unknown. Recent success with therapies targeting mutationally activated EGFR and constitutively active EML4-ALK serve as proof of principle that drugs targeting genetically activated drivers of lung cancer result in better, more durable therapeutic responses in patients. In an effort to identify novel mutationally activated drivers of lung cancer, we performed a targeted siRNA screen to knockdown all somatically mutated genes in a panel of six NSCLC cell lines. Using this approach we have identified three mutationally activated drivers that include MLK1, PAK7 and FGFR4. We demonstrate that mutations in these genes are activating, that the cancer cells that harbour the genetically activated oncogenes rely on these drivers to maintain cell proliferation and survival and inhibition of these activated kinases results in specific killing of the lung cancer cells. As cancer genomic data accumulates at an unprecedented rate, approaches must be developed to filter through this data to identify druggable drivers that could lead to better therapeutic options for patients in the clinic. Our studies demonstrate that combining targeted siRNA screens with cancer genomics will be a successful approach to identify novel drivers of cancer. Citation Format: Shameem Fawdar, Eleanor W. Trotter, Yaoyong Li, Sara Ientile, Crispin Miller, John Brognard. Targeted depletion of all somatically mutated genes in lung cancer cells facilitates identification of mutationally activated novel drivers of lung cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2999. doi:10.1158/1538-7445.AM2013-2999
Importance of Dressing Removal Before Radiolabeled WBC Imaging for Musculoskeletal Infection
Authors: MUNIR GHESANI, E. GORDON DEPUEY, STEVEN PARMETT, ANDREW DEROGATIS, STEVE MELANCON, RINA RISKINA
Journal: Clinical Nuclear Medicine (1996)

Leukocyte imaging performed with In-111 or Tc-99m is gaining widespread acceptance as a method for detection of osteomyelitis associated with soft tissue injury or infection. The authors present three cases in which initial imaging was suggestive of a focal infectious process in bone and soft tissue. However, repeat imaging after the removal of wound dressings, which revealed serosanguineous discharge in all cases, resulted in a scan appearance that was much less remarkable for focal radiotracer accumulation in the bone. The authors conclude that accumulation of labeled WBCs in wound discharge can result in scans that are false-positive for osteomyelitis. Therefore, the authors recommend that wounds should be cleaned and dressings changed before imaging in order to avoid scans that are false-positive for osteomyelitis.
HIV protease inhibitor (PI) therapy for liposarcoma
Authors: W. A. Chow, S. Guo, F. Valdes-Albini
Journal: Journal of Clinical Oncology (2006)

9564 Background: Liposarcomas are the second most common soft-tissue sarcoma. Highly-active anti-retroviral therapy (HAART) with HIV PIs results in “HIV-1 protease inhibitor associated lipodystrophy syndrome,” characterized by peripheral fat wasting, central fat accumulation, insulin resistance, and hyperlipidemia. Based upon this syndrome, we hypothesized that HIV PIs might represent a novel liposarcoma therapy. Methods: SW872, LiSa-2, and FU-DDLS-1 liposarcoma, and control 293 embryonic kidney and HT1080 fibrosarcoma cell lines were treated with HIV PIs and subjected to cellular and molecular assays. Results: Clonogenic assays with SW872 cells using HIV PIs (saquinavir, ritonavir, indinavir, nelfinavir, and amprenavir) were performed. Nelfinavir demonstrated the most potent clonogenic inhibition without affecting 293 and HT1080 clonogenicity, and was studied further. Nelfinavir inhibited SW872 and LiSa-2 proliferation dose-dependently, and HT1080 proliferation at the highest concentration, without affecting FU-DDLS-1 nor 293 proliferation. Nelfinavir induced a G 1 cell cycle arrest in SW872 and HT1080, but not in 293 cells. It also induced dose-dependent apoptosis in SW872, but not in 293 nor HT1080 cells. Western analyses for sterol regulatory element binding protein-1 (SREBP-1) expression, a key transcriptional regulator of fatty acid and cholesterol synthesis, were performed. Nelfinavir induced expression of SREBP-1 in nelfinavir-sensitive SW872 and LiSa-2 cells, and modestly in HT1080 cells, but not in insensitive FU-DDLS-1 nor 293 cells. Additionally, nelfinavir reduced protein expression of proliferating cell nuclear antigen (PCNA) in sensitive SW872 and LiSa-2 cells, and induced expression of the anti-proliferative protein, p21, as well as pro-apoptotic proteins, Bax and Fas, in a dose-dependent manner. Finally, forced expression of SREBP-1 with a Tet-On inducible SW872 cell line, in the absence of nelfinavir, induced expression of p21, Bax, Fas, reduced expression of PCNA, and inhibited cell proliferation. Conclusions: These studies demonstrate that nelfinavir inhibits cellular proliferation, and induces apoptosis in sensitive-liposarcoma cells through upregulation of SREBP-1. These studies validate nelfinavir as a potential, novel targeted therapy for liposarcoma. No significant financial relationships to disclose.
1073 INTEGRATED GENOMIC ANALYSIS IN HEPATOCELLULAR ADENOMA
Authors: C. Pilati, S. Imbeaud, A. Boulai, K. Poussin, G. Morcrette, G. Couchy, J. Calderaro, P. Bioulac-Sage, E. Letouz'e, J. Zucman- Rossi
Journal: Journal of Hepatology (2013)
The duality of art: Body and soul
Authors: George E Newman
Journal: Behavioral and Brain Sciences (2013)

Bullot & Reber (B&R) make a strong case for the role of causal reasoning in the appreciation of artwork. Although I agree that an artistic design stance is important for art appreciation, I suggest that it is a subset of a more general framework for evaluating artworks as the causal extensions of individuals, which includes inferences about the creator's mind, as well as more physical notions of essence.
A Rare Case of Hepatic Carcinoid
Authors: LUCA TAGLIABUE, GIAN L. TAROLO, ALBERTO BESTETTI, CLAUDIO DI LEO, ANGELO DEL SOLE
Journal: Clinical Nuclear Medicine (2001)

TAGLIABUE, LUCA M.D.; TAROLO, GIAN L. Prof.; BESTETTI, ALBERTO M.D.; DI LEO, CLAUDIO M.D.; DEL SOLE, ANGELO M.D. Author Information
THU0160 The Effect of VX-509, a Selective Oral Jak3 Inhibitor, on Plasma Biomarkers of Disease Activity in Patients with Rheumatoid Arthritis
Authors: I. M. Catlett, A. K. Legedza, L. Sewell, T. Hoock
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Janus kinase 3 (JAK3) plays a critical role in intracellular signal transduction and is required for activation of lymphocytes. Oral VX-509 selectively inhibits JAK3 and improves signs and symptoms in patients with active RA. <h3>Objectives</h3> To evaluate the pharmacodynamic effect of VX-509 on inflammatory biomarkers of RA disease activity including interleukin 6 (IL-6), IL-2 receptor alpha (CD25), and chemokine ligand 18 (CCL18), and markers of bone erosion (matrix metalloproteinase, MMP-3). These analyses advance our understanding of the response to VX-509 treatment in RA patients. <h3>Methods</h3> Two hundred and four RA patients with inadequate response to DMARDs were enrolled in a 12-week, phase 2a, double-blind, randomized, placebo-controlled study of oral VX-509 monotherapy with 25 mg, 50 mg, 100 mg, 150 mg bid, or placebo. Plasma was collected at baseline, week 6, and week 12. Samples from 93 study completers were stratified to represent the non-responder, ACR20, ACR50, and ACR70 responses observed within each dosage group. Markers of RA associated with inflammation were analyzed by Luminex multiplex technology. The mean, median, and change from baseline were calculated; the 25 mg bid group was not included. <h3>Results</h3> Patients treated with VX-509 at dosages of 50 mg, 100 mg, and 150 mg bid had decreases from baseline in levels of IL-6, CD25, CCL18, and MMP-3 at week 12 that were dose-related (Table 1). <h3>Image/graph</h3> <h3>Conclusions</h3> VX-509 treatment modulated biomarkers of RA associated with inflammation (IL-6, CD25, and CCL18) and bone erosion (MMP-3). These changes are consistent with the efficacy of VX-509 in improving RA signs and symptoms. <h3>Disclosure of Interest</h3> I. Catlett Shareholder of: Vertex Pharmaceuticals Incorporated, Employee of: Vertex Pharmaceuticals Incorporated, A. Legedza Shareholder of: Vertex Pharmaceuticals Incorporated, Employee of: Vertex Pharmaceuticals Incorporated, L. Sewell Shareholder of: Vertex Pharmaceuticals Incorporated, Employee of: Vertex Pharmaceuticals Incorporated, T. Hoock Shareholder of: Vertex Pharmaceuticals Incorporated, Employee of: Vertex Pharmaceuticals Incorporated
PREDICTORS OF CORONARY ARTERY DISEASE IN PATIENTS WITH POLYCYTHEMIA VERA AND ESSENTIAL THROMBOCYTOSIS: RESULTS FROM THE NATIONAL INPATIENT SAMPLE 2009-10
Authors: Parasuram Krishnamoorthy, Varun Mittal, Jalaj Garg, Neeraj Shah, Nainesh Patel, John C. Leighton, Vincent Figueredo
Journal: Journal of the American College of Cardiology (2016)
Evaluation of Changes in Plasma Protein Profiles during Neoadjuvant Chemotherapy in HER2-Positive Breast Cancer Using MALDI-TOF/MS Procedure.
Authors: C. Mazouni, K. Baggerly, D. Hawke, S. Tsavachidis, F. André, A. Buzdar, P. Martin, R. Kobayashi, L. Pusztai
Journal: Cancer Research (2009)

Abstract Background: Comparison of protein profiles of the plasma before chemotherapy and after completion of neoadjuvant chemotherapy may reveal tumor markers that could be used to monitor tumor response.Patients and Methods: We examined matching pre- and post-treatment serum samples 39 HER2-postive breast cancer patients (n=78 samples) who all received 6 months of preoperative chemotherapy with or without trastuzumab in the context of a randomized clinical trial. Serum was analyzed with an Applied Biosystems 4700 Proteomics Analyzer matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometer. Samples were grouped and pooled into those who achieved pathological complete response (pCR, n=20) and those who had residual disease (RD, n=19). We compared matching baseline and post-chemotherapy/pre-surgery samples separately in both response groups and also compared baseline samples between the two response groups.Results: MALDI-TOF analysis revealed a total of 2329 and 3152 peaks in pooled samples of cases with pCR and RD, respectively. A total of 32 peaks were differentially expressed between base line and post-chemotherapy pCR samples and 643 peaks in cases with RD (false discovery rate ≤ 20%). A total of 8 differentially expressed proteins were identified in the before- and after-chemotherapy samples from their peptides after digestion and LC-MALDI-TOF/TOF. These included 4 AFM, C3, hemopexin, SAP in pCR samples and AP1, hemopexin, Complement B, amyloid P component in the RD group.Conclusion: Our study suggests that MALDI mass spectrometry may be used to detect differences in baseline serum profiles of patients who are highly sensitive to chemotherapy and those who are less sensitive. Also, changes occur in the serum during chemotherapy and this may offer the possibility of monitoring response to treatment in the future. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 2037.
Role of Daunosamine and Hydroxyacetyl Side Chain in Reaction With Iron and Lipid Peroxidation by Anthracyclines
Authors: L. Gianni, L. Vigano, C. Lanzi, M. Niggeler, V. Malatesta
Journal: JNCI Journal of the National Cancer Institute (1988)

Journal Article Role of Daunosamine and Hydroxyacetyl Side Chain in Reaction With Iron and Lipid Peroxidation by Anthracyclines Get access Luca Gianni, Luca Gianni * 3Laboratory of Clinical Pharmacology, Division of Medical Oncology, Istituto Nazionale per lo Studio e la Cura dei TumoriMilan, Italy. *Correspondence to: Dr. Luca Gianni, Laboratory of Clinical Pharmacology, Division of Medical Oncology, Istituto Nazionale Tumori, Via Venezian 1, 20133 Milan, Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar Lucia Vigano, Lucia Vigano 3Laboratory of Clinical Pharmacology, Division of Medical Oncology, Istituto Nazionale per lo Studio e la Cura dei TumoriMilan, Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cinzia Lanzi, Cinzia Lanzi 6Division of Experimental Therapy, Istituto Nazionale per lo Studio e la Cura dei TumoriMilan, Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar Michela Niggeler, Michela Niggeler 3Laboratory of Clinical Pharmacology, Division of Medical Oncology, Istituto Nazionale per lo Studio e la Cura dei TumoriMilan, Italy. Search for other works by this author on: Oxford Academic PubMed Google Scholar Vincenzo Malatesta Vincenzo Malatesta 4Division of Research and Development, Farmitalia Carlo Erba, Ltd.Milan. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 80, Issue 14, 21 September 1988, Pages 1104–1111, https://doi.org/10.1093/jnci/80.14.1104 Published: 21 September 1988 Article history Received: 25 April 1988 Accepted: 08 June 1988 Published: 21 September 1988
A HIGHLY PREDICTIVE RISK MODEL FOR NEW PERMANENT PACEMAKER IMPLANTATION AFTER BALLOON-EXPANDABLE TRANSCATHETER AORTIC VALVE REPLACEMENT
Authors: Yoshio Maeno, Hiroyuki Kawamori, Yoshio Kazuno, Nobuyuki Takahashi, Yigal Abramowitz, Shunsuke Kubo, Mohammad Kashif, Kazuaki Okuyama, Tarun Chakravarty, Mamoo Nakamura, Wen Cheng, Raj Makkar, Hasan Jilaihawi
Journal: Journal of the American College of Cardiology (2016)
MULTI-MODALITY IMAGES - COLOR COMPOSITE ANALYSIS OR CLUSTER ANALYSIS.
Authors: Barry L. Engelstad, H. Joseph Meyers, William A. Hanson, J. William OʼConnell, Robert C. Taylor, Ralph Bernstein
Journal: Clinical Nuclear Medicine (1988)

Engelstad, Barry L.; Joseph Meyers, H.; Hanson, William A.; William O'Connell, J.; Taylor, Robert C.; Bernstein, Ralph Author Information
Detection of Residual Acute Lymphoblastic Leukemia Cells in Cultures of Bone Marrow Obtained during Remission
Authors: Zeev Estrov, Tom Grunberger, Ian D. Dubé, Yao-Ping Wang, Melvin H. Freedman
Journal: New England Journal of Medicine (1986)

We used a semisolid culture assay to quantitate leukemia cells in the bone marrow of patients with childhood acute lymphoblastic leukemia (ALL). In bone marrow cultures from 40 patients with newly diagnosed disease, the colonies that developed in vitro consisted of lymphoblasts with the same surface markers and abnormal karyotype as the original diagnostic marrow specimens. We also studied marrow cultures from 13 patients in chemotherapy-induced remission; 6 of these, including 1 obtained from a patient during successful engraftment after marrow transplantation, also yielded lymphoblast colonies in culture, with the same immunologic phenotype or abnormal karyotype as the original leukemic marrow. Four of these patients, including the one who underwent marrow transplantation, relapsed within 2 to 30 months of the abnormal cultures; the other two are still In remission, one of them 30 months after diagnosis. Bone marrow cultures from eight normal controls and from the other seven patients in remission did not yield lymphoblast colonies; all seven of the latter are still in remission. This assay appears to allow detection of small numbers of residual leukemic cells. We conclude that the technique will be valuable in monitoring the efficacy of chemotherapy and allogeneic bone marrow transplantation in acute lymphoblastic leukemia, as well as in evaluating the quality of purged marrow for autologous marrow transplantation. (N Engl J Med 1986; 315: 538–42.)
Antithrombotic Agents and Thromboembolic Disease
Authors: Bruce M. Ewenstein
Journal: New England Journal of Medicine (1997)

Among patients undergoing elective hip replacement, the incidence of deep-vein thrombosis in the absence of prophylactic anticoagulation approaches 50 percent.1,2 Thrombus formation is multifocal, occurring principally in the surgically manipulated leg, where trauma to blood vessels and venous stasis would be expected to be most severe. Since approximately half of thrombi are found in large proximal veins, the risk of pulmonary embolism is high. An optimal therapeutic regimen should therefore be capable of preventing the initiation and propagation of venous thrombi without increasing the risk of perioperative bleeding or interfering with wound healing.The efficacy of several pharmacologic agents, . . .
Abstract 4040: Silence of miR-203 by promoter methylation in endometrial cancer
Authors: Yi-Wen Huang, Janet S. Rader, Gary D. Stoner, Paul J. Goodfellow, Tim H-M. Huang
Journal: Cancer Research (2012)

Abstract MicroRNAs (miRNAs), a class of small non-coding RNAs, play important roles in cancer development by perturbing the expression of target genes. DNA methylation, a well-studied epigenetic event, also influences gene expression and aberrant methylation is frequently observed in cancer. We previously reported a new paradigm in which hypermethylation-mediated silencing of a miRNA de-repressed its oncogenic target in cancer cells. SOX4, an oncogene, was found to be overexpressed in endometrial cancer, partly because of hypermethylation of miR-129-2. Herein, thirteen additional miRNAs targeting on the 3′-end of untranslated regions of SOX4, and encompassing CpG islands, were identified using computational analysis. Hypermethylation of eight of the thirteen miRNAs was detected in at least two of seven endometrial cancer cell lines. miR-203 was selected for further analysis because this locus was predominantly hypermethylated in endometrial cancer cell lines, but not in normal endometrium. miR-203 expression can be reactivated by pharmacologic induction of DNA demethylation and histone acetylation, indicating that the loss of miR-203 expression is associated with promoter hypermethylation in endometrial cancer. Restoration of miR-203 by cell transfection decreased SOX4 expression and reduced proliferation of endometrial cancer cells. To confirm these in vitro findings in primary endometrial tumors, specimens from two cohorts were analyzed for miR-203 methylation by quantitative pyrosequencing or MassARRAY. In one cohort, miR-203 was significantly hypermethylated in endometrial tumors (n=31), but not in adjacent or un-related normal (n=18) specimens. Methylation of this locus is related to lymphatic and vascular invasion. In the other cohort, increased methylation was observed in primary tumors (n=114), but not in normal controls (n=22). Hypermethylation of miR-203 was positively associated with MLH1 methylation and MSI status. In conclusion, we present an emerging phenomenon that epigenetic silencing of multiple miRNAs could lead to overexpression of a single oncogene in endometrial cancer. This work is supported, in part, by NIH grants U54 CA113001 (THH) and P50 CA134254 (PJG, THH). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4040. doi:1538-7445.AM2012-4040