tbuckley/cabot-search huggingface dataset:
AVAILABILITY OF CENSUS REPORTS
Journal: JAMA (1941)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
BOOKS IN REVIEW 1992
Authors: ERIC J. SEIFTER
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article BOOKS IN REVIEW 1992 Get access Breast Cancer Treatment: A Comprehensive Guide to Management Barbara Fowble , Robert L. Goodman , John H. Glick , Ernest F. Rosato . St. Louis : Mosby-YearBook , 1991 . 647 pp., illus. $89. Reviewed by Carol Fabian (first citation) and Michael S. Simon (second citation) (J Natl Cancer Inst 84: 975–976 , 1992 ). ERIC J. SEIFTER ERIC J. SEIFTER Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 2, 20 January 1993, Page 158, https://doi.org/10.1093/jnci/85.2.158-a Published: 20 January 1993
Motor-Vehicle Occupant Fatalities and Restraint Use Among Children Aged 4-8 Years--United States, 1994-1998
Journal: JAMA (2000)

In the United States, more children aged 4-8 years die as occupants in motor-vehicle-related crashes than from any other form of unintentional injury (1). To reduce the number of deaths and injuries caused by motor-vehicle-related trauma, child passengers in this age group should be restrained properly in a vehicle's back seat (2). To characterize fatalities, restraint use, and seating position among occupants aged 4-8 years involved in fatal crashes, CDC analyzed 1994-1998 data from the Fatality Analysis Reporting System (FARS), which is maintained by the National Highway Traffic Safety Administration (NHTSA). This report summarizes the results of that analysis, which indicate that during 1994-1998, little change occurred in the death rate, restraint use, and seating position among children aged 4-8 years killed in crashes.
SI Units
Authors: Allan R. Glass
Journal: Annals of Internal Medicine (1990)

Letters and Corrections15 September 1990SI UnitsAllan R. Glass, MDAllan R. Glass, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-113-6-484_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editors: In a recent issue of ACP Observer, you indicated that you were interested in focusing on material that would "help . . . in the day-to-day practice of [the] profession." To this end, you could follow through on the recent initiative by Annals of Internal Medicine to use only SI units in its articles. This change has made the articles less useful to practicing physicians, as laboratory results on patients are still reported almost exclusively in traditional units. This dichotomy inhibits the rapid and intuitive transfer of material from articles to use in the clinic.I would... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Allan R. Glass, MDAffiliations: Walter Reed Army Medical Center Washington, DC 20307-5001 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 September 1990Volume 113, Issue 6Page: 484-485KeywordsResearch laboratories ePublished: 1 December 2008 Issue Published: 15 September 1990 PDF downloadLoading ...
Use of Longitudinal Analysis of Peripheral Blood Counts to Validate Historical Reconstructions of Benzene Exposure
Authors: Howard M. Kipen, Ronald P. Cody, Bernard D. Goldstein
Journal: Environmental Health Perspectives (1989)

We studied over 17,000 peripheral blood counts, accumulated during hematologic surveillance from 1940 through 1975, from a cohort of 459 benzene-exposed workers. Linear regressions demonstrated significant decreases in white and red cell counts, as well as hemoglobin, for workers exposed during the 1940s, without persistent trends over the ensuing 25 years. Strongly positive correlations were observed between these blood count fluctuations and fluctuations in retrospective estimates of benzene exposures for these workers in the earlier period of surveillance (mean estimated exposure 1940 to 1948, 75 ppm), but not for later years, (mean estimated exposure 1948 to 1975, 15 to 20 ppm). These data suggest substantial limitations of hematologic examination of populations to detect abnormalities in populations currently exposed to benzene. The analysis also demonstrates a novel approach to the biological validation of exposure estimates based upon limited industrial hygiene and historical record data. The application of biologic monitoring data may be useful for assisting decisions in reconstruction of a previous exposure.
Deactivating Implantable Cardioverter Defibrillators
Authors: Heather M. Ross
Journal: Annals of Internal Medicine (2005)

Letters1 November 2005Deactivating Implantable Cardioverter DefibrillatorsHeather M. Ross, MS, APRN, NPHeather M. Ross, MS, APRN, NPFrom St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-143-9-200511010-00015 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Berger (1) raises the important issue of advances in technology outstripping advances in ethical decision-making practices. His comparison of implantable cardioverter defibrillator (ICD) deactivation with hemodialysis discontinuation is valuable in helping to clarify the issues inherent in decisions to remove active and invasive therapies. I am very concerned, however, about the parallel drawn between deactivation of an ICD and deactivation of a permanent pacemaker. The nature of implanted cardiac devices and their functions related to the dying process are inherently different and must be considered as such. An ICD delivers therapy to terminate a life-threatening arrhythmia by ...Reference1. Berger JT. The ethics of deactivating implanted cardioverter defibrillators. Ann Intern Med. 2005;142:631-4. [PMID: 15838070] LinkGoogle Scholar Author, Article, and Disclosure InformationAffiliations: From St. Joseph's Hospital and Medical Center, Phoenix, AZ 85013.Disclosures: None disclosed. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoThe Ethics of Deactivating Implanted Cardioverter Defibrillators Jeffrey T. Berger Deactivating Implantable Cardioverter Defibrillators James M. Beattie , Michael J. Connolly , and John E. Ellershaw Deactivating Implantable Cardioverter Defibrillators Joanne Lynn Deactivating Implantable Cardioverter Defibrillators Jeffrey T. Berger Metrics Cited ByEthical issues on defibrillator deactivation in end-of-life patients 1 November 2005Volume 143, Issue 9Page: 690KeywordsArrhythmiaCardiac electrophysiologyConflicts of interestEuthanasiaHeartHomicide ePublished: 1 November 2005 Issue Published: 1 November 2005 CopyrightCopyright © 2005 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Is initial treatment with enoxaparin beneficial in unstable angina/non-ST segment elevation patients who later undergo percutaneous coronary interventon (PCI)? Keith A. A. Fox, Elliott M. Antman, Marc Cohen, Frederique Bigonzi, David Radley, On behalf of the ESSENCE &amp; TIMI 11B investigators. The Royal Infirmary of Edinburgh, Edinburgh, United Kingdom
Journal: Journal of the American College of Cardiology (2001)
Books Received
Authors: Nicoletta Sonino, Giovanni A. Fava, Chantal Henry, Katia M'Baïlara, Rollon Poinsot, Anne-Aurelie Casteret, Frédéric Sorbara, Marion Leboyer, Eduard Vieta, Ludwig Grepmair, Ferdinand Mitterlehner, Thomas Loew, Egon Bachler, Wolfhardt Rother, Marius Nickel, Axel Schweickhardt, Astrid Larisch, Michael Wirsching, Kurt Fritzsche, Carlo Faravelli, Mario Catena, Alessandra Scarpato, Valdo Ricca, Michael Martini Jørgensen, Martin Härter, Harald Baumeister, Katrin Reuter, Frank Jacobi, Michael Höfler, Jürgen Bengel, Hans-Ulrich Wittchen, Robert Zachariae, Axel Skytthe, Kirsten Kyvik, R. Zachariae, K. Paulsen, M. Mehlsen, A.B. Jensen, A. Johansson, H. von der Maase, Fabio Facchinetti, Fedra Ottolini, Marta Fazzio, Marco Rigatelli, Annibale Volpe, Naheed K. Hossain, Jane Irvine, Paul Ritvo, Helen S. Driver, Colin M. Shapiro, Constance Dalenberg, Richard Loewenstein, David Spiegel, Chris Brewin, Ruth Lanius, Steven Frankel, Steven Gold, Bessel Van der Kolk, Daphne Simeon, Eric Vermetten, Lisa Butler, Cheryl Koopman, Christine Courtois, Paul Dell, Ellert Nijenhuis, James Chu, Vedat Sar, Oxana Palesh, Carlos Cuevas, Kelsey Paulson, Harrison G. Pope, Jr., Steven Barry, J. Alexander Bodkin, James Hudson, Carlo Lai, Silvia Daini, Maria Lucia Calcagni, Isabella Bruno, Sergio De Risio, Marco Chiesa, Peter Fonagy, Sabine Loeber, Bernhard Croissant, Helmut Nakovics, Anke Zimmer, Alexander Georgi, Sabine Klein, Carsten Diener, Andreas Heinz, Karl Mann, Herta Flor
Journal: Psychotherapy and Psychosomatics (2007)
Infant Mortality—United States, 1991
Journal: JAMA (1994)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Operative Surgery.
Journal: JAMA (1921)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Neural control of sweat secretion: a review
Authors: Y. Hu, C. Converse, M.C. Lyons, W.H. Hsu
Journal: British Journal of Dermatology (2018)

Humans have four million sweat glands, which can be classified into two types: eccrine (which make up about 90% of our sweat glands) and apocrine glands. In the 1980s, scientists discovered a third type, the apoeccrine sweat gland. However, this has been disputed by some scientists and it is not well understood. The functions of sweat glands are to maintain body temperature, to release waste products, and to respond to emotional stresses. Sweating which is involved in body temperature regulation and responding to emotional stress is controlled by signals from the body's central nervous system to the peripheral nervous system using neurotransmitters, which are chemical messengers that carry signals between cells in the body, including neurons. This means that the body's nervous systems are crucial to sweating. This review looks at the science behind sweating, in particular the neural (nervous system) control of sweat secretion and the mechanisms by which neurotransmitters trigger sweating. The researchers, from the U.S.A., also discuss sweating disorders associated with neural anomaly such as hyperhidrosis (in which people sweat too much) and hypohydrosis (not enough). The study also outlines the possible treatments for such disorders, and their effectiveness.
Disordered Fat Storage and Mobilization in the Pathogenesis of Insulin Resistance and Type 2 Diabetes
Authors: G. F. Lewis
Journal: Endocrine Reviews (2002)

The primary genetic, environmental, and metabolic factors responsible for causing insulin resistance and pancreatic β-cell failure and the precise sequence of events leading to the development of type 2 diabetes are not yet fully understood. Abnormalities of triglyceride storage and lipolysis in insulin-sensitive tissues are an early manifestation of conditions characterized by insulin resistance and are detectable before the development of postprandial or fasting hyperglycemia. Increased free fatty acid (FFA) flux from adipose tissue to nonadipose tissue, resulting from abnormalities of fat metabolism, participates in and amplifies many of the fundamental metabolic derangements that are characteristic of the insulin resistance syndrome and type 2 diabetes. It is also likely to play an important role in the progression from normal glucose tolerance to fasting hyperglycemia and conversion to frank type 2 diabetes in insulin resistant individuals. Adverse metabolic consequences of increased FFA flux, to be discussed in this review, are extremely wide ranging and include, but are not limited to: 1) dyslipidemia and hepatic steatosis, 2) impaired glucose metabolism and insulin sensitivity in muscle and liver, 3) diminished insulin clearance, aggravating peripheral tissue hyperinsulinemia, and 4) impaired pancreatic β-cell function. The precise biochemical mechanisms whereby fatty acids and cytosolic triglycerides exert their effects remain poorly understood. Recent studies, however, suggest that the sequence of events may be the following: in states of positive net energy balance, triglyceride accumulation in "fat-buffering" adipose tissue is limited by the development of adipose tissue insulin resistance. This results in diversion of energy substrates to nonadipose tissue, which in turn leads to a complex array of metabolic abnormalities characteristic of insulin-resistant states and type 2 diabetes. Recent evidence suggests that some of the biochemical mechanisms whereby glucose and fat exert adverse effects in insulin-sensitive and insulin-producing tissues are shared, thus implicating a diabetogenic role for energy excess as a whole. Although there is now evidence that weight loss through reduction of caloric intake and increase in physical activity can prevent the development of diabetes, it remains an open question as to whether specific modulation of fat metabolism will result in improvement in some or all of the above metabolic derangements or will prevent progression from insulin resistance syndrome to type 2 diabetes.
THE PLACEBO EFFECT IN PSYCHOTHERAPY
Journal: JAMA (1967)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
GLANDULAR ORGANS AS ARTICLES OF DIET
Journal: JAMA (1920)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
"CHRISTIAN SCIENCE" AND DEATH CERTIFICATES.
Journal: JAMA (1899)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Five-year follow-up after intracoronary gamma radiation therapy for in-stent restenosis: Results from a randomized clinical trial
Authors: Ron Waksman, Andrew E. Ajani, Larry R. White, Edouard F. Cheneau, Augusto D. Pichard, Lowell F. Satler, Kenneth M. Kent, Regina Deible, Verne Mattox, Ellen Pinnow, Peter Iloanya, Joseph Lindsay
Journal: Journal of the American College of Cardiology (2003)
Abstract B22: Increased phosphorylation of eIF4E induces resistance to treatment with mTOR inhibitors together with AR antagonists in advanced prostate cancer
Authors: Leandro S. D'Abronzo, Michael Crapuchettes, Ryan Beggs, Ruth Vinall, Clifford Tepper, Salma Siddiqui, Maria Mudryj, Frank Melgoza, Blythe Durbin-Johnson, Ralph deVere White, Paramita Ghosh
Journal: Cancer Research (2017)

Abstract The anti-androgen bicalutamide is widely used in the treatment of advanced prostate cancer (CaP) in many countries, but its effect on castration resistant CaP (CRPC) is limited. We previously showed that resistance to bicalutamide results from increased activation of the mechanistic target of rapamycin (mTOR); indicating a role for mTOR inhibitors in CaP treatment. Interestingly, a clinical trial testing combinations of the mTOR inhibitor RAD001 with bicalutamide were initially effective (PSA decline&amp;gt;50%) in 62.5% CRPC patients, but many initial responders later developed resistance. Here we investigate causes for their difference in response. Evaluation of various CRPC cell lines identified resistant vs sensitive in vitro models, and revealed that increased eIF4E phosphorylation at S209 is associated with resistance to the combination. To recognize potential causes of resistance, we demonstrated using a human tumor xenograft mouse model, that bicalutamide use is associated with an increase in eIF4E(S209) phosphorylation. Investigations revealed that AR suppressed eIF4E phosphorylation, while the use of anti-androgens relieved this suppression, thereby triggering its increase. Additional investigation on the consequences of increased eIF4E phosphorylation in human prostatectomy samples revealed that increased eIF4E phosphorylation strongly correlated with the cell proliferation marker Ki67, indicating a role for eIF4E in tumor growth. Inhibition of eIF4E phosphorylation by siRNA suppression or treatment with CGP57380 (an inhibitor of MAPK interacting serine-threonine kinases Mnk1/2, the eIF4E upstream kinase,) sensitized CRPC cells to RAD001+bicalutamide, while eIF4E overexpression induced resistance. Our results demonstrate that bicalutamide treatment induced an increase in eIF4E phosphorylation by inhibition of AR which otherwise suppressed this phosphorylation. Increased eIF4E phosphorylation then induced resistance to the combination of anti-androgens with mTOR inhibitors by increasing proliferation. These results also indicate that resistance to RAD001+bicalutamide can be prevented by the concurrent use of a Mnk1/2 inhibitor. Citation Format: Leandro S. D'Abronzo, Michael Crapuchettes, Ryan Beggs, Ruth Vinall, Clifford Tepper, Salma Siddiqui, Maria Mudryj, Frank Melgoza, Blythe Durbin-Johnson, Ralph deVere White, Paramita Ghosh. Increased phosphorylation of eIF4E induces resistance to treatment with mTOR inhibitors together with AR antagonists in advanced prostate cancer. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr B22.