tbuckley/cabot-search huggingface dataset:
Re: Nader Al Nakouzi, Sylvestre Le Moulec, Laurence Albigès, et al. Cabazitaxel Remains Active in Patients Progressing After Docetaxel Followed by Novel Androgen Receptor Pathway Targeted Therapies. Eur Urol. In press. http://dx.doi.org/10.1016/j.eururo.2014.04.015
Authors: Robert J van Soest, Ronald de Wit, Wytske M van Weerden
Journal: European Urology (2014)
Errors in Data
Authors: Scott Fears
Journal: JAMA Psychiatry (2016)

Scott C. Fears, MD, PhD; Susan K. Service, MS; Barbara Kremeyer, PhD; Carmen Araya, Lic; Xinia Araya, Lic; Julio Bejarano, MS; Margarita Ramirez, Lic; Gabriel Castrillón, BSc; Juliana Gomez-Franco, MD; Maria C. Lopez, MSW; Gabriel Montoya, MD, MSc; Patricia Montoya, MA; Ileana Aldana, MPH; Terri M. Teshiba, BA; Zvart Abaryan, BSc; Noor B. Al-Sharif, BSc; Marissa Ericson, PhD; Maria Jalbrzikowski, PhD; Jurjen J. Luykx, MD, PhD; Linda Navarro, MS; Todd A. Tishler, PhD; Lori Altshuler, MD; George Bartzokis, MD; Javier Escobar, MD; David C. Glahn, PhD; Jorge Ospina-Duque, MD; Neil Risch, PhD; Andrés Ruiz-Linares, MD, PhD; Paul M. Thompson, PhD; Rita M. Cantor, PhD; Carlos Lopez-Jaramillo, MD, PhD; Gabriel Macaya, PhD; Julio Molina, MD; Victor I. Reus, MD; Chiara Sabatti, PhD; Nelson B. Freimer, MD; Carrie E. Bearden, PhD
Fitz-Hugh and Curtis syndrome in a man
Authors: G. L. Fung
Journal: JAMA (1981)

<h3>To the Editor.—</h3> With reference to the observation, "in a country with less than 10% literacy" made by Arneson and Hammerschmidt (1980;244:1139), I would like to point out that India's literacy is mentioned as, "total: 33.3%, male: 46.3%, female: 18.8%" in the new<i>Encyclopaedia Britannica, Micropaedia</i>, vol 10, p 983. The<i>Bri</i><i>tannica</i>mentions many countries, unfortunately, with less than 10% literacy. India is not one of them. I would assume that Arneson and Hammerschmidt have attempted to guess the figure unessential to their otherwise excellent photoessay
Abstract SY31-01: Development and validation of a clinical-grade cell-free DNA profiling assay: MSK-ACCESS
Authors: Dana Wai Yi Tsui
Journal: Cancer Research (2019)

Abstract Cell-free DNA profiling noninvasively reveals the underlying tumor genomic profiles to guide treatment decisions, especially important when the tumor is in a site that is difficult or risky to access. It has the potential to guide treatment stratification, monitor disease responses, identify resistance mechanisms and detection of minimal residual disease or relapse.Clinical implementation of molecular profiling assay requires the establishment of robust quality controls throughout the process including pre-analytical procedures, such as sample collection and processing, analytical steps such as molecular assay specification and bioinformatics algorithm, as well as data reporting. This talk will describe an academic institutional effort to develop and validate a clinical-grade cell-free DNA profiling assay for patient care. We will discuss considerations behind the development, including factors such as analytical sensitivity required for individual clinical applications, operational and logistical efficiency, regulatory requirement and clinical annotation to guide decisions. We will also present the validation studies required by the New York State Department of Health to demonstrate robustness of the assay before clinical deployment. The assay we have developed, called MSK-ACCESS (Analysis of Circulating cfDNA to Evaluate Somatic Status), is a custom next-generation sequencing assay covering selected exons from 129 cancer-related genes for ultra-sensitivity detection of somatic mutations from plasma. Using ultra-high depth (&amp;gt;15,000x) sequencing, with duplex unique molecular indexing (UMI), unique dual sample barcodes, and background error suppression, MSK-ACCESS is able to detect low-frequency (0.1%) variants with high confidence. We validated MSK-ACCESS using plasma samples collected from healthy non-cancer individuals and cancer patients with known mutations in selected genes of interest. We evaluated the analytical performance of the assays such as accuracy, intra- and inter-assay reproducibility using control samples and samples with known mutation data established by orthogonal assays. With the growing interest on cell-free DNA profiling for molecular diagnostics, it is crucial to ensure robustness of each assay to deliver high-quality data to guide decisions. Establishing analytical performance is the first step precedes large-scale prospective trials to further demonstrate clinical utility of cell-free DNA as a biomarker. Citation Format: Dana Wai Yi Tsui. Development and validation of a clinical-grade cell-free DNA profiling assay: MSK-ACCESS [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr SY31-01.
Formation and Fate of Gaseous and Particulate Mutagens and Carcinogens in Real and Simulated Atmospheres
Authors: James N. Pitts
Journal: Environmental Health Perspectives (1983)

The growing use of coal for heating and electric power generation and diesel engines in light duty motor vehicles will increase not only the existing atmospheric concentrations of criteria pollutants such as NO2, SO2, O3 and fine particulates, but also the concentrations of a number of highly reactive gaseous copollutants such as HONO, HONO2, PAN and the nitrate radical, NO3. These gaseous noncriteria pollutants are of interest not only because of their roles in the chemistry of the "clean" and polluted troposphere, including "acid rain," but also because they may pose health risks disproportionate to their relatively low ambient concentrations, and through complex heterogeneous reactions, they may serve as precursors or catalysts in the formation of "nonclassical" particulate mutagens and carcinogens such as certain nitroarenes associated with combustion generated particulate polycyclic organic matter (POM). Results of research efforts to establish current ambient levels of these noncriteria pollutants and to develop an understanding of their sources, formation and sinks are reported here. First, long pathlength (greater than or equal to 1 km) infrared and UV-visible spectroscopic studies of ambient levels of gaseous HONO, NO3, HONO2, PAN, HCHO and HCOOH in southern California atmospheres are described, and data given on their ambient concentrations. Second, an integrated chemical/microbiological investigation is described. It is directed toward identifying the nature of direct-acting mutagens found in extracts of diesel and ambient POM, as well as those formed upon exposure of environmentally relevant PAH to simulated natural and polluted atmospheres. The identification of certain of these mutagens, including a newly identified class of mutagenic PAH-lactones is discussed, along with the mechanisms of their formation and fate in the natural and polluted troposphere.
Treatment of malignant pericardial effusion
Authors: P. T. Vaitkus
Journal: JAMA (1994)

<h3>Objective.</h3> —To discuss the diagnosis and treatment of malignant pericardial Objective.—To fusion and focus on quantitating the success and complication rates of the many treatment modalities and updating recent advances in the field. <h3>Data Sources.</h3> —English-language publications were identified by a computerized search (MEDLINE) of these key words:<i>cancer, tumor, malignancy, pericardium</i>, and<i>pericardial effusion</i>. This computerized search was supplemented by a manual search of the bibliographies of original research articles and textbooks. <h3>Study Selection.</h3> —Studies were included if the outcome of patients undergoing treatment for malignant pericardial effusion was reported separately from the outcome of patients with other causes of pericardial effusions. Studies that only reported the combined results of patients with malignant and nonmalignant effusions were excluded. <h3>Data Extraction.</h3> —To determine success rates for the various treatment modalities, we examined freedom from symptomatic recurrence of pericardial effusion requiring reintervention as the key end point. Where appropriate, we also examined procedural mortality rates. <h3>Results.</h3> —Initial relief of symptoms is achieved in most cases with percutaneous pericardiocentesis that, with echocardiographic guidance, can be performed with low morbidity and mortality. In many cases, drainage for several days with an indwelling catheter alleviates the effusion without subsequent recurrence. Systemic antitumor therapy with chemotherapy or radiation therapy is effective in controlling malignant effusions in cases of sensitive tumors such as lymphomas, leukemias, and breast cancer. Local sclerotherapy with tetracycline hydrochloride or bleomycin sulfate is also effective and associated with low morbidity. Sclerotherapy with other agents or radionuclides offers no advantages. Of the several surgical options, subxiphoid pericardiotomy has the advantage of low morbidity and mortality, can often be performed under local anesthesia, and is highly effective in preventing recurrence. Percutaneous balloon pericardiotomy has recently been described. This intervention is performed with local anesthesia, is effective in preventing reaccumulation, and has a low morbidity. <h3>Conclusions.</h3> —Treatment of malignant pericardial effusions must be individualized with consideration given to the patient's condition and tumor type, the success rates and risks of the various modalities, and local availability and expertise. (<i>JAMA</i>. 1994;272:59-64)
FOOTBALL AND DEVELOPMENT.
Journal: JAMA (1900)

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
Abstract 2939: Developing new therapeutic strategy to bladder cancer by targeting CK1 delta
Authors: Yu-Chen Lin, Mei-chuan Chen, Jing-Ping Liou, Chun-Han Chen
Journal: Cancer Research (2019)

Abstract Bladder cancer is a common malignancy with high recurrent rate, but targeted therapy other than immune checkpoint inhibitors is currently unavailable. Hence, there is an unmet medical need for the discovery of new therapeutic approach to bladder cancer. By investigating Oncomine database, the mRNA level of CK1 delta is higher in bladder cancer compared to normal tissue, which correlates with survival rate. The aim of this study is to develop new CK1 delta inhibitors and examine their therapeutic potential to bladder cancer as well as the pharmacological mechanisms. Cell viability, cell cycle progression, apoptosis, migration and downstream signaling pathway were analyzed. The results showed that treatment of CK1 delta inhibitors decreased cell viability and inhibited wnt/β-catenin pathway in bladder cancer cell lines. CK1 delta inhibitors increased the accumulation of sub-G1 phase by flow cytometry analysis, as well as the activation of caspase-3, 8, 9 and PARP cleavage by western blot, indicating the promotion of cell apoptosis. Meanwhile, necroptosis was also involved as evident by the rescuing effects by knocking down MLKL in bladder cancer cells. In conclusion, this study demonstrates that CK1 delta is a potential target for bladder cancer therapy in the future. Note: This abstract was not presented at the meeting. Citation Format: Yu-Chen Lin, Mei-chuan Chen, Jing-Ping Liou, Chun-Han Chen. Developing new therapeutic strategy to bladder cancer by targeting CK1 delta [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 2939.
ALCOHOL IN THE NAVY.
Journal: JAMA (2007)

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
PARIS
Journal: JAMA (1924)

<h3>The Gabrilovitch Tuberculin</h3> In previous letters I have mentioned the exploitation of the Gabrilovitch tuberculin (phagolysin) as "a truly curative and specific remedy" for tuberculosis (The Journal, March 3, 1923, p. 640, and Jan. 26, 1924, p. 316). Recently Dr. Kresser presented to the Société de médecine of Paris a communication on this remedy in which he claimed that he had obtained 74.2 per cent, of clinical cures. Dr. Levassort has more recently suggested that all communications on the treatment of tuberculosis be submitted hereafter, before presentation, to a special commission for investigation. It would then be possible to avoid publishing communications that awaken hope which proves unfounded. In the meantime, Dr. Tilmant presented to the Société de médecine a number of documents that show the deceitful methods used to advertise the Gabrilovitch tuberculin. There appeared in the<i>Gazette des hôpitaux</i>, Jan. 6, 1923, an article entitled, "Is There an
Late recurrence (beyond ten years) of cutaneous malignant melanoma. Report of two cases and a review of the literature
Authors: H. K. Koh
Journal: JAMA (1984)

Two patients experienced a recurrence of cutaneous malignant melanoma more than ten years after initial diagnosis, treatment, and presumed cure. A review of the literature shows that delayed metastases (more than ten years) have been clearly documented in only seven previous patients with cutaneous malignant melanoma. With the rising incidence of cutaneous malignant melanoma, physicians may begin to see more cases of late recurrence in patients with a history of presumably cured disease. Although uncommon, late recurrence has important implications in the long-term management of all patients with malignant melanoma. (<i>JAMA</i>1984;251:1859-1862)
Raynaud's disease and scleroderma
Authors: O. Horwitz
Journal: JAMA (1979)

<h3>To the Editor.—</h3> I should like to take Orville Horwitz, MD, of Philadelphia, to task on one point that he made concerning Raynaud's disease in answering a question forThe Journal(184:85, 1963). I had occasion to read his response lately and was horrified to note the following: "Raynaud's disease itself is a nuisance rather than a serious condition and endangers neither life nor limb. It is, however, frequently a prelude to scleroderma (50% to 90% of the time, depending on whose series)." I feel certain that today's response would be: "Raynaud's disease is on rare occasions a prelude to scleroderma, but in the great majority of cases it is a mere transient phenomenon." Almost any general practitioner would have told this to Horwitz. The trouble was that most of the literature on Raynaud's disease at that time was written by academic surgeons who saw almost exclusively the most severe
Citrate Excretion in Renal Tubular Acidosis
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
Medication Error Made by Elderly Chronically Ill Patients
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
Probable cure of acute lymphocytic leukemia following relapses
Authors: P. G. Dyment
Journal: JAMA (1979)

THE TREATMENT of children with acute lymphocytic leukemia using current chemotherapy regimens along with radiotherapy and intrathecal chemotherapy for CNS prophylaxis has resulted in a large number of long-term survivors. Most of these patients continue in remission following cessation of three years or more of therapy.<sup>1</sup>However, these successfully treated patients have almost always been in continuous remission since their initial induction treatment at the time of diagnosis. Bone marrow or extramedullary relapse almost always heralds a series of recurrent relapses and progressively shorter remissions in children with acute lymphocytic leukemia. A child underwent both testicular and bone marrow relapse at different times and yet subsequently has become apparently cured of his disease. He has been free of all signs of acute lymphocytic leukemia for the 11 years since his last relapse, even though his antileukemic therapy was stopped six years ago. We hope this report will encourage physicians
Abstract 28: Dihydrolipoyl dehydrogenase is a key molecule inducing ferroptotic cell death
Authors: Jaewang Lee, Daiha Shin, Jong-Lyel Roh
Journal: Cancer Research (2019)

Abstract Ferroptosis is iron-dependent, non-apoptotic cell death from lipid peroxidation. Cystine-glutamate transporter (xCT) and glutathione peroxidase 4 (GPX4) are recognized as the key regulators of ferroptosis. Glutathione depletion via cystine deficiency or inhibition of xCT or GPX4 accumulates cellular lipid peroxidation and ferrous iron, resulting in ferroptosis. Glutamine is an amino acid essential for growth of cancer cells as well as induction of ferroptotic cell death via the production of alpha-ketoglutarate (αKG) from glutaminolysis. However, it is still unclear whether αKG or its relevant metabolic process is engaged in ferroptotic cell death. Therefore, we examined the role of αKG dehydrogenase (αKGDH) in induction of ferroptosis in head and neck cancer (HNC) cells. Cystine-deficient conditioned medium or xCT inhibition with sulfasalazine induced typical ferroptotic cell death, which was prevented by the inhibition of glutaminolysis or αKG production. Next, we focused the dihydrolipoyl dehydrogenase (DLD) and dihydrolipoyl succinyltransferase (DLST), consisting of the E3 and E2 components of αKGDH respectively. Ferroptosis was significantly prevented by genetic inhibition of the DLD but not the DLST, which was rescued by re-insertion of the DLD gene. Cellular reactive oxygen, lipid peroxidation, and ferrous iron accumulation were induced by the increased function of αKGDH, that is mainly the DLD, when αKG was converted to succinate in the tricarboxylic acid cycle. Sulfasalazine did not significantly suppress the in vivo growth of the shDLD-transfected HNC cells but vector control transplanted in nude mice. Taken together, our data support that the DLD is a key molecule inducing ferroptosis in cancer cells. Note: This abstract was not presented at the meeting. Citation Format: Jaewang Lee, Daiha Shin, Jong-Lyel Roh. Dihydrolipoyl dehydrogenase is a key molecule inducing ferroptotic cell death [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 28.