tbuckley/cabot-search huggingface dataset:
As Genes Differ, So Should Interventions for Cancer
Authors: J. Stephenson
Journal: JAMA (2001)

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
Highlights
Journal: JAMA Oncology (2016)

Kroenke and colleagues aimed to evaluate the association between body mass index (BMI) and colorectal cancer (CRC) outcomes.They evaluated 3408 men and women aged 18 to 80 years with stage I to III CRC.Body mass index at (and following) diagnosis of CRC was associated with all-cause and disease-specifi c mortality, with diff erent spectrums of BMI associated with diff erent risk.Renehan and Sperrin provide an Editorial.
Latino Individuals’ Diabetes Risk Increases With US Lifestyle
Journal: JAMA (2015)

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Clinical Pharmacology of Cyclothiazide
Journal: JAMA (1963)

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
John Waterlow
Authors: J. Lyall
Journal: BMJ (2011)

<h3>Abstract</h3> Small cell lung cancer (SCLC) is a recalcitrant malignancy that urgently needs new therapies. Four master transcription factors (ASCL1, NEUROD1, POU2F3, and YAP1) are identified in SCLC, and each defines the transcriptome landscape of one molecular subtype. These master factors have not been directly druggable, and targeting their transcriptional coactivator(s) could provide an alternative approach. Here, we identify that BET bromodomain proteins physically interact with NEUROD1 and function as its transcriptional coactivators. Using CRISPR knockout and ChIP-seq, we demonstrate that NEUROD1 plays a critical role in defining the landscapes of BET bromodomain proteins in the SCLC genome. Targeting BET bromodomain proteins by BET inhibitors leads to broad suppression of the NEUROD1-target genes, especially those associated with superenhancers, and reduces SCLC growth <i>in vitro</i> and <i>in vivo</i>. LSAMP, a membrane protein in the IgLON family, was identified as one of the NEUROD1-target genes mediating BET inhibitor sensitivity in SCLC. Altogether, our study reveals that targeting transcriptional coactivators could be a novel approach to blocking the master transcription factors in SCLC for therapeutic purposes. <h3>Significance</h3> Small cell lung cancer (SCLC) is the most aggressive form of lung malignancies, and little progress has been made to improve its outcome in the past two decades. It is now recognized that SCLC is not a single disease but has at least four molecular subtypes, and each subtype features the expression of one master transcription factor. Unfortunately, these master transcription factors are not directly druggable. Here, we identified BET bromodomain proteins as the transcriptional coactivators of NEUROD1, one of the master transcription factors in SCLC. Blocking BET bromodomain proteins with inhibitors suppresses NEUROD1-target genes and reduces tumor growth. Our results demonstrate that blocking transcriptional coactivators could be an alternative approach to targeting the master transcription factors in SCLC.
Missed malignant melanomas
Authors: R. M MacKie, V. R Doherty
Journal: BMJ (1986)

Australia supports the concept that lesions in Australia have a better prognosis than those in Oxford because they are diagnosed at an earlier stage owing to greater public and professional awareness.4At Queen's University, Belfast, we have now started a teaching programme to improve the recognition ofmelanomas by medical students.We plan to extend this into the postgraduate educational programme for general practitioners and other doctors.The public should also be made more aware of the possible dangers inherent in certain types of pigmented lesions and the curability of melanoma in its early stages.Un- necessary deaths can be prevented.
Abstract 626: Shear Stress Regulates Angiotensin Type One Receptor Expression in Endothelial Cells
Authors: Bhama Ramkhelawon, Jose Vilar, Alain Tedgui, Lehoux Stephanie
Journal: Circulation (2007)

Several studies have shown that angiotensin II tends to favour atherosclerotic lesion formation and progression, acting mainly through angiotensin type one receptors (AT1R). Conversely, shear stress (SS) confers atheroprotective effects in the vasculature. However, whether SS regulates endothelial AT1R expression remains unknown. Using en face staining of C57BL/6 mouse aortas, we found a pronounced expression of AT1R in the inner regions of the aortic arch and at collateral artery branch points, known to have low flow and to be atheroprone, compared with neighboring high SS regions. Furthermore, staining of vessels from hypercholesterolemic LDLR−/−mice demonstrated a clear expression of AT1R only in endothelium overlying plaques. Using HUVECs exposed to a laminar SS of 15dynes/cm2, we observed a biphasic decrease in AT1R protein expression characterized by a first reduction at 1 hr (31+4% of static control, p&lt;0.001), partial recovery at 3 hr (65+9%), and a second more prolonged decrease at 6, 12 and 24 hrs (48+9%, 36+9%, 33+5% of static control, respectively)(p&lt;0.001). AT2R levels remained unchanged in these conditions. Shear-induced downregulation of AT1R was abolished by treatment with L-NAME (10–7M), suggesting that NO regulates AT1R in sheared endothelial cells. In accordance, stimulating static HUVECs with a NO donor for 1 hour decreased AT1R protein expression. The acute loss of AT1R at 1 hour SS suggested a rapid endocytosis and degradation of the protein. Indeed, immunocytochemical staining demonstrated a clear colocalisation of AT1R with caveolin-1 in HUVECs submitted to 5 mins SS, similar to that observed in angII-stimulated cells. Cholesterol depletion with methyl-beta-cyclodextrin prevented AT1R-caveolin colocalisation. No colocalisation of AT1R with clathrin was observed. In comparison, AT2R did not undergo endocytosis under any conditions tested. Finally, RT-PCR revealed a significant (p&lt;0.001) decrease of AT1R mRNA in HUVECs exposed to SS during 6 (4+1% of static control), 12 (4+1%) and 24 hours (15+4%), suggesting a transcriptional downregulation of AT1R at length. Hence, our results demonstrate that SS may convey some of its atheroprotective effects through degradation and downregulation of AT1R in endothelial cells.
Outcomes in Elderly Patients After Intensive Care
Authors: Robert J. Boland
Journal: JAMA (1993)

<h3>To the Editor.</h3> —Chelluri and associates<sup>1</sup>should be commended on their evaluation of the relationship between age and longterm outcome of intensive care patients. In a time when geriatricians are referring to the elderly in terms of<i>youngold</i>and<i>old-old</i>, it becomes clear that age alone is too crude a measure of functioning, and the thought that it might be used "as a criterion for allocating health care" is vaguely chilling. In looking at their choices for outcome measures, it is unfortunate that they did not choose to look specifically at neuropsychological functioning in their population. Quality of life, activities of daily living, and perhaps even depression, although related to cognitive functioning, are not predictive of it. Cognitive status testing may, on the other hand, be a more reliable predictor of those and other outcome measurements. With a number of well-validated mental status screens available (particularly in view of
Physician Not Dead
Journal: JAMA (1952)

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Tolerability and efficacy of chemotherapy in older men with metastatic castrate-resistant prostate cancer (mCRPC) in the TAX 327 trial.
Authors: B. Seruga, A. M. Horgan, G. R. Pond, S. M. H. Alibhai, E. Amir, R. De Wit, M. A. Eisenberger, I. Tannock
Journal: Journal of Clinical Oncology (2011)

4530 Background: The TAX 327 trial established 3-weekly docetaxel (Dq3w) as standard of care in men with mCRPC. Observational data suggest older men experience substantial toxicity (e.g. infection, diarrhea) when treated with Dq3w (Shepard DR et al, ASCO 2010). The tolerability and efficacy of Dq3w in men ≥75yrs in the TAX 327 study is investigated in this exploratory analysis. Methods: Of 1,006 men in the TAX 327 trial, 207 were ≥75 yrs. Tolerability and efficacy was compared for men receiving Dq3w between three age groups (<65, 65-74 and ≥75 yrs), as well as for men ≥75 yrs between the three treatment regimens (Dq3w, weekly docetaxel [Dq1w] and mitoxantrone [Mtx]). Cox proportional hazards, χ2 and Wilcoxon rank sum tests were used. Results: At baseline older men had poorer performance status (ECOG 2: 6%, 16% and 18% by age group), higher PSA (PSA ≥ 20ng/ml: 82%, 89% and 93%) and more visceral disease (18%, 24% and 27%). Infection of any grade occurred more often in older men (24%, 35% and 42%; p=0.03) and there was a trend to increased frequency of diarrhea of any grade (30%, 29% and 40%; p=0.25). Although older men required more frequent dose reductions and trended to more treatment discontinuations due to toxicity, Dq3w had similar efficacy in all age groups (Table). In men ≥75 yrs there were higher rates of infection and diarrhea of any grade with Dq3w and Dq1w as compared to those treated with Mtx (42%, 45% and 21%; p=0.005, and 40%, 42% and 10%; p< 0.001, respectively). Dq3w and Dq1w resulted in more dose reductions and discontinuations due to toxicity than Mtx, but there was a trend to better efficacy of Dq3w (Table). Conclusions: Dq3w remains the preferred treatment strategy in older men with mCRPC, but close monitoring for toxicity is advised. Dq3w ≥75 yrs Variable < 65 yrs n=126 % 65-74 yrs n=141 % ≥75 yrs n=68 % P Dq3w n=68 % Dq1w n=71 % Mtx n=68 % P Dose reduction 7 12 22 0.01 22 8 6 <0.01 Discontinuation 3 14 19 NS 19 23 12 0.01 Improvement in QoL 19 26 20 NS 20 12 12 NS Pain response 34 38 28 NS 28 44 7 <0.01 PSA response 44 48 43 NS 43 39 32 NS Tumor response 17 7 13 NS 13 6 8 NS Median survival (mo) 20 19 19 NS 19 16 13 NS Abbreviations: NS, not significant; QoL, quality of life.
XI. PNEUMOCOCCUS VACCINE
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
Sudden Unexpected Death in Infancy and Milk Sensitivity
Journal: JAMA (1963)

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
Quality of life is rarely and poorly measured in randomised controlled trials
Journal: BMJ (1998)

Terms used to describe trials may have different meanings for patientsLittle is known about patients' perspectives of participation in randomised controlled trials.On p 1177 Featherstone and Donovan explore the understandings of randomisation among middle aged and elderly men participating in a trial of treatments for benign prostatic disease.Most men were able to recall and describe basic aspects of randomisation such as the involvement of chance, but they also developed alternative accounts to help them make sense of their experiences.The use of terms with different meanings for patients and trialists (such as "trial") caused confusion, as did inaccuracies in patient information.Providing clear and accurate patient information is crucial, and patients need to be able to discuss their concerns about concepts such as randomisation if they are to give truly informed consent to participate in randomised controlled trials.
Correction: <i>Incidence rates of immune-related adverse events and their correlation with response in advanced solid tumours treated with NIVO or NIVO+IPI: a systematic review and meta-analysis</i>
Authors: Kenji Fujiwara, Hao Jing, Brian Herbst, MacKenzie Zarecki, Annie Wu, Elaine Bigelow, Keyu Li, Neolle Jurcak, Alex B Blair, Michael Wichroski, Jordan Blum, Nathan Cheadle, Jennifer Koenitzer
Journal: Journal for ImmunoTherapy of Cancer (2020)

Incidence rates of immune-related adverse events and their correlation with response in advanced solid tumours treated with NIVO or NIVO+IPI: a systematic review and meta-analysis', the author noticed that the second corresponding author was not designated in the article.
Society Proceedings
Journal: JAMA (1925)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Demanding dignity, and competence, in older people's care
Authors: None The Lancet
Journal: The Lancet (2012)

Picture a typical children's hospital in the UK: the walls are brightly painted; cheerful assistants are employed simply to entertain; a blood sample is skilfully extracted by two nurses in a choreographed procedure designed to distress the patient as little as possible. In other words, the focus is the patient and his or her needs as a child.
The changing epidemiology of invasive meningococcal disease in Canada, 1985 through 1992. Emergence of a virulent clone of Neisseria meningitidis
Authors: C. M. Whalen
Journal: JAMA (1995)

<h3>Objective.</h3> —To describe the occurrence of invasive meningococcal disease (IMD) in Canada with respect to demographic variables and characteristics of the isolated strains of<i>Neisseria meningitidis</i>. <h3>Design.</h3> —National surveillance case series. <h3>Setting.</h3> —Canada, 1985 through 1992. <h3>Outcome Measures.</h3> —Morbidity and mortality. <h3>Main Results.</h3> —The incidence of IMD averaged 1.38 per 100 000 person-years, with considerable regional variation. In 1988, serogroup C organisms became more common, with one strain of the electrophoretic type 37 (ET-37) complex of<i>N meningitidis</i>, termed ET-15, the predominant group C strain identified. With the increase in group C disease, a greater proportion of cases were older than 5 years. By 1991, ET-15 was the most common strain identified in most parts of the country. Electrophoretic type 15 had a case fatality of 17.8% vs 8.1% for all other IMD (<i>P</i>&lt;.001). Among cases 20 years and older the case fatality for ET-15 was 22.4%. <h3>Conclusions.</h3> —The group C, ET-15 strain of<i>N meningitidis</i>, first identified in Canada, was more virulent than other prevalent strains during this period. Active surveillance, rapid identification, and typing of<i>N meningitidis</i>will assist public health decision making in the control of emerging strains. (<i>JAMA</i>. 1995;273:390-394)
Clinical Implications of Prostaglandin and Thromboxane A<sub>2</sub>Formation
Authors: John A. Oates, Garret A. FitzGerald, Robert A. Branch, Edwin K. Jackson, Howard R. Knapp, L. Jackson Roberts
Journal: New England Journal of Medicine (1988)

(First of Two Parts)THE prostaglandins and thromboxane A2 are biologically active metabolites of arachidonic acid.1 , 2 Their actions and the pharmacologic agents that influence their formation affect almost every aspect of medical practice.The interactions of platelets with the vessel wall in catastrophic events in the coronary and cerebral arteries, as well as in diseases of smaller arterial vessels, have drawn attention to the participation of thromboxane A2 and prostacyclin (prostaglandin I2) in these pathophysiologic processes. Similarly, important medical consequences follow from the participation of prostaglandins in the pathophysiologic activities of the kidney, the mast cell, . . .