tbuckley/cabot-search huggingface dataset:
Abstract 3254: A novel TGFβRI inhibitor suppresses tumor progression by increasing T-cell infiltration into tumor
Authors: Xu Zusheng, Yangtong Lou, Qiang Zhao, Wei Wang
Journal: Cancer Research (2019)

Abstract TGF-beta (TGF-β) pathways, despite serving as tumor suppressor in early stage of carcinogenesis, have shown to be one of the key tumor-promoting factors in later-stage tumor progression. TGF-β receptor type 1 (TGFβRI) inhibitors have shown great potentials in their anti-tumor and anti-metastasis efficacy in preclinical studies and some of them are being tested in the clinical settings. A specific TGFβRI inhibitor YL-13027 was developed at Yingli Pharmaceutical. Our previous data have shown that YL-13027 significantly inhibited the T cell differentiation into Treg and the secretion of IL-10 in vitro, as well as tumor growth in immune-competent mice with CT26 tumors. Our further studies indicated that the anti-tumor efficacy of YL-13027 was largely mediated by T cells. More importantly, YL-13027 synergistically enhanced the anti-tumor efficacy of anti-PD-L1 antibody in CT26 model. YL-13027 displayed significant anti-tumor efficacy in other syngeneic mouse tumor models tested including orthotopic murine breast carcinoma 4T1 model in BALB/c mice and murine hepatocellular carcinoma Hepa1-6 model in C57BL/6 mice. YL-13027 is well tolerated by the animals with no treatment-related toxicity observed in these efficacy studies. Analyses of tumors treated with YL-13027 revealed that YL-13027 significantly increased the number of tumor-infiltrating lymphocytes in tumors. These data suggest that YL-13027, a novel TGFβRI inhibitor, represents a promising and safe immune modulator and shows great potential as a cancer immuno-therapeutics. Citation Format: Xu Zusheng, Yangtong Lou, Qiang Zhao, Wei Wang. A novel TGFβRI inhibitor suppresses tumor progression by increasing T-cell infiltration into tumor [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 3254.
Glycohydrolases as markers of hepatic ischemia-reperfusion injury and recovery
Authors: W Liu
Journal: Hepatology (1996)

Advances in liver surgery and transplantation have lead to a steady increase in the number of these interventions. Prompt quantitative assessment of hepatic of hepatic function and a patient's subsequent morbidity and mortality following surgery remain difficult despite the currently utilized historic markers of hepatic parenchymal injury (e.g., aspartate transaminase [AST], lactate dehydrogenase [LDH] γ-glutamyl transpeptidase [GGT]). Increases in serum glycohydrolase activities appear to provide sensitive and quantitative markers of hepatic ischemia/reperfusion injury. In 10 male swine (25 to 35 kg body weight) following 30, 45, and 90 minutes of acute hepatic ischemia, the systemic release of eight different glycohydrolases and lipid peroxides into serum were determined and compared with pre- and postischemic serum levels of LDH, GGT, and AST. The rapid release of glycohydrolases into serum was directly proportional to the length of the ischemic period from 30 to 90 minutes; e.g., β-glucosidase, mean 1.9-fold increase at 30 minutes; 8.3-fold at 45 minutes; and 22.8-fold at 90 minutes; P < .002 and the activities peaked within the first 3 hours postischemia. In constrast, AST, LDH, and GGT were released slowly and peaked 20 to 30 hours after hepatic blood flow was restored. In swine with fatal outcomes (90 minutes of ischemia), all enzyme levels increased continuously during the final hours of life. However, in swine that survived hepatic ischemia/reperfusion injury (45 minutes of ischemia) the glycohydrolases, but not AST, LDH, and GGT, declined after 2 to 3 hours postischemia and the serum lipid peroxide levels followed the same pattern. Serum β-galactosidase and β-glucosidase levels are sensitive markers that rise as quickly as traditional enzyme markers (AST, LDH, GGT) following hepatic ischemic injury; moreover, the glycohydrolases have the added value of serving as predictors of survival.
Anticoagulants During Pregnancy
Authors: J. Ginsberg
Journal: Annual Review of Medicine (1989)

Anticoagulant therapy during pregnancy is problematic because both heparin and oral anticoagulants can potentially produce adverse maternal and fetal effects. Reviewing the relevant literature makes it clear that heparin is safer for the fetus than are oral anticoagulants. For the prophylaxis and treatment of venous thromboembolic disease in pregnant patients, heparin is the preferred anticoagulant because its efficacy and safety are established. However, because the efficacy of heparin in preventing systemic embolism in patients with prosthetic heart valves is not established, either adjusted-dose heparin or a combination of heparin and oral anticoagulants can be used.
The Spider
Authors: Kevin Kuntz
Journal: JAMA (1988)

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
Trends in the use of administrative databases in urologic oncology: 2000 – 2019.
Authors: Zev Leopold, Priya Dave, Adarsh Menon, Hiren V. Patel, Arnav Srivastava, Isaac Yi Kim, Thomas L Jang, Eric A. Singer
Journal: Journal of Clinical Oncology (2021)

356 Background: Administrative databases (AD) provide investigators with nationally representative study populations to answer research questions using large sample sizes. We aimed to quantify the trends and incidence of AD use in published manuscripts in urologic oncology. We examined six commonly used databases: National Cancer Database (NCDB), Surveillance, Epidemiology and End Results Database (SEER), SEER-Medicare (SEER-M), Nationwide Inpatient Sample (NIS), National Surgical Quality Improvement Program (NSQIP), and Premier Healthcare Database (PHD). Methods: A literature review powered by PubMed and DistillerSR from 7/1/2000 to 6/30/2019 aggregated manuscripts that used the aforementioned databases to study a genitourinary malignancy. Included publications were categorized by database used, corresponding author department affiliation, organ, journal, year, and contribution – defined as temporal treatment trends, outcomes and survival, comparative effectiveness research, or cost-effectiveness. Results: There were 2,265 publications across 302 journals that met the inclusion criteria. Between 2000 and 2019 the compound annual growth rate of these publications was 18.7%. SEER contributed most heavily over the study period, with a 14.6% growth rate. NCDB use grew 75.6% annually starting in 2012. Prostate cancer comprised the majority of publications (51.3%), followed by kidney (23.1%) and bladder (22.5%) cancer. Journals publishing these manuscripts had a median impact factor of 3.28 (IQR = 1.84 – 5.74) in 2019. Urologists published 52.5% of AD manuscripts over the study period. Conclusions: Our results show substantial growth in the use of ADs for the study of urologic oncology. Given the broad use of ADs, investigators and specialty societies should advocate for continued improvement in the data captured by them.
A phase 2 randomized, double-blind, placebo-controlled trial of hormone therapy (HT) ± radium-223 dichloride (Ra-223) in HER2<sup>-</sup> hormone receptor<sup>+</sup> breast cancer patients (pts) with bone metastases (mets).
Authors: Robert E. Coleman, Liping Huang, Oana Petrenciuc, Paola Zaccarini
Journal: Journal of Clinical Oncology (2015)

TPS1104 Background: Treatment of bone-metastatic breast cancer (MBC) is limited. Multimodality therapy may improve symptom control and survival. In a phase 2a study of advanced breast cancer pts with bone-dominant and no visceral disease, Ra-223, a first-in-class α-emitter selectively targeting bone mets, reduced baseline bone biomarker levels with favorable safety (Coleman et al. Breast Cancer Res Treat 2014). This study (NCT02258464) evaluates Ra-223 efficacy and safety vs placebo (pbo) in HER2- hormone receptor+ breast cancer pts with bone mets receiving single-agent HT. Methods: Pts receive (1:1) Ra-223 50 kBq/kg IV or pbo q 4 wk (6 cycles) + concurrent single-agent HT + best supportive care. Stratification is by geographic region, prior lines of HT for MBC, and number of prior skeletal events. Pts are assessed for efficacy and safety, and followed to symptomatic skeletal event (SSE), radiologic progression, death, or withdrawal. Primary endpoint is SSE-free survival. Eligible pts are pre- or postmenopausal with estrogen receptor+, HER2-, bone-dominant MBC with ≥ 2 bone mets and ≥ 1 or 2 prior SSEs (external beam radiotherapy for bone pain, pathologic bone fracture, spinal cord compression, orthopedic surgery). Pts had ≥ 1 line of HT for MBC; are taking bisphosphonates or denosumab for ≥ 1 month before study; are eligible for endocrine treatment; and have evaluable disease (RECIST 1.1), asymptomatic or mildly symptomatic bone disease (Brief Pain Inventory), ECOG score 0-1, and adequate hematologic, renal, and liver function. Pts may not have had visceral or brain mets or leptomeningeal disease, need for chemotherapy for mets, and untreated spinal cord compression. Assuming a 1-sided α of 0.1, power of 90%, ~ 119 SSEs are required for the analysis. Time-to-event variable analysis will use a log-rank test, accounting for stratification. Kaplan-Meier estimates and survival curves will be given for each treatment group. Safety analyses will be descriptive. Target enrollment is 227 pts. First pt first visit is expected in early 2015. Clinical trial information: NCT02258464.
<i>Taenia solium</i>
Authors: Cyriac A Philips, Amrish Sahney
Journal: New England Journal of Medicine (2017)

A 48-year-old man presented with abdominal discomfort and lethargy. Examination revealed pallor, and laboratory studies showed mild anemia. Colonoscopy revealed a proglottid from a tapeworm, shown in a video, in the rectosigmoid colon.
Update: Influenza Activity—United States and Worldwide, 1999-2000 Season, and Composition of the 2000-2001 Influenza Vaccine
Journal: JAMA (2000)

To monitor influenza activity and to detect antigenic changes in the circulating strains of influenza viruses, CDC conducts surveillance in collaboration with the World Health Organization (WHO) and its international network of collaborating laboratories and with state and local health departments in the United States. This report summarizes surveillance for influenza in the United States and worldwide during the 1995-96 season and describes the composition of the 1996-97 influenza vaccine.
Annual Scientific Meeting of the American Society of Cytology
Journal: JNCI Journal of the National Cancer Institute (1985)

Journal Article Annual Scientific Meeting of the American Society of Cytology Get access JNCI: Journal of the National Cancer Institute, Volume 74, Issue 6, June 1985, Page 1365, https://doi.org/10.1093/jnci/74.6.1365-b Published: 01 June 1985
The coronary care unit. New perspectives and directions
Authors: B. Lown
Journal: JAMA (1967)

In the past two decades there have been momentous advances in the care of patients with cardiovascular ailments. Yet, mortality from coronary-artery disease has remained unaffected. Year after year myocardial infarction and its complications exact the highest toll of any single disease.<sup>1</sup>In large metropolitan hospitals, the death rate from this condition 30 years ago ranged from 30% to 40% and remains unaltered today. Certain facts are forcing reevaluation of the problem. Peak mortality occurs at the very onset of myocardial infarction and then recedes almost exponentially, with 65% of deaths occurring in the initial three days and 85% during the first week of attack. Arrhythmias probably account for 40% of deaths. Of these about two thirds are due to ventricular fibrillation and one third to bradycardia, heart block, and asystole.<sup>2</sup>It is well established that these electrical catastrophes are usually not due to irreversible cardiac damage. On
Discontinuance of cigarette smoking: "natural" and with "therapy". A ten-week and ten-month follow-up study of 298 adult participants in a five-day plan to stop smoking
Authors: D. S. Thompson
Journal: JAMA (1966)

Two hundred and ninety-eight cigarette smokers attended the first session of the Five Day Plan to Stop Smoking; 201 of them also attended the fifth session. Of the latter group, 146 (72.6%) had not smoked a cigarette during the preceding 24 hours. Ten weeks after the plan, 287 of the 298 original participants were contacted by telephone: 84 (29.4%) had not smoked a cigarette during the preceding seven days. Ten months after the plan, 49 participants from a previously selected subgroup of 50 who attended the first and fifth sessions were contacted by telephone: 41 were still smoking cigarettes but eight (16%) had not smoked a cigarette since the plan ended. The "therapeutic success" rate of the plan (discontinuance of cigarette smoking ten months after the plan) was 16%.
HOSPITALS MAINTAINED BY NATIONAL, STATE AND LOCAL GOVERNMENTS
Journal: JAMA (1926)

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
CHLOROMA, OR GREEN TUMORS.
Journal: JAMA (1903)

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 1780: iSCREAM - an unbiased pipeline to screen for activating kinase mutations
Authors: Deepankar Chakroborty, Kari J. Kurppa, Ilkka Paatero, Laura L. Elo, Klaus Elenius
Journal: Cancer Research (2019)

Abstract Cancer tissues harbor thousands of mutations, and a given oncogene may be mutated at hundreds of sites. Most of these somatic mutations are expected to be inconsequential passenger mutations that reflect the general instability of the tumors. The discovery of most of the currently known driver mutations has been facilitated by their accumulation in mutation hot-spots within their respective genes. However, a vast majority of mutations in cancer tissues are rare and no information is currently available about their functional significance. Several lines of in vitro and in vivo clinical evidence also indicate that there is a significant number of, as yet unidentified, activating driver mutations that could serve as predictive markers in oncology. An unbiased iSCREAM (in vitro screen for activating mutations) platform was developed to functionally characterize thousands of variants of a kinase oncogene in a single assay. The functional genetics screen was based on expressing random variants of a cDNA encoding a tyrosine kinase in a cell line in which the activating mutations provide growth-advantage. Targeted next-generation sequencing of the cDNA inserts was used to quantitatively analyze variants that provided growth-advantage. iSCREAM is able to identify activating mutations from a library of thousands of random mutations of a tyrosine kinase. The pipeline can also be modified to identify mutations conferring resistance to a tyrosine kinase inhibitor. Citation Format: Deepankar Chakroborty, Kari J. Kurppa, Ilkka Paatero, Laura L. Elo, Klaus Elenius. iSCREAM - an unbiased pipeline to screen for activating kinase mutations [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 1780.
Abstract 95: Synthetic essentiality of chromatin remodeling factor CHD1 in PTEN deficient cancer
Authors: Di Zhao
Journal: Cancer Research (2019)

Abstract Prostate cancer (PCa) is one of the most common cancer types in mem. Advanced PCa, especially metastatic castration resistant prostate cancer (mCRPC), has high morbidity and mortality. ~50% advanced PCa shows PTEN deletion or mutation, therefore, identification of specific therapeutic targets for PCa harboring PTEN deficiency holds hope for patients with advanced PCa. Taking advantage of the vast public available prostate cancer genome database, we recently explored a novel approach to identify potential therapeutic targets by screening for “synthetic essential” genes that were occasionally deleted in cancer but always retained in the context of tumor suppressor gene deficiency. Using this method, we identified the chromodomain-helicase-DNA-binding protein 1 (CHD1) as a synthetic essential gene in PTEN-deficient PCa. Both human PCa xenograft models and genetically engineered PCa mouse models suggested that depletion of CHD1 suppresses the tumor growth and progression of PTEN-deficient PCa, but has minimal effects on normal prostate tissue or PTEN-intact PCa. Importantly, CHD1 inhibition leads to a significantly prolonged overall survival in PTEN-loss PCa mouse model. Mechanistically, we found that PTEN-PI3K-AKT-GSK3βpathway regulates CHD1 phosphorylation, followed by ubiquitination and degradation via β-TrCP mediated proteasome pathway. The ChIP-seq and transcriptional profiling analyses uncovered that, in PCa with PTEN loss, CHD1 is stabilized and interacts with epigenetic marker H3K4me3, resulting in the transcriptional activation of NF-κB network genes. Furthermore, immunophenotyping using Mass Cytometry (CyTOF) and functional validation suggested that CHD1 contributes to the immunosuppressive tumor microenvironment in PCa through stimulating the expansion and activation of myeloid-derived suppressor cell (MDSCs) and reducing tumor-infiltrating CD8+ T-cells. Together, this study demonstrated that CHD1 plays important roles in tumor initiation and progression of PTEN-deficient PCa, and presents a promising context-specific therapeutic target in PCa. In addition, the novel approach of “synthetic essentiality” we proposed provides a good tool to identify context-specific therapeutic targets for undruggable tumor suppressor deficiency in cancer genome. Citation Format: Di Zhao. Synthetic essentiality of chromatin remodeling factor CHD1 in PTEN deficient cancer [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 95.
Twentieth Century Practice. An International Encyclopedia of Modern Medical Science. By leading authorities of Europe and America.
Journal: JAMA (1895)

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
The Guarantee
Authors: CARL SPIVACK
Journal: Annals of Internal Medicine (1980)

Ad Libitum1 December 1980The GuaranteeCARL SPIVACK, M.D.CARL SPIVACK, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-93-6-930 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptOn the night before surgery, as the patient lay in bed, the surgeon came to his side. "Tomorrow we shall remove one breast," the surgeon said. "We shall sever and excise it, and when this is done the disease that oppresses you will be cured. This is what the operation will accomplish."The patient looked at his breast. He nodded. He said to the surgeon, "And then the disease will be ended, and then I shall be cured. Is that not so?" "Yes," the surgeon replied. "One breast must be sacrificed for the body to be reprieved. We shall sacrifice... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: CARL SPIVACK, M.D.Affiliations: NEW YORK, NEW YORK PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTP 1 December 1980Volume 93, Issue 6Page: 930-930KeywordsSurgeonsSurgery ePublished: 1 December 2008 Issue Published: 1 December 1980 PDF downloadLoading ...