tbuckley/cabot-search huggingface dataset:
Infection Due to<i>Actinobacillus actinomycetemcomitans</i>and<i>Haemophilus aphrophilus</i>
Authors: Malcolm I. Page, Elizabeth O. King
Journal: New England Journal of Medicine (1966)

OVER a period of ten years the laboratory responsible for the identification of miscellaneous types of bacteria at the Communicable Disease Center received 63 strains of Actinobacillus actinomycetemcomitans and 83 strains of Haemophilus aphrophilus. The cultural and serologic studies of 67 of these strains have been the subject of a previous report.1 These organisms are seldom encountered and infrequently identified even when isolated. Although seemingly unrelated by generic designation, they are in fact closely related and frequently confused. It is unlikely that any physician would be able to collect a comparable number of cases of either infection to report. For . . .
Abstract 4963: An integrated approach for functional analysis of 11q13 amplification target genes in HNSCC
Authors: Tatiana Lepikhova, Henna Pehkonen, Riku Louhimo, Ping Chen, Nina Peitsaro, Anni Nieminen, Misa Imai, Juha Klefstrom, Sampsa Hautaniemi, Outi M. Monni
Journal: Cancer Research (2011)

Abstract Gene amplification is one of the most common mechanisms for oncogenic activation in human cancer. Some genomic regions are more frequently amplified than others. For example, amplification of 11q13 occurs at high frequencies in several human cancers, such as lung, bladder, breast and ovarian carcinomas, as well as head and neck squamous cell carcinoma (HNSCC). Approximately 40% of HNSCC are affected by this specific amplification, which is associated with the presence of lymph node metastasis and poor prognosis. Distinct core regions of amplified areas within the 11q13 locus have been identified, and these can be amplified independently or concurrently in various combinations. A number of oncogenes or potential cancer-related genes have been mapped to the 11q13 chromosomal region, however it is still not known whether these genes, that undergo co-amplification and over-expression, cooperate in promoting tumorigenesis. We have used a complementary approach to comprehensively characterize the functional basis for selection and maintenance of 11q13 amplification in HNSCC. To facilitate this approach, each of the 15 HNSCC cell lines used in this study has undergone molecular characterization for genomic and transcriptomic alterations. We performed a loss-of-function screen on 11q13 positive HNSCC cell lines to identify the genes essential for growth and survival. Next we applied gain-of-function analysis using ORFs for CTTN, FADD, PPFIA1, ORAOV1, CCND1 on 11q13 negative HNSCC cell lines. A single or multiple genes mapping to the amplicon were stably co-overexpressed in different combinations and related phenotypes were analysed in several in vitro and in vivo assays for growth, invasion and sensitivity/resistance to drugs. In addition, changes associated with overexpression of those genes were analysed by exon arrays in order to identify deregulated signaling pathways associated with 11q13 amplification. Our preliminary data suggests that this integrated approach is an efficient method at identifying genes that co-operate due to their location in the same amplicon. Such information is particularly valuable for elucidating oncogenic drivers and addressing the relevance of 11q13 amplification to drug sensitivity/resistance in 11q13 positive HNSCC. 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 4963. doi:10.1158/1538-7445.AM2011-4963
REDUCTION IN LIPOPROTEIN (A) WITH EVOLOCUMAB: ELUCIDATION OF THE ROLE OF THE LDL RECEPTOR FROM CLINICAL TRIALS AND IN-VITRO MODELS
Authors: Frederick J. Raal, Robert P. Giugliano, Marc Sabatine, Michael Koren, Dirk Blom, Nabil G. Seidah, Narimon Honarpour, Armando Lira Pineda, Allen Xue, Simon Jackson, Mei Di, Matthew Peach, Ransi Somaratne, Scott Wasserman, Robert Scott, Evan Stein
Journal: Journal of the American College of Cardiology (2016)
Abstract 4145: Increased anti-tumor effect of sorafenib by depleting tumor associated macrophages
Authors: Sun Hui-Chuan, Wei Zhang, Xiao-Dong Zhu, Zhao-You Tang
Journal: Cancer Research (2010)

Abstract Background: Sorafenib prolonged survival in patients with unresectable hepatocellular carcinoma (HCC), but the effect is modest and tumor finally progressed even under continuous sorafenib therapy. The aim of this study is to investigate the mechanism of tumor progression under sorafenib treatment. Methods: Tumor growth, local invasion and lung metastasis were observed in MHCCLM3-R, a human HCC xenograft nude mouse model, when treated by sorafenib (30 mg/kg qd, n=6 per group) and vehicle as control. Macrophage infiltration was measured in the peripheral blood and macrophage in tumor after sorafenib treatment by immunohistochemistry and flow cytometry with F4/80 antibody, and the effect of macrophage depletion on tumor angiogenesis and metastasis after sorafenib treatment, using two drugs target macrophages, zoledronic acid (ZA) and clodrolip, in a mouse model of human hepatocellular carcinoma (HCC). Results: Sorafenib treatment significantly inhibited tumor growth and lung metastasis, but also induced significant increase in peripheral F4/80-positive cells and intratumoral macrophages infiltration, which was associated with elevation of colony stimulating factor-1, stromal-derived factor 1α and vascular endothelial growth factor in tumor and plasma VEGF of mouse origin in peripheral blood, suggesting the role of macrophage in tumor progression during sorafenib treatment. Depletion of macrophage by clodrolip or ZA in combination with sorafenib significantly inhibited tumor progression, tumor angiogenesis and lung metastasis compared to that of mice treated with sorafenib alone. ZA was more effective than clodrolip. Conclusions: Macrophage may have an important role in tumor progression under sorafenib treatment. Zoledronic acid is promising when combined with sorafenib to enhance its anti-tumor effect. 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 4145.
THE INCIDENCE AND RISK FACTORS OF LATE CATCH UP PHENOMENON AFTER SECOND GENERATION DES DEPLOYMENT
Authors: Takahiro Tokuda, Toshiya Muramatsu, Reiko Tsukahara, Yoshiaki Ito, Hiroshi Ishimori, Keisuke Hirano, Masatsugu Nakano, Masahiro Yamawaki, Motoharu Araki, Norihiro Kobayashi, Hideyuki Takimura, Yasunari Sakamoto, Masakazu Tsutsumi, Takuro Takama, Hiroya Takafuji
Journal: Journal of the American College of Cardiology (2015)
Impact of Dual-Time-Point F-18 FDG PET/CT in the Assessment of Pleural Effusion in Patients With Non-Small-Cell Lung Cancer
Authors: Khaled Alkhawaldeh, Hans-J Biersack, Anna Henke, Samer Ezziddin
Journal: Clinical Nuclear Medicine (2011)

The aim of this study was to assess the utility of dual-time-point F-18 fluorodeoxyglucose positron emission tomography (F-18 FDG PET) in differentiating benign from malignant pleural disease, in patients with non-small-cell lung cancer.A total of 61 patients with non-small-cell lung cancer and pleural effusion were included in this retrospective study. All patients had whole-body FDG PET/CT imaging at 60 ± 10 minutes post-FDG injection, whereas 31 patients had second-time delayed imaging repeated at 90 ± 10 minutes for the chest. Maximum standardized uptake values (SUV(max)) and the average percent change in SUV(max) (%SUV) between time point 1 and time point 2 were calculated. Malignancy was defined using the following criteria: (1) visual assessment using 3-points grading scale; (2) SUV(max) ≥2.4; (3) %SUV ≥ +9; and (4) SUV(max) ≥2.4 and/or %SUV ≥ +9. Analysis of variance test and receiver operating characteristic analysis were used in statistical analysis. P < 0.05 was considered significant.Follow-up revealed 29 patient with malignant pleural disease and 31 patients with benign pleural effusion. The average SUV(max) in malignant effusions was 6.5 ± 4 versus 2.2 ± 0.9 in benign effusions (P < 0.0001). The average %SUV in malignant effusions was +13 ± 10 versus -8 ± 11 in benign effusions (P < 0.0004). Sensitivity, specificity, and accuracy for the 5 criteria were as follows: (1) 86%, 72%, and 79%; (2) 93%, 72%, and 82%; (3) 67%, 94%, and 81%; (4) 100%, 94%, and 97%.Dual-time-point F-18 FDG PET can improve the diagnostic accuracy in differentiating benign from malignant pleural disease, with high sensitivity and good specificity.
Fluorine-18 Fluorodeoxyglucose Splenic Uptake From Extramedullary Hematopoiesis After Granulocyte Colony-stimulating Factor Stimulation
Authors: HUSSEIN M. ABDEL-DAYEM, GERALD ROSEN, HOSSAM EL-ZEFTAWY, SLEIMAN NADDAF, MITHILESH KUMAR, SAADET ATAY, ADRIENNE CACAVIO
Journal: Clinical Nuclear Medicine (1999)

Two patients with sarcoma, one with recurrent osteosarcoma of the spine and the other with metastatic synovial cell sarcoma, were treated with high-dose chemotherapy that produced severe leukopenia. The patients received granulocyte colony-stimulating factor (G-CSF) to stimulate the bone marrow (480 mg given subcutaneously twice daily for 5 to 7 days); their responses were seen as a marked increase in peripheral leukocyte count with no change in the erythrocyte or platelet counts. The patients had fluorine-18 fluorodeoxyglucose (F-18 FDG) imaging 24 hours after the end of G-CSF treatment. Diffusely increased uptake of F-18 FDG was seen in the bone marrow in both patients. In addition, markedly increased uptake in the spleen was noted in both, indicating that the spleen was the site of extramedullary hematopoiesis. The patients had no evidence of splenic metastases. The first patient had a history of irradiation to the dorsal spine, which was less responsive to G-CSF administration than was the nonirradiated lumbar spine.
Abstract 5502: Vintafolide: a first-in-class small molecule drug conjugate targeting folate receptor positive tumors.
Authors: Christopher P. Leamon, Joseph A. Reddy, Brian B. Haines, Isabelle Dussault
Journal: Cancer Research (2013)

Abstract Targeted anti-cancer therapies offer the promise of more efficacious treatments with fewer side effects. Vintafolide (also known as EC145) is a rationally designed small molecule drug conjugate consisting of one folic acid moiety which serves as a stable high affinity binding ligand for the folate receptor, and one vinca alkaloid unit (desacetylvinblastine hydrazide; DAVLBH), which serves as the cytotoxic warhead. Vintafolide is thus designed to target cancer cells by binding with high affinity to folate receptors which are more commonly expressed at high levels on tumors compared to normal tissues. Vintafolide is internalized following binding to folate receptors and is cleaved in endosomes to release DAVLBH. Like all vinca alkaloids, DAVLBH binds to tubulin and disrupts the mitotic spindle which leads to cell death. Pre-clinical in vitro and in vivo experiments show that vintafolide requires interaction with the folate receptor for its activity and that it is more efficacious and better tolerated than untargeted DAVLBH. Vintafolide is currently being investigated in clinical trials in ovarian (Phase III) and lung (Phase II) cancer patients who express folate receptors on their tumors as determined by the investigational companion imaging agent, etarfolatide. Etarfolatide is also a folate-based conjugate consisting of folic acid linked to a peptidic metal-chelating moiety labeled with 99mTechnetium. In a randomized Phase II study in patients with advanced ovarian cancer, patients treated with vintafolide had a significantly longer period of progression free survival compared with the control. This was driven by patients who were identified by etarfolatide as having tumors with functional folate receptors. Vintafolide and etarfolatide is the first pair of therapeutic and non-invasive, imaging diagnostic to be co-developed for the treatment of cancer. Citation Format: Christopher P. Leamon, Joseph A. Reddy, Brian B. Haines, Isabelle Dussault. Vintafolide: a first-in-class small molecule drug conjugate targeting folate receptor positive tumors. [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 5502. doi:10.1158/1538-7445.AM2013-5502
ESTUDIO PROSPECTIVO COMPARATIVO DOBLE CIEGO DEL PAPEL DE LA ECOENDOSCOPIA vs. COLANGIO-RNM CON SECRETINA EN EL ESTUDIO ETIOLÓGICO DE LA PANCREATITIS AGUDA IDIOPÁTICA
Authors: JJ Vila, S Goñi, M Gómez, M Basterra, M Garaigorta, E Rubio, J Urman, F Bolado, I Fernández-Urién, FJ Jiménez
Journal: Endoscopy (2011)

Introducción: El rendimiento diagnóstico de USE y Colangio-RNM con secretina (CRNM-s) en pacientes con pancreatitis aguda idiopática (PAI) no ha sido comparado.
781 A CLINICAL TRIAL ON ANTI-HBV-DC VACCINE COMBINED WITH LAMIVUDINE AND THYMOSIN-a1 IN THE HBeAg POSITIVE PATIENTS OF CHRONIC HEPATITIS B VIRUS INFECTION
Authors: B.-F. Wu, J.-Y. Yang, Y.-L. Zhang, Y. Liu, H.-H. Zhou, X.-Q. Wang, F.-Q. Li, C.-Q. Hou, X.-S. Li, X.-H. Huang, Z.-S. Xiao, M. Yang, F.-X. Lin, Y.-P. Fu, S. Zheng, W. Chen, Y. Zhou, J. Yang, X.-H. Wan, H. Huang
Journal: Journal of Hepatology (2013)
Tc-99m Sestamibi Bone Marrow Scintigraphy in Gaucher Disease
Authors: Dvora Aharoni, Yodphat Krausz, Deborah Elstein, Irith Hadas-Halpern, Ari Zimran
Journal: Clinical Nuclear Medicine (2002)

Purpose No imaging technique has been found to be adequate to assess the severity and extent of bone involvement in patients with Gaucher disease. Marrow involvement, as determined by Tc-99m sulfur colloid, correlated well with the clinical and radiologic changes of the skeleton, but a normal pattern was found in the early stages of the disease. Subsequently, Tc-99m sestamibi (MIBI) has been suggested for direct visualization of glycolipid deposits in the bone marrow. This study was initiated as a pilot using MIBI to detect various forms of bone disease in patients with Gaucher disease of varying severity. Materials and Methods Eleven patients (9 men; median age, 39.9; age range, 21 to 61 years) were evaluated. The clinical severity of disease was scored at presentation, and four patients with moderate to severe disease were treated with enzyme replacement therapy. Each patient underwent a radiographic skeletal survey, bone densitometry, and MIBI scintigraphy. The scan included static images of the lower limbs, with a whole-body scan acquired between the early and late acquisition. Tracer uptake in the bone marrow was graded and correlated with clinical and objective variables. Results All but one patient had increased MIBI uptake in the bone marrow. No correlation was noted between MIBI uptake and severity score, radiographic changes, densitometry z score, or treatment status. Conclusions MIBI scanning is a sensitive technique for detecting bone marrow deposits in Gaucher disease, but it is inadequate for early identification of patients at high risk for skeletal complications or for the follow-up of patients treated with enzyme replacement.
Role and epigenetic regulation of p16Ink4a-MMP-1 axis in OA-associated senescence-like phenotype and hypertrophy of chondrocytes
Authors: D Philipot, D Guerit, E Olivotto, D Platano, P Chuchana, J Piette, C Jorgensen, R M Borzi, D Noel, J-M Brondello
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Backgroundand objectives</h3> Osteoarthritic (OA) chondrocyte is characterised by altogether DNA damage accumulation, eroded telomeres, expression of senescence marker such as p16<sup>Ink4a</sup> and establishment of one specific secretome including IL-1b, IL-8 and MMP-1/-3/-13. Recent data have proposed that tissue specific accumulation of p16<sup>Ink4a</sup>-positive cells would be deleterious for the tissue function and could be the consequence of the inherent age-associated disorders. Here the authors evaluate the role of p16<sup>Ink4a</sup>-dependent pathway and its epigenetic regulation by microRNAs in osteoarthritis-associated phenotypes. <h3>Materials and methods</h3> The authors performed a genome wide miRNA-array analysis in order to identify microRNAs regulating senescence-associated phenotypes found in OA. The authors used primary OA chondrocytes in 3D culture, IL-1β treatment and gain or loss of function experiments to validate their regulatory effects on senescence-associated targets. chondrogenic differentiation was induced by culture of mesenchymal stromal cells in micropellets in inductive medium for 21 days. Expression of chondrocyte markers was performed by RT-qPCR. <h3>Results</h3> By miR-array analysis, the authors identified the downregulation of miR-24, one epigenetic known regulator of p16<sup>Ink4a</sup>. miR-24 expression is repressed upon IL-1 β treatment while p16<sup>Ink4a</sup> protein accumulates. Based on gain or loss of functions approaches, our results suggest that miR-24 downregulation or p16<sup>Ink4A</sup> overexpression, are sufficient to trigger chondrocyte premature ageing characterised by activation of p16<sup>Ink4a</sup>-MMP-1 axis as shown by RT-qPCR and ELISA. This reverse correlation is also observed during hypertrophic stage induced by an in vitro chondrogenic differentiation of mesenchymal stromal cells. <h3>Conclusions</h3> Altogether, our preliminary data show that, in Il-1 β -treated chondrocytes, miR-24 expression is downregulated leading to p16<sup>ink4A</sup> accumulation. In turn, p16<sup>Ink4a</sup> controls the expression of MMP-1 probably via the transcriptional induction of the transcription factor, ZNF-410. Future experiments are required to validate this last hypothesis and would open new perspectives for putative pharmacological targets to delay OA or other p16<sup>ink4a</sup>-dependent diseases.
Abstract A45: The tumor suppressor role of ARID1A in gynecologic cancer
Authors: Bin Guan, Tian-Li Wang, le-Ming Shih
Journal: Cancer Research (2011)

Abstract ARID1A (BAF250A), a gene participating in the formation of a BRG1 SWI/SNF chromatin remodeling complex, has emerged as a potential tumor suppressor because of its frequent inactivating mutations in gynecological cancer (approximately 50% of ovarian clear cell and 30% of ovarian endometrioid carcinomas). The mutation is associated with loss of protein expression as assessed by immunohistochemistry. In this study, we analyzed ARID1A expression in a wide variety of carcinomas to determine the prevalence of ARID1A inactivation in carcinomas using immunohistochemical staining. Immunoreactivity was not detected in 36 (3.6%) of 995 tumors. Uterine low-grade endometrioid carcinomas showed a relatively high-frequency loss of ARID1A expression, as 15 (26%) of 58 cases were negative. Mutational analysis showed 10 (40%) of 25 uterine endometrioid carcinomas; none of 12 uterine serous carcinomas and none of 56 ovarian serous and mucinous carcinomas harbored somatic ARID1A mutations. These findings suggest that the molecular pathogenesis of low-grade uterine endometrioid carcinoma is similar to that of ovarian low-grade endometrioid and clear cell carcinoma, tumors that have previously been shown to have a high-frequency loss of expression and mutation of ARID1A. We further studied the functions of ARID1A and found that restoration of wild-type ARID1A expression in ovarian cancer cells harboring ARID1A mutations suppressed cellular proliferation and tumor growth in mice. Gene silencing of ARID1A in non-transformed epithelial cells enhanced cellular proliferation and tumorigenecity. Mutations in ARID1A and TP53 were mutually exclusive in tumor specimens, and knockdown of ARID1A affected multiple p53-regulated genes and pathways, including CDKN1A and SMAD3. The ARID1A/BRG1 complex bound to the promoters and enhanced transcriptional activity of CDKN1A and SMAD3 in a p53-dependent manner. We further showed that p21 mediated, at least in part, the tumor suppressive functions of ARID1A. These results provide new evidences that ARID1A functions as tissue-type-restricted tumor suppressor by directly modulating transcriptional activity of several p53-regulated genes. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the Second AACR International Conference on Frontiers in Basic Cancer Research; 2011 Sep 14-18; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2011;71(18 Suppl):Abstract nr A45.
Chemotherapeutic Evaluation Using Clinical Criteria in Spontaneous, Autochthonous Murine Breast Tumors1
Authors: R. L. Stolfi, L. M. Stolfi, R. C. Sawyer, D. S. Martin
Journal: JNCI Journal of the National Cancer Institute (1988)

Six drugs, three of which are considered to be active against human breast cancer [melphalan (PAM), cyclophosphamide (CTX), and 5-fluorouracil (FUra)] and three of which have failed to demonstrate activity against human breast cancer [N-phosphonacetyl-L-aspartate (PALA), cytarabine (ara-C), and 6-thioguanine (TG)], were tested at optimal weekly doses in (BALB/-cfC3H × DBA/8)F1 (CD8F1) mice bearing spontaneous, autochthonous breast tumors averaging 300 mg. When treatment was evaluated by laboratory criteria (i.e., tumor growth inhibition in comparison to vehicle-treated, size-matched controls), all six of the drugs tested were judged to be active. However, when the criteria for positive drug activity consisted of the attainment of tumor regressions of ≧50% in ≧20% of the treated individuals (i.e., analogous to clinical criteria), only the three drugs that are known to be active against human breast cancer (PAM, CTX, and FUra) were judged active against the spontaneous murine breast tumors. PALA, ara-C, and TG failed to demonstrate regressing activity against the spontaneous murine breast tumors. With a cavea concerning the limited spectrum of drugs evaluated in this study, it can be concluded that the CD8F1 breast tumor model demonstrated 100% correlation with human breast cancer in terms of both positive and negative drug sensitivity when the criteria for evaluation were parallel. [J Natl Cancer Inst 1988;80:52–55]