tbuckley/cabot-search huggingface dataset:
Stat Bite: Uterine Cancer Incidence and Mortality, C. Kosary
Authors: C. Kosary
Journal: JNCI Journal of the National Cancer Institute (1994)

Journal Article Stat Bite: Uterine Cancer Incidence and Mortality, C. Kosary Get access Carol Kosary Carol Kosary Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 86, Issue 17, 7 September 1994, Page 1271, https://doi.org/10.1093/jnci/86.17.1271 Published: 07 September 1994
A retrospective study of D-index in acute myeloid leukemia patients undergoing induction chemotherapy
Authors: Yuhei Shibata, Takuro Matsumoto, Nobuhiko Nakamura, Junichi Kitagawa, Akemi Morikawa, Nobuhiro Kanemura, Takeshi Hara, Hisashi Tsurumi
Journal: Annals of Oncology (2015)
Abstract 704: Upregulation of the human equilibrative nucleoside transporter 1 (hENT1) expression by indole-3-carbinol (I3C) in pancreatic cancer cell lines
Authors: Honggang Wang, Beverly Word, Berverly Lyn-Cook
Journal: Cancer Research (2011)

Abstract Pancreatic adenocarcinoma is the fourth most common cause of death in cancer in the Western world. In the past years, gemcitabine (GEM) has become the standard chemotherapeutic agent for patients with pancreatic cancer. However, a substantial number of patients fail to respond to therapy due to inherent or developed GEM chemoresistance. GEM is transported into cells mainly by the human equilibrative nucleoside transporter 1 (hENT1). Overexpression of hENT1 mRNA and protein in pancreatic carcinoma is known to correlate with better outcomes. In recent years, indole-3-carbinol (I3C), a dietary compound in cruciferous vegetables, has been shown to alter cancer cell survival by inducing apoptosis in vivo. I3C has also been shown to reverse multiple drug resistance by inhibiting efflux transporter, P-glycoprotein (P-gp) expression. In this study, the potential of I3C to modulate hENT1 expression and activity was evaluated in a panel of human pancreatic cancer cell lines, AsPC-1, BxPC-3, MiaPaca2, PANC-1 and PL-45. Our data showed that I3C at 50 and 100 uM significantly increased hENT1 mRNA and protein expression in BxPC-3 cell, MiaPaca2 cells and PANC-1 cells compared with the vehicle controls. In contrast, no such effect was observed in AsPC-1 and PL-45 cells with same treatment. The potential synergistic cytotoxic effect of I3C and GEM was also examined in all five pancreatic cancer cell lines. Pancreatic cancer cells were incubated with or without I3C at 50 uM for 24 h and then treated with GEM at different concentrations with or without I3C at 50 uM and a specific hENT1 inhibitor, NBMPR, at 50nM for 48 hours. MTS assay was used for cell viability measurement. Our data showed that I3C decreased IC50 by 6.8, 8.1 and 8.4 folds in PANC-1, MiaPaca2 and BxPC-3 cells respectively, and only 2.7 and 2.0 folds in AsPC-1 and PL-45 cells respectively, compared with GEM alone treated cells. Investigation also found that NBMPR, a specific inhibitor of hENT1, only abrogated a part of the augmented effect of I3C in response to GEM in all five pancreatic cell lines. The present study provides evidence that increasing hENT1 expression is a novel mechanism of the antitumor effect of I3C. The combination of GEM and I3C may be an effective strategy to overcome the GEM chemoresistance in pancreatic cancer patients. This affirms our hypothesis that I3C could be an adjuvant therapy improving the response to GEM treatment in patients with pancreatic 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 704. doi:10.1158/1538-7445.AM2011-704
Tracheotomy in Children
Authors: Peter Oliver, John R. Richardson, Robert W. Clubb, Carlyle G. Flake
Journal: New England Journal of Medicine (1962)

TRACHEOTOMY is performed at every age of life. The indications for tracheotomy vary considerably in childhood from those in adult life. In a small child the operation requires a more meticulous surgical technic than the same procedure in a fully developed adult. Mortality, postoperative complications and the ease of decannulation differ substantially in children and in mature persons. Recent reviews1 2 3 4 of the procedure have included patients of all ages in describing the indications, technics, complications and results of tracheotomy. The purpose of this study is to review and analyze the problems of tracheotomy peculiar to childhood. The ages of the . . .
Conversion by new treatment modalities of nonresectable to resectable hepatocellular cancer.
Authors: J V Sitzmann, S E Order, J L Klein, P K Leichner, E K Fishman, G W Smith
Journal: Journal of Clinical Oncology (1987)

Eleven patients with hepatocellular cancer had nonresectable lesions, ten as determined by laparotomy and one by computed tomographic (CT) evidence of inferior vena caval invasion. These patients were treated with a variety of new modalities, particularly radiolabeled antiferritin antibodies. Following treatment, seven of the 11 patients were considered to have converted their lesions to possible resectability. Six patients had complete resections, and one patient was partially resected. All patients had the common features of either nodular massive or nodular multifocal hepatocellular cancer. Relative to the patient's initial status, the quality of life remains high, and a new approach in the treatment of the nodular form of nonresectable hepatoma has been demonstrated. The present rate of such conversion to resectability is unknown. However, with further advances in radiolabeled antibody therapy, these results offer a new opportunity in the management of hepatocellular cancer.
Abstract 917: mTOR kinase inhibition relieves feedback inhibition of RTK and PI3K signaling in breast cancer cells
Authors: Vanessa S. Rodrik-Outmezguine, Sarat Chandarlapaty, Nen Cao, Paul Smith, Sylvie Guichard, Neal Rosen
Journal: Cancer Research (2011)

Abstract Activation of mitogenic signaling by receptor tyrosine kinases is regulated by negative feedback. Feedback is in part mediated by mTORC1/S6K dependent downregulation of IRS proteins which downregulate IGF/insulin receptor signaling. Rapamycin, an mTORC1 inhibitor, relieves this feedback and causes induction of phosphorylation of AKT at Serine 473 via IGF activation of mTORC2 leading to the activation of AKT kinase and signaling. This relief of feedback inhibition of mTORC2/AKT signaling may attenuate or abolish the antitumor activity of rapamycin. mTOR kinase inhibitors that inhibit both mTORC1 and mTORC2 complexes have now been developed to circumvent these problems. We now find that AZD8055 is a potent and selective inhibitor of both mTORC1 and mTORC2 and thus abolishes AKT phosphorylation at Ser473 as well as 4EBP1 and S6K phosphorylation, in contrast to rapamycin which effectively inhibits only the last and which activates the first. This drug potently inhibited the proliferation of tumor cells, especially those in which PI3K/AKT signaling is dysregulated and sometimes induced their death. However, AZD8055 does potently reactivate receptor tyrosine kinase signaling. It enhanced receptor tyrosine kinase phosphorylation and expression and caused a profound, HER-kinase dependent activation of ERK and PI3K signaling. It reactivated phosphorylation of AKT Thr308 and AKT substrates, but not that of Ser473 AKT. These data suggest that inhibition of the phosphorylation of AKT at Serine 473 is not sufficient to inhibit AKT signaling. Furthermore, relief of feedback inhibition of RTK function by mTOR kinase inhibitors leads to reactivation of both ERK and AKT signaling. 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 917. doi:10.1158/1538-7445.AM2011-917
Early Enhancing Lesion Seen on Computed Tomography Consistent with Focal Nodular Hyperplasia
Authors: CHRISTOPHER A. SWINGLE, WILLIAM A. FAJMAN, NAOMI ALAZRAKI
Journal: Clinical Nuclear Medicine (2003)

SWINGLE, CHRISTOPHER A. D.O.; FAJMAN, WILLIAM A. M.D.; ALAZRAKI, NAOMI M.D. Author Information
AB0489 Pulse Cyclophosphamide Therapy of Lupus-Nephritis and Its Course through the Maintenance Therapy
Authors: J. Lukac, O. Lukacova, A. Canicova, A. Tuchynova, J. Rovensky, E. Zanova
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Lupus-nephritis (LN) is a serious organ involvement and important factor of morbidity and mortality in patients (pts) with systemic lupus erythematosus. As initial treatment of LN, high doses of glucocorticoids (GK), pulses of cyclophosphamide (PT CY) or mycophenolate mofetil (MMF) is recommended. Initial treatment is followed by subsequent (maintenance) therapy. There are few information about course and relapses of LN through the maintenance therapy. <h3>Methods</h3> In retrospective study, 36 pts with SLE and LN were hospitalized in National Institute of Rheumatic Diseases Piestany from 1996 – 2013 years. Effectiveness of initial treatment of PT CY on LN activity, course of LN and occurrence of relapses through maintenance therapy was evaluated. <h3>Results</h3> Total 36 patients (pts) with SLE and LN were treated with PT CY 0,5-1 g/m<sup>2</sup> monthly for 6 month. There were 31 female and 5 male pts with with a mean age 38.7 yrs on the onset of SLE, with disease duration 9.62 yrs (2 to 25 yrs). Anti-dsDNA antibodies were positive in 25 pts at the onset of the therapy and in 12 pts persisted after PT CY. Hypocomplementemia before therapy was recorded in 34 of 36 pts. Renal failure with creatinine elevation at the beginning of the PT CY was in 6 of 36 pts. Overall SLE activity was evaluated by SELENA SLEDAI. After initial treatment of PT CY, complete renal response was reached in 34 pts, partial in 2 pts. Low complement was normalized in 64.7%. After that, four types of maintenance therapy was introduced: 12 pts PT CY 0,5-1 g/m<sup>2</sup> each three months, 8 pts azathioprine from 50 to 100 mg a day, 6 pts MMF 2 g per day, 10 pts cyclosporine A 100 to 150 mg a day. Combination with belimumab had 1 pts and with hydroxychloroquine 10 pts. The dosage of GK through the maintenance therapy was from 10 – 25 mg of prednisone. In 16 pts suppression persist through the following up, in 20 pts relapse of LN appeared. Time to relapse after PT CY was 43 months in average (5 - 116 months). At AZA therapy, there were 11 relapses, 3 at MMF, 2 at cyclosporine A, 4 at GK maintenance therapy. In group of pts with LN relaps, 13 pts had anti-dsDNA autoantibodies. In another 5 pts were anti-dsDNA antibodies negative in time of LN reactivation. After LN relapse, PT CY was repeatedly introduced – again with complete or partial renal response. <h3>Conclusions</h3> Pulse CY therapy is effective almost in all pts with SLE and LN. Relapses in the phase of maintenance therapy occurred in more than 50% of pts. Relapses of LN can appear even in pts without anti-dsDNA antibodies. Tight control of SLE activity is necessary in all pts. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3905
Dimeric Inhibin A as a Marker for Down's Syndrome in Early Pregnancy
Authors: David A. Aitken, Euan M. Wallace, Jennifer A. Crossley, Ian A. Swanston, Yvonne van Pareren, Merel van Maarle, Nigel P. Groome, James N. Macri, J. Michael Connor
Journal: New England Journal of Medicine (1996)

In screening for Down's syndrome in the second trimester of pregnancy, the concentrations of alpha-fetoprotein, the β subunit of human chorionic gonadotropin, and intact human chorionic gonadotropin in maternal serum are widely used markers. We investigated a new marker, dimeric inhibin A, and compared its predictive value with that of the established markers.
S42 Effect of iron deficiency on oxygen transport in hypoxaemic patients: implications for haemodynamics and clinical management
Authors: V Santhirapala, LC Williams, HC Tighe, JE Jackson, CL Shovlin
Journal: Thorax (2013)

<h3>Background</h3> Oxygen transport in the blood depends not only upon oxygen partial pressure (or saturation, SaO<sub>2</sub>), but also the concentration of haemoglobin to which oxygen binds, and blood volume in any given period. In current clinical studies and guidelines, it is rare for these components to be discussed together. <h3>Methods</h3> An observational cohort study was performed in 165 consecutive unselected patients with pulmonary arteriovenous malformations, including 98 before and after embolisation. 159 (96%) had hereditary haemorrhagic telangiectasia (HHT). Prior to statistical analyses, patients were stratified by self-reported exercise tolerance, and serum iron/ferritin. <h3>Results</h3> Patients were aged 17–87 (median 49)ys, with median SaO<sub>2</sub> 95% (range 78·5–99%) Many had biochemical/haematinic evidence of iron deficiency, predominantly attributable to HHT-blood loss, but several had undergone venesection for secondary polycythaemia, as recommended in current UK haematological guidelines. Haemoglobin ranged from 7.7–20.9g/dl (median 14.1g/dl), and was higher in patients with lower SaO<sub>2</sub>: For every 1% fall in SaO<sub>2</sub>, haemoglobin rose on average, by 0·82g/dl (p &lt; 0·0001). SaO<sub>2</sub> explained only 0·1% of the variance in oxygen carriage per unit blood volume. Embolisation treatment increased SaO<sub>2</sub> (median + 2·5%), but usual subsequent haemoglobin falls restored oxygen carriage/unit volume. Concurrent iron deficiency reduced erythrocyte haemoglobin content. Secondary erythrocytosis was achievable with low ferritin, but only if serum iron was high-normal. Oxygen carriage was lower if iron deficiency was present (median 16·1 [IQR 14·7, 18·1]mls/dL compared to 19·0 [IQR 17·4, 20·2]mls/dL, p &lt; 0·0001), implying ~15% higher cardiac outputs were required to maintain oxygen delivery. At rest, this was not met by a higher pulse in the iron deficiency group, indicating stroke volume would need be higher. Self reported exercise tolerance was used as a crude indicator of whether compensating for reduced oxygen carriage was achievable in this patient group. There was a very clear inverse correlation between exercise grade and oxygen carriage such that exercise tolerance was worse in patients with lower oxygen carriage (coefficient -0.0012 (95% CI -0.0017, -0.00061) p &lt; 0.0001). The trend was evident across all grades of exercise tolerance. <h3>Conclusions</h3> Low oxygen carriage per unit volume, and not low PaO<sub>2</sub>/SaO<sub>2 </sub><i>per se</i>, are predictors of impaired exercise tolerance in PAVM patients.
The Incidence of Multiple Primary Cancers. I. Development of Further Cancers in Patients With Lymphomas, Leukemias, and Myeloma
Authors: John W. Berg
Journal: JNCI Journal of the National Cancer Institute (1967)

This prospective study of 1,561 patients with leukemia, 1,871 with lymphosarcomas, 1,028 with Hodgkin's disease, and 207 with myeloma revealed the following: In all, 95 further cancers were found during the 9,840 patient-years of observation when only 45.4 were expected from New York State incidence rates for a population of this sex and age distribution. Prostate, bladder, endometrial, and breast cancers were somewhat more frequent than expected. The four patients with Kaposi's sarcoma only confirm the association of this tumor with the index diseases. The greatest increase was in skin cancers: 6 were expected, whereas 43 patients developed over 60 asynchronous carcinomas. This increase is significant, even allowing for a likely 2½-fold underregistration in the control tabulation. The minimum increases were 9-fold after myeloid leukemia, 4-fold after lymphatic leukemia, 2½-fold after lymphosarcoma, and 2-fold after Hodgkin's disease. Squamous carcinomas, basal cell carcinomas, and melanomas all had the same degree of increase. No single common cause for this increase was found, though a number of patients reported specific exposures to carcinogenic situations.
O05 * FOXG1 IS A CANDIDATE TRANSCRIPTIONAL MASTER REGULATOR IN NEURAL STEM CELLS AND GLIOBLASTOMA
Authors: H. Bulstrode, S. Pollard
Journal: Neuro-Oncology (2014)

INTRODUCTION: FOXG1 is a forebrain-specific forkhead box transcription factor, whose high level expression is necessary for telencephalic development in the embryo. Glioblastoma-derived cell cultures also consistently express high levels of FOXG1, and expression in the primary tumour is negatively correlated with patient survival. We and other groups have shown that FOXG1 cooperates with SOX2 to reprogram normal differentiated cells to a neural stem state. METHOD: We have investigated the function of FOXG1 in neural stem cells and their glioblastoma-derived equivalents, and using shRNA knockdown and Crispr/Cas knockout, as well as constitutive and inducible overexpression. We have characterised FOXG1's transcriptional targets using ChIP-Seq and Taqman array assays. We are in the process of exploring FOXG1's reprogramming capabilities in normal and neoplastic brain cell cultures. RESULTS: Functional data supports a role for FOXG1 in establishing and maintaining a neural stem identity, although some established tumour lines show evidence of escape from this regulation. We present a profile of downstream DNA-binding targets, including genes with established roles in self-renewal, lineage selection, cell cycle and chromatin regulation. CONCLUSION: FOXG1 is a candidate master regulator of neural stem cell identity. We believe that its consistent overexpression in GBM cell lines reflects a key role in glioma initiation, and we anticipate that FOXG1's downstream targets will present important novel therapeutic targets.
ECG ABNORMALITIES COMPARED TO EXTENT OF MYOCARDIAL FIBROSIS IN BOYS WITH DUCHENNE MUSCULAR DYSTROPHY
Authors: Kan N. Hor, Sharath Subramanian, Tyler Moran, Kathleen Lao, Bipul Gnyawali, Linda Cripe, Karolina Zareba, Subha Raman
Journal: Journal of the American College of Cardiology (2016)
AB0319 Reactivation of Hepatitis B Virus in Patients with Rheumatoid Arthritis
Authors: H. Iwase, Y. Kanayama, H. Inagaki, A. Murase, M. Saeki, S. Shimizu, T. Saeki, M. Murata
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> The risk of the HBV reactivation in patients who receive immunosuprressive therapy was pointed out these days. The frequency of the patients over 50 years old with resolver hepatitis B virus in our country is 20–25%, and it is difficult in medical economics to carry out preventional medication of nucleic acid analog to all the patients.The guidline against HBV developed by immunosuppression, chemotherapy (2013) was published by the Japan society of hepatology, which said that if anti-HBs or anti-HBc is positive,HBV-DNA and ALT/AST should be observed every one-three mouths, and the dosage of the nucleic acid analog is recommended if HBV-DNA is more than 2.1log copies/mL. HBV-DNA monitoring situation in our department was examined this time. <h3>Methods</h3> In our department, 134 patients are under medical treatment of RA. 38 RA patients were positive either anti-HBs or anti- HBc. We enrolled 22 patients with RA (8 men and 14 women) who had anti-HBs or anti HBc and who had received treatment with anti rheumatic drugs,including biological drugs.The average age was 64 years old. The monitoring span of HBV-DNA quantity and the generating situation of HBV reactivation were examined. <h3>Results</h3> In the first-time inspection, HBV-DNA had not detected in all patients and monitoring was performed in every 4-8 weeks. The average monitoring interval was every 5.2 weeks. The average monitoring period was 10.7 months. Although very-small-quantity of HBV-DNA (&lt;2.1 log copies/mL) was observed twice in one patient medicated with methotrexate (MTX) and mizoribine (MZB) and infliximab (IFX),after entecavir medication started, HBV-DNA was undetected promptly, and re-detectation was not seen and did not show the rise of AST and ALT, either. <h3>Conclusions</h3> We experienced one patient who developed reactivation of HBV-DNA during HBV-DNA monitoring. It was expected that the risk of HBV revitalization was high for this patient,because immunosuppressant and biological medicine were given. But as a result of monitoring of HBV-DNA for every month, HBV-DNA was able to detect in a little stages. RA patients with resolver hepatitis B virus should be monitored based on guideline. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2867
Automated treatment for flight phobia: a 3 1/2 year follow-up
Authors: M S Denholtz, L A Hall, E Mann
Journal: American Journal of Psychiatry (1978)

The authors contacted 43 patients who had been given audiovisual treatment for flight phobia 3 1/2--5 1/2 years previously. Of the 26 subjects who had flown successfully by the end of treatment, 23 had maintained their ability to fly at follow-up. Eighteen said their attitude toward flying was more positive since treatment, and 21 rated their comfort level while flying as "much better" or "better"; however, only 3 said they were "cured." Eleven patients said the treatment had helped to alleviate other fears or anxieties.
Abstract LB-339: MicroRNA modulators regulate oncogenes and tumor suppressors in glioblastoma
Authors: Pavel Sumazin, Xuerui Yang, Wei-Jen Chung, Mukesh Bansal, Andrea Califano
Journal: Cancer Research (2011)

Abstract MicroRNAs, including miR-21, MiR-26a and miR-221/2, are potential key regulators of gene expression in glioblastoma, the most common and the most aggressive type of primary human brain tumor. Their activity is modulated by post-transcriptional factors that regulate mRNA processing pathways and by the abundance of their targets. Despite recent efforts to identify microRNA modulators, this mode of regulation is still poorly understood, and the repertoire and extent that microRNA modulators regulate gene expression in tumors and affect tumorigenesis remain unknown. We developed a genome-wide approach to identify glioblastoma-specific microRNA modulators. We identified hundreds of candidate modulators, including modulators that either activate or suppress miRISC-mediated regulation, and mRNAs that act as decoys and compete for microRNA binding in glioblastoma. Validation experiments were done in SNB19 cell line by measuring differential expression of mature microRNAs and their targets after ectopic expression or inhibition of predicted regulator proteins. 3′ UTR luciferase assays were used to establish the post-transcriptional nature of the regulation. Focusing on two known drivers of gliomagenesis and progression, we showed that PTEN is post-transcriptionally up regulated by WNT7A through miR-21 and down regulated by PALB2 through miR-106a, and that RUNX1 is post-transcriptionally down regulated by WIPF2 through miR-17–5p. Further, we showed that PTEN and RUNX1, which are widely considered functionally unrelated, act as decoys for one another by competing for a common microRNA-regulatory program: they post-transcriptionally regulate one another through their microRNA regulators. In addition, other modulators with prognosis-predictive genetic alterations act through common microRNA-regulatory programs to regulate PTEN and RUNX1 expression. For example, prognosis-predictive genetic alterations at the CTBP2 locus significantly alter both CTBP2 and PTEN expression in glioblastoma; siRNA-mediated silencing of CTBP2 resulted in a 30% reduction in the expression of PTEN 3′ UTR luciferase reporters. Our results demonstrate that microRNA modulators regulate the expression of key glioblastoma drivers, and that genetic alterations at microRNA modulators lead to aberrant post-transcriptional regulation of these drivers. Taken together, these results suggest that microRNA modulation plays a significant role in tumorigenesis and progression of gliobalstoma. 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 LB-339. doi:10.1158/1538-7445.AM2011-LB-339