tbuckley/cabot-search huggingface dataset:
Abstract P3-01-21: Is lymph node ratio (LNR) having additional contribution for predict prognosis on pathologic lymph node staging in node-positive breast cancer patients?
Authors: MA Kaplan, H Odabasi, N Ozdemir, H Harputluoglu, M Aliustaoglu, V Berk, Y Gunaydin, D Uncu, T Elkiran, D Aydin, A Isikdogan
Journal: Cancer Research (2016)

Abstract PURPOSE: The aim of the study was to determine whether LNR have additional contribution on pathologic lymph node staging. METHODS: To examine the prognostic value of LNR examined the original histopathological reports of 2049 node-positive breast cancer patients treated in the references centers of the Turkey. The LNR was defined as the number of positive lymph nodes (LNs) over the total number of LNs removed. The LNR cutoffs were defined as low-risk, 0.01-0.20; intermediate-risk, 0.21- 0.65; and high-risk, LNR &amp;gt;0.65. RESULTS: The median follow-up was 11.8 years. Median Disease free survival (DFS) was 191.8, 110.6 and 78.2 months in patients with pN1, pN2 and pN3 tumor, respectively (p&amp;lt;0.001). Median DFS was 191.9, 106.4 and 78.1 months in patients with LNR low, intermediate and high risk tumor, respectively (p&amp;lt;0.001). Median DFS was not reached and 200.1 months in patients with pN2 and LNR low risk patients, pN1 and LNR high risk patients, respectively (p=0.254). CONCLUSIONS: LNR is an important prognostic parameter for DFS and might provide potentially more information than pN-stage in patients with pN1/LNR high risk and pN2/LNR low risk. Citation Format: Kaplan MA, Odabasi H, Ozdemir N, Harputluoglu H, Aliustaoglu M, Berk V, Gunaydin Y, Uncu D, Elkiran T, Aydin D, Isikdogan A. Is lymph node ratio (LNR) having additional contribution for predict prognosis on pathologic lymph node staging in node-positive breast cancer patients?. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P3-01-21.
Inhibition of Mammary-Gland Development and Mammary-Tumor Formation in Female C3H Mice Following Ingestion of Thiouracil&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;
Authors: Celia S. Dubnik, Harold P. Morris, Albert J. Dalton
Journal: JNCI Journal of the National Cancer Institute (1950)

Journal Article Inhibition of Mammary-Gland Development and Mammary-Tumor Formation in Female C3H Mice Following Ingestion of Thiouracil Get access Celia S. Dubnik, Celia S. Dubnik Search for other works by this author on: Oxford Academic PubMed Google Scholar Harold P. Morris, Harold P. Morris Search for other works by this author on: Oxford Academic PubMed Google Scholar Albert J. Dalton Albert J. Dalton National Cancer Institute, National Institutes of Health, Public Health Service, Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 10, Issue 4, February 1950, Pages 815–841, https://doi.org/10.1093/jnci/10.4.815 Published: 01 February 1950 Article history Received: 27 July 1949 Published: 01 February 1950
Abstract B2-27: Systems biological identification of optimal drug targets for combination therapy of non-small cell lung cancer
Authors: Jonghoon Lee, Kwang-Hyun Cho
Journal: Cancer Research (2015)

Abstract Non-small cell lung cancer (NSCLC) is the major subtype of lung cancer, accounting for about 85% of all lung patients. Recently, molecularly targeted inhibitors of receptor tyrosine kinase (RTK) such as epidermal growth factor receptor (EGFR) and fibroblast growth factor receptor (FGFR) signalling pathways have been highlighted as promising anti-tumor drugs because of the prevalence of genetic alterations within EGFR and FGFR signalling pathways in NSCLC patients. However, their functional effects have been reported as varying over a wide range depending on the patient-specific mutational conditions. To understand the underlying mechanism of the heterogeneous responses to EGFR and FGFR inhibitors and to find the optimal strategy for combination therapy, we have developed an integrative Boolean network model of EGFR, FGFR and DNA damage signalling pathways by integrating previous experimental evidences from the literature. Systematic perturbation analysis revealed that the multiple feedback regulations embedded in the signalling pathways play important roles in determining the responses to EGFR and FGFR inhibitors. We further analyzed the mechanism for the heterogeneous responses of cells to the EGFR and FGFR inhibitors under various mutational conditions and identified key genetic alterations that can lead to undesirable responses. Finally, extensive combinatorial perturbation analysis and subsequent comparison of the attractor profiles in the presence and absence of targeted inhibitors identified novel candidate drug targets for combinatorial therapy. Our analysis provides a new insight into the underlying mechanism of the heterogeneous cellular responses to EGFR and FGFR inhibitors and the optimal combinatorial treatment strategies. Acknowledgements: This work was supported by the National Research Foundation of Korea (NRF) grants funded by the Korea Government, the Ministry of Science, ICT &amp; Future Planning (2014R1A2A1A10052404, 2013M3A9A7046303, and 2010-0017662) and by a grant of the Korean Health Technology R&amp;D Project, Ministry of Health &amp; Welfare, Republic of Korea. (HI13C2162). Citation Format: Jonghoon Lee, Kwang-Hyun Cho. Systems biological identification of optimal drug targets for combination therapy of non-small cell lung cancer. [abstract]. In: Proceedings of the AACR Special Conference on Computational and Systems Biology of Cancer; Feb 8-11 2015; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2015;75(22 Suppl 2):Abstract nr B2-27.
Transplantation versus chemotherapy in acute leukemia.
Authors: E A Copelan
Journal: Journal of Clinical Oncology (1989)

Article Tools Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.1989.7.5.684 Journal of Clinical Oncology - published online before print September 22, 2016 PMID: 2651584 Transplantation versus chemotherapy in acute leukemia. E A CopelanxE A CopelanSearch for articles by this author https://doi.org/10.1200/JCO.1989.7.5.684 PDF "Transplantation versus chemotherapy in acute leukemia.." Journal of Clinical Oncology, 7(5), pp. 684–685© 1989 by American Society of Clinical Oncology
Heart Failure Considerations of Antihyperglycemic Medications for Type 2 Diabetes
Authors: Eberhard Standl, Oliver Schnell, Darren K. McGuire
Journal: Circulation Research (2016)

Prevalent and incident heart failure (HF) is increased in people with type 2 diabetes mellitus, with risk directly associated with the severity of hyperglycemia. Furthermore, in patients with type 2 diabetes mellitus, mortality is increased ≈10-fold in patients with versus without HF. Reducing HF with antihyperglycemic therapies, however, has been unsuccessful until recently. In fact, HF as an important outcome in patients with type 2 diabetes mellitus seems to be heterogeneously modulated by antihyperglycemic medications, as evidenced by results from cardiovascular outcome trials (CVOTs) and large observational cohort studies. Appropriately powered and executed CVOTs are necessary to truly evaluate cardiovascular safety and efficacy of new antihyperglycemic medications, as reflected by the guidance of the US Food and Drug Administration and other regulatory agencies since 2008. In light of the best available evidence at present, metformin and the sodium-glucose-co-transporter 2-inhibitor empagliflozin seem to be especially advantageous with regard to HF effects, with their use associated with reduced HF events and improved mortality. Acarbose, the dipeptidyl-peptidase 4-inhibitor sitagliptin, the glucagon-like peptide 1-receptor agonist lixisenatide based on presently available CVOT results comprise reasonable additional options, as significant harm in terms of HF has been excluded for those drugs. Additions to this list are anticipated pending results of ongoing CVOTs. Although no HF harm was seen in CVOTs for insulin or sulfonylureas, they should be used only with caution in patients with HF, given their established high risk for hypoglycemia and some uncertainties on their safety in patients with HF derived from epidemiological observations. Pioglitazone is contraindicated in patients with HF&gt;New York Heart Association I, despite some benefits suggested by CVOT subanalyses.
Surgery for temporal lobe epilepsy
Authors: R. D C Elwes
Journal: BMJ (2002)

In a worldwide review of epilepsy surgery carried out in 1985, 53 centres were found that had undertaken about 3500 operations for intractable epilepsy. Five years later this had increased to over 8000 operations done in 118 centres.1 In both surveys most patients underwent resections for temporal lobe epilepsy. Specialist services for epilepsy and intensive electroencephalography monitoring are now more widely available and presurgical evaluation has become easier due to advances in neuroimaging.

Any doubts that surgery is not effective have been dispelled by a recent randomised study.2 Patients were assigned to surgery or a one year waiting list control group where they received optimum medical treatment. This study design avoided any ethical objections to delaying surgery. Fortunately, only 10% of the patients were excluded after investigation so an appropriate intention to treat analysis could be undertaken. With medical treatment only 5% remitted, while after surgery 65% were completely seizure free. The study design did however restrict comparative outcomes to one year of follow up, …
The emerging role of viral vectors as vehicles for DMD gene editing
Authors: Ignazio Maggio, Xiaoyu Chen, Manuel A. F. V. Gonçalves
Journal: Genome Medicine (2016)

Duchenne muscular dystrophy (DMD) is a genetic disorder caused by mutations in the dystrophin-encoding DMD gene. The DMD gene, spanning over 2.4 megabases along the short arm of the X chromosome (Xp21.2), is the largest genetic locus known in the human genome. The size of DMD, combined with the complexity of the DMD phenotype and the extent of the affected tissues, begs for the development of novel, ideally complementary, therapeutic approaches. Genome editing based on the delivery of sequence-specific programmable nucleases into dystrophin-defective cells has recently enriched the portfolio of potential therapies under investigation. Experiments involving different programmable nuclease platforms and target cell types have established that the application of genome-editing principles to the targeted manipulation of defective DMD loci can result in the rescue of dystrophin protein synthesis in gene-edited cells. Looking towards translation into the clinic, these proof-of-principle experiments have been swiftly followed by the conversion of well-established viral vector systems into delivery agents for DMD editing. These gene-editing tools consist of zinc-finger nucleases (ZFNs), engineered homing endonucleases (HEs), transcription activator-like effector nucleases (TALENs), and RNA-guided nucleases (RGNs) based on clustered, regularly interspaced, short palindromic repeats (CRISPR)–Cas9 systems. Here, we succinctly review these fast-paced developments and technologies, highlighting their relative merits and potential bottlenecks, when used as part of in vivo and ex vivo gene-editing strategies.
Abstract P2-06-02: BIN3 is an 8p21 tumor suppressor regulating the epithelial attachment checkpoint
Authors: J Silva, N Marshall, F Sanchez-Garcia, R Parsons, D Pe'er
Journal: Cancer Research (2016)

Abstract An important characteristic of multicellular organisms is the control that tissue architecture exerts on the growth and differentiation of individual cells. Epithelial cells sense their location through interactions with the extracellular matrix (ECM) as well as neighboring cells. These interactions generate input signals, including survival, that are critical to maintain tissue and cellular homeostasis. When attachment is compromised, epithelial cells undergo an intrinsically programmed cell death (apoptosis) that is termed anoikis (from the Greek "loss of home"). Importantly, failure to execute the anoikis program could result in adherent epithelial cells surviving in suspension or being able to proliiferate at sites different from their original environment. Thus, anoikis is a line of defense that must be circumvented by cancerous epithelial cells for them to leave their home niche, thrive in inappropriate ECM environments, and establish long distance metastases. Thus, elucidating how epithelial cancer cells escape anoikis is critical to understanding cancer progression. In order to uncover genes that modulate the anoikis response and are altered in human cancers, we performed a functional genomics study. We couple genome wide RNAi to identify gene functions that, when silenced, induce resistance to anoikis with a novel computational method, ISAR-DEL, specifically aimed at pinpointing candidate tumor suppressor genes based on recurrent loss of copy number. Our studies identified Bridging Integrator 3 (BIN3) as a novel tumor suppressor located on the chromosomal region 8p21.3, one of the most frequently lost regions in epithelial cancers. Mechanistically, we link BIN3 tumor suppression function to its ability to sense changes in the curvature of the cell membrane and relocate to the cell membrane after cell detachment to induce a proapoptotic cascade. Once BIN3 has translocated to the cell membrane it modulates the relocation and function of CDC42. In these conditions, CDC42 transmits the signal that leads to the activation of the stress protein P38-α and programmed cell death mediated by accumulation of the apoptotic facilitator BimEL. Overall, our results explain how changes in cell geometry are integrated in the cellular signaling network and present, for the first time, BIN3 as a novel breast cancer tumors suppressor. Citation Format: Silva J, Marshall N, Sanchez-Garcia F, Parsons R, Pe'er D. BIN3 is an 8p21 tumor suppressor regulating the epithelial attachment checkpoint. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P2-06-02.
Spinal Cord Tumors Induced by &lt;italic&gt;N&lt;/italic&gt;-Ethyl-&lt;italic&gt;N&lt;/italic&gt;-nitrosourea in Rats: Presence of Spinal Subpial Target Cells&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: M Naito, Y Naito, A Ito, H Watanabe, K Kawashima
Journal: JNCI Journal of the National Cancer Institute (1984)

The correlation between induction of spinal cord tumor by N-ethyl-N-nitrosourea (ENU) (CAS: 759-73-9; 1-ethyl-1-nitrosourea) and postnatal cellular differentiation of the spinal cord was examined in 6 different strains of rats [noninbred Wistar and inbred F344, WF, LE, WF (female) X LE (male), and LE (female) X WF (male)]. By perinatal injection of 40 mg ENU/kg, 258 spinal cord tumors were induced in 175 of 372 ENU-treated rats. The spinal cords of rats at ages ranging from day 1 to day 8 after birth were particularly susceptible to the oncogenic effect of ENU. All spinal cord tumors developed in the white matter without any segmental predilection site. Moreover, most (93%) were found in the subpial region of the spinal cord and were classified as oligodendrogliomas. Morphologic and autoradiographic examinations revealed accumulation of spinal subpial immature glial cells from day 1 to day 8 after birth when the spinal cord had a high susceptibility and most of the cells were destined to differentiate into oligodendrocytes. These data show the existence of target cells in the spinal cords of rats after ENU carcinogenesis.
Trend of Lung-Cancer Mortality in the United States: Some Limitations of Available Statistics
Authors: Benno K. Milmore, M.D.
Journal: JNCI Journal of the National Cancer Institute (1955)

Trend of Lung-Cancer Mortality in the United States: Some Limitations of Available Statistics Get access Benno K. Milmore, M.D. Benno K. Milmore, M.D. National Cancer Institute,2Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 16, Issue 1, August 1955, Pages 267–284, https://doi.org/10.1093/jnci/16.1.267 Published: 01 August 1955 Article history Received: 11 January 1955 Published: 01 August 1955
Brief versus standard hospitalization: the differential costs
Authors: J Endicott, M I Herz, M Gibbon
Journal: American Journal of Psychiatry (1978)

The authors compared the use of inpatient and day care services, number of readmissions, use of special services, use of drugs, costs to family and community, and differential dollar costs of three treatment approaches--brief hospitalization followed by day care, brief hospitalization followed by outpatient care, and standard hospitalization. They found that, among patients who had families willing to care for them, brief hospitalization followed by either day or outpatient care was less expensive in terms of hospital costs and costs to the family than standard hospitalization.
Depression in women treated for gynecological cancer: clinical and neuroendocrine assessment
Authors: D L Evans, C F McCartney, C B Nemeroff, D Raft, D Quade, R N Golden, J J Haggerty, V Holmes, J S Simon, M Droba
Journal: American Journal of Psychiatry (1986)

To determine the prevalence of major depression in cancer patients and assess the usefulness of the dexamethasone suppression test (DST) and the thyrotropin-releasing hormone (TRH) stimulation test for diagnosing major depression in these patients, the authors studied 83 women hospitalized for gynecological cancer. Nineteen (23%) had major depression according to DSM-III criteria. The sensitivity and specificity of the DST were 40% and 88%, respectively. No relationship between DST and TRH test results was found. These findings indicate a high prevalence of depression in cancer patients, but further research on these tests in cancer patients is needed; their routine use with cancer patients is premature at this time.
A dog model for human psychopathology
Authors: W G Reese
Journal: American Journal of Psychiatry (1979)

The author reviews studies of the development and scientific exploitation of two true-breeding strains of pointer dogs, one of which is basically normal and one of which is nervous, particularly around people. Basic studies, which generally contrast the nervous dogs with the normal dogs, include studies of inheritance, early experience, conditioning, psychophysiology, neuropharmacology, and neurochemistry. The author suggests that the nervous line is an animal model of human psychopathology and probably of cardiac pathology.
Complement Fixation in Animal Neoplasia. I. A Study of Techniques for Measurement of the Reaction in Rabbit Serum with Special Reference to the Temperature of Inactivation&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;&lt;xref ref-type="fn" rid="fn2"&gt;&lt;sup&gt;3&lt;/sup&gt;&lt;/xref&gt;
Authors: Helen Thornton, L. D. Ellerbrook, M. C. Rhees, E. C. Stowell, Jr., S. W. Lippincott
Journal: JNCI Journal of the National Cancer Institute (1950)

Journal Article Complement Fixation in Animal Neoplasia. I. A Study of Techniques for Measurement of the Reaction in Rabbit Serum with Special Reference to the Temperature of Inactivation Get access Helen Thornton, Helen Thornton Search for other works by this author on: Oxford Academic PubMed Google Scholar L. D. Ellerbrook, L. D. Ellerbrook Search for other works by this author on: Oxford Academic PubMed Google Scholar M. C. Rhees, M. C. Rhees Search for other works by this author on: Oxford Academic PubMed Google Scholar E. C. Stowell, Jr., E. C. Stowell, Jr. Search for other works by this author on: Oxford Academic PubMed Google Scholar S. W. Lippincott S. W. Lippincott Clinical Trials Unit, Cancer Control Branch, National Cancer Institute, National Institutes of Health, U. S. Public Health Service, and the Department of Pathology, School of Medicine, University of Washington, Seattle, Wash. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 11, Issue 1, August 1950, Pages 97–124, https://doi.org/10.1093/jnci/11.1.97 Published: 01 August 1950 Article history Received: 27 April 1950 Published: 01 August 1950
Prognostic Impact of the Serum Levels of Soluble CD23 in B-Cell Chronic Lymphocytic Leukemia
Authors: Irmgard Langenmayer, Michael Hallek, Berthold Emmerich, Dagmar Adorf, Christoph Nerl, Theodor Zwingers, Wolfgang U Knauf, Bärbel Ehlers, Birgitt Mohr, Eckhard Thiel
Journal: Blood (1997)
ROTATIONAL ATHERECTOMY FOLLOWED BY CUTTING BALLOON PLAQUE MODIFICATION BEFORE DRUG-ELUTING STENT IMPLANTATION IN CALCIFIED CORONARY LESIONS
Authors: Shinichi Fumichi, Tetsuya Tobaru, Ryuta Asano, Yusuke Watanabe, Itaru Takamisawa, Atsushi Seki, Tetsuya Sumiyoshi, Hitonobu Tomoike
Journal: Journal of the American College of Cardiology (2012)
Erratum to: A benchmark for RNA-seq quantification pipelines
Authors: Mingxiang Teng, Michael I. Love, Carrie A. Davis, Sarah Djebali, Alexander Dobin, Brenton R. Graveley, Sheng Li, Christopher E. Mason, Sara Olson, Dmitri Pervouchine, Cricket A. Sloan, Xintao Wei, Lijun Zhan, Rafael A. Irizarry
Journal: Genome biology (2016)

After the publication of this work [1] it was noticed that there were typographical errors in the following equations: equation 5 in column 2, equation 7 in column 2, equation 8 in column 1.
The Action of Tissue Extracts on Cell Division&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;
Authors: L. V. Heilbrunn, W. L. Wilson, Drusilla Harding
Journal: JNCI Journal of the National Cancer Institute (1951)

The Action of Tissue Extracts on Cell Division Get access L. V. Heilbrunn, L. V. Heilbrunn Search for other works by this author on: Oxford Academic PubMed Google Scholar W. L. Wilson, W. L. Wilson Search for other works by this author on: Oxford Academic PubMed Google Scholar Drusilla Harding Drusilla Harding Department of Zoology, University of Pennsylvania, Philadelphia Pa., and the Marine Biological Laboratory, Woods Hole, Mass. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 11, Issue 6, June 1951, Pages 1287–1298, https://doi.org/10.1093/jnci/11.6.1287 Published: 01 June 1951 Article history Received: 11 April 1951 Published: 01 June 1951