tbuckley/cabot-search huggingface dataset:
Variation in the Cost of Managing Actinic Keratosis
Authors: Joslyn S. Kirby, Tanner Gregory, Guodong Liu, Douglas L. Leslie, Jeffrey J. Miller
Journal: JAMA Dermatology (2017)

Actinic keratosis (AK), a skin growth induced by ultraviolet light exposure, requires chronic management because a small proportion can progress into squamous cell skin cancer. Spending for AK management was more than $1 billion in 2004. Investigating geographic variation in AK spending presents an opportunity to decrease waste or recoup excess spending.To evaluate geographic variation in health care cost for management of AKs and the association with patient-related and health-related factors.This retrospective cohort study was performed using data from the MarketScan medical claims database of 488 324 continuously enrolled members with 2 or more claims for AK. Data from January 1, 2008, to December 31, 2012, was used.Annual costs of care were calculated for outpatient visits, AK destruction, and medications for AKs, and the total of these components. Costs were adjusted for inflation to 2014 US dollars. To display cost variation, we calculated the ratio of mean cost in the highest quintile (Q5) relative to the mean in the lowest quintile (Q1), or the Q5:Q1 ratio; Q5:Q1 ratios were adjusted based on age, sex, history of nonmelanoma skin cancer, US geographic region, and population density (metropolitan statistical area).Overall, data from 488 324 continuously enrolled members (mean [SD] age, 53.1 [7.5] years; 243 662 women) with 2 or more claims for AK were included. Overall, patients had 1 085 985 claims related to AK, and dermatologists accounted for 71.0% of claims. The 2-year total cost was $111.5 million, with $52.4 million in 2011 and $59.1 million in 2012. The unadjusted Q5:Q1 ratios for total annual cost per patient ranged from 9.49 to 15.10. Adjusted ratios ranged from 1.72 to 1.80.There is variation in AK management cost within and between regions. This is not fully explained by differences in patient characteristics such as age, sex, or comorbidities. The annual cost for 10 common conditions from Medicare had lower Q5:Q1 ratios that ranged from 1.33 (joint degeneration of back/neck) to 1.69 (chronic sinusitis) when compared with 1.72 to 1.80 for AKs. This suggests an opportunity to investigate and improve the value of health care delivery in the management of AKs.
The burden of skin disease in the United States
Authors: Henry W. Lim, Scott A.B. Collins, Jack S. Resneck, Jean L. Bolognia, Julie A. Hodge, Thomas A. Rohrer, Marta J. Van Beek, David J. Margolis, Arthur J. Sober, Martin A. Weinstock, David R. Nerenz, Wendy Smith Begolka, Jose V. Moyano
Journal: Journal of the American Academy of Dermatology (2017)
Young Adults with Acute Lymphoblastic Leukemia (ALL) Treated with Adapted Augmented Berlin-Frankfurt-Munster (ABFM) Therapy
Authors: Michael Rytting, Deborah Thomas, Anna Franklin, William Wierda, Stefan Faderl, Farhad Ravandi, Brenda Muriera, Hagop M. Kantarjian, Susan O’Brien
Journal: Blood (2008)
Abstract P5-10-04: Spectrum of hereditary breast and ovarian cancer gene variants in an African American cohort
Authors: PD Shah, L Digiovanni, KN Maxwell, AR Bradbury, J Van Den Akker, S Kim, E Gil, MS Simon, KL Nathanson, SM Domchek
Journal: Cancer Research (2017)

Abstract Background: Few reports describe the spectrum of mutations in breast and ovarian cancer predisposition genes found specifically in African Americans. Methods: 560 women who self-identified as African American (AA) from the University of Pennsylvania and Wayne State University were included in this IRB-approved, case-control study. Cases (n=218 with a personal history of breast and/or ovarian cancer) and controls (n=342 without breast or ovarian cancer) underwent germline genetic testing using the Color Genomics 19-gene breast and ovarian cancer risk panel. The subset of AA patients diagnosed with breast cancer ≤40 (n=185) was compared to an institutional cohort of white patients with breast cancer diagnosed ≤40 (n=189). Results: Of 218 AA cases, 70 had pathogenic or likely pathogenic (P/LP) mutations (BRCA1: n=36; BRCA2: n=24; TP53: n=3; RAD51D: n=2; ATM: n=2; CHEK2: n=2 and MSH6: n=1). Forty-two of 218 patients (19%) had at least one variant of uncertain significance (VUS). Of 342 AA controls, 5 women had P mutations in 5 distinct genes: BRCA2, ATM, BRIP1, PALB2 and PMS2. 55 control patients (16%) had at least one VUS. Many of the 75 P/LP mutations (cases, 70 mutations; controls, 5 mutations) in the full AA cohort were unique variants. In the 135 patients who had BRCA1/BRCA2 sequencing prior to testing under this protocol, the Color Genomics platform identified all 56 pathogenic mutations. Among AA patients diagnosed with breast cancer ≤40 (n=185), the incidence of TP53 and ATM pathogenic mutations was similar to the white, early-onset breast cancer cohort (n=189): TP53, 1% in both cohorts; ATM = 1% in AA patients and 2% in whites. However, no patients in the AA, early-onset cohort had germline CHEK2 mutations, compared to 4% of white, early-onset breast cancer patients (p=0.007). Conclusions: Taken together, the results of this study demonstrate the importance of considering germline mutation testing in the AA population. Examination of mutations and disease phenotypes within the AA population may facilitate understanding of the clinical risk associated with variants of uncertain significance. Further comparative data between the AA and white cohorts will be presented. Citation Format: Shah PD, Digiovanni L, Maxwell KN, Bradbury AR, Van Den Akker J, Kim S, Gil E, Simon MS, Nathanson KL, Domchek SM. Spectrum of hereditary breast and ovarian cancer gene variants in an African American cohort [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P5-10-04.
Seven-Year Follow-up Data on Sequential Prospective Trials of Imatinib 400mg Vs 800mg Daily Schedule for Front-Line Treatment of Chronic Myeloid Leukemia (CML).
Authors: Naveen Pemmaraju, Hagop Kantarjian, Susan O'Brien, Srdan Verstovsek, Elias Jabbour, Alfonso Quintas-Cardama, Guillermo Garcia-Manero, Gautam Borthakur, Farhad Ravandi, Jianqin Shan, Jorge E. Cortes
Journal: Blood (2010)
Krüppel-like Transcription Factor KLF10 Suppresses TGFβ-Induced Epithelial-to-Mesenchymal Transition via a Negative Feedback Mechanism
Authors: Vivek Kumar Mishra, Malayannan Subramaniam, Vijayalakshmi Kari, Kevin S. Pitel, Simon J. Baumgart, Ryan M. Naylor, Sankari Nagarajan, Florian Wegwitz, Volker Ellenrieder, John R. Hawse, Steven A. Johnsen
Journal: Cancer Research (2017)

TGFβ-SMAD signaling exerts a contextual effect that suppresses malignant growth early in epithelial tumorigenesis but promotes metastasis at later stages. Longstanding challenges in resolving this functional dichotomy may uncover new strategies to treat advanced carcinomas. The Krüppel-like transcription factor, KLF10, is a pivotal effector of TGFβ/SMAD signaling that mediates antiproliferative effects of TGFβ. In this study, we show how KLF10 opposes the prometastatic effects of TGFβ by limiting its ability to induce epithelial-to-mesenchymal transition (EMT). KLF10 depletion accentuated induction of EMT as assessed by multiple metrics. KLF10 occupied GC-rich sequences in the promoter region of the EMT-promoting transcription factor SLUG/SNAI2, repressing its transcription by recruiting HDAC1 and licensing the removal of activating histone acetylation marks. In clinical specimens of lung adenocarcinoma, low KLF10 expression associated with decreased patient survival, consistent with a pivotal role for KLF10 in distinguishing the antiproliferative versus prometastatic functions of TGFβ. Our results establish that KLF10 functions to suppress TGFβ-induced EMT, establishing a molecular basis for the dichotomy of TGFβ function during tumor progression. Cancer Res; 77(9); 2387-400. ©2017 AACR.
Antitumor Activity of Amphibian Ribonucleases, Onconase and R-Amhinase, on Tumor Cells From B-Cell Lymphoproliferative Disorders
Authors: Piotr Smolewski, Malgorzata Zwoliñska, Barbara Cebula-Obrzut, Agata Majchrzak, Malgorzata Misiewicz, Aleksandra Jeske, Zbigniew Darzynkiewicz, Wojciech Ardelt, Barbara Ardelt, Shailendra K Saxena, Charles Muniz, Tadeusz Robak
Journal: Blood (2010)
Hospital readmission after surgical cytoreduction for epithelial ovarian carcinoma: An assessment of risk.
Authors: Rachel Marie Clark, Whitfield Board Growdon, Andrew Wiechert, Marcela G del Carmen, Annekathryn Goodman, David M. Boruta, Leslie Bradford, Leslie A. Garrett, John O. Schorge
Journal: Journal of Clinical Oncology (2012)

e15545 Background: Hospital readmissions are common, possibly avoidable, and may be used as a metric for assessing an institution’s quality of care. We performed a retrospective analysis to determine risk factors associated with readmission after ovarian cancer cytoreduction surgery. Methods: We identified all patients with stage II-IV ovarian cancer who underwent cytoreduction at our institution between 2003-2011. A retrospective chart review was performed and clinical variables extracted. Utilizing linear and logistic regression these variables were correlated with risk of readmission. Results: A total of 463 patients were included in the analysis. Average age was 62 years. Median length of stay was 8.6 days (range 2-55). Optimal cytoreduction (&lt;1.0cm residual disease) was obtained in 368 patients (81%) and 233 patients (50%) underwent bowel resection or radical upper abdominal procedure (splenectomy, liver resection, diaphragmatic surgery). Perioperative complications were observed in 148 patients (32%). A large proportion of our cohort was discharged to rehabilitation facilities (12%) or with a visiting nurse (38%). Of the entire cohort, 55 (12%) were readmitted within 30 days. Readmission was significantly associated with increased length of stay (OR 1.05, 95% 1.01 – 1.1) and perioperative complications (OR 3.5, 95% 2.0 – 6.3). Radical surgery was associated with an increased length of stay (p &lt;0.001) but not with readmission (p = 0.8). Multivariate logistic regression revealed that complications were the only independent factor associated with readmission (OR 3.2, 95% 1.7- 6.0). Further multivariate analysis revealed that reoperation was associated with the greatest risk (OR 8.4, 95% 3.3 -21.1) of readmission. Conclusions: Readmission after ovarian cancer cytoreduction affected 12% of our population. While perioperative complications and increased length of stay were associated with an increased risk of readmission, multivariate analyses suggested that perioperative complications, specifically reoperation, placed the patient at the greatest risk. Comorbidities, radical surgery and the use of ancillary/rehabilitation services had no significant effects on the risk of readmission.
Non-invasive prenatal screening should be banned for sex selection, says ethics report
Authors: Anne Gulland
Journal: BMJ (2017)

Testing a fetus to determine its sex should be banned, and the marketing practices of manufacturers and private companies offering the tests should be more closely monitored, a report has recommended.1

The Nuffield Council on Bioethics’ report on non-invasive prenatal screening (NIPT), a method of testing for genetic conditions by taking a blood sample from the mother at nine or 10 weeks of pregnancy, said that sex determination should not be offered unless it is being used to diagnose a medical condition. The tests are carried out by private sector providers, and some evidence shows that sex selective terminations do occur in the UK, the report said.

A consultation by the council found that many respondents thought that sex selection was “sexist and wrong.” …
Erratum to: Metastatic Merkel cell carcinoma response to nivolumab
Authors: Frances M. Walocko, Benjamin Y. Scheier, Paul W. Harms, Leslie A. Fecher, Christopher D. Lao
Journal: Journal for ImmunoTherapy of Cancer (2017)

Following publication of this article [[1][1]], it was noticed that the Clinical Trial Number in the last paragraph of the conclusions section was incorrectly listed as [NCT02155647][2]. The correct Clinical Trials Number is [NCT02488759][3]. 1. 1.[↵][4]1. 2. Walocko FM , 3.
Prostate Cancer, Version 2.2014
Authors: James L. Mohler, Philip W. Kantoff, Andrew J. Armstrong, Robert R. Bahnson, Michael Cohen, Anthony Victor D’Amico, James A. Eastham, Charles A. Enke, Thomas A. Farrington, Celestia S. Higano, Eric Mark Horwitz, Christopher J. Kane, Mark H. Kawachi, Michael Kuettel, Timothy M. Kuzel, Richard J. Lee, Arnold W. Malcolm, David Miller, Elizabeth R. Plimack, Julio M. Pow-Sang, David Raben, Sylvia Richey, Mack Roach, Eric Rohren, Stan Rosenfeld, Edward Schaeffer, Eric J. Small, Guru Sonpavde, Sandy Srinivas, Cy Stein, Seth A. Strope, Jonathan Tward, Dorothy A. Shead, Maria Ho
Journal: Journal of the National Comprehensive Cancer Network (2014)

Prostate cancer has surpassed lung cancer as the most common cancer in men in the United States. The NCCN Guidelines for Prostate Cancer provide multidisciplinary recommendations on the clinical management of patients with prostate cancer based on clinical evidence and expert consensus. NCCN Panel guidance on treatment decisions for patients with localized disease is represented in this version. Significant updates for early disease include distinction between active surveillance and observation, a new section on principles of imaging, and revisions to radiation recommendations. The full version of these guidelines, including treatment of patients with advanced disease, can be found online at the NCCN website.
Incidence and Outcome in Aplastic Anemia Diagnosed 2000-2011 - a Nationwide Swedish Registry Study
Authors: Krista Vaht, Magnus Göransson, Kristina Carlson, Cecilia Isaksson, Stig Lenhoff, Anna Sandstedt, Bertil Uggla, Per T. Ljungman, Mats Brune, Per-Ola Andersson
Journal: Blood (2016)
Final Results of the BP22333 Study Demonstrate Non-Inferior Pharmacokinetics (PK) and Safety of Subcutaneous (SC) Administration of Rituximab Compared with Intravenous (IV) Administration As Maintenance Therapy in Patients with Follicular Lymphoma (FL)
Authors: Antonio Salar, Irit Avivi, Jean-Francois Larouche, Andrea Janikova, Juliana Pereira, Mike Brewster, Olivier Catalani, Christine McIntyre, Pakeeza Sayyed, Andrew Haynes
Journal: Blood (2012)
Mesothelin/mucin 16 signaling in activated portal fibroblasts regulates cholestatic liver fibrosis
Authors: Yukinori Koyama, Ping Wang, Shuang Liang, Keiko Iwaisako, Xiao Liu, Jun Xu, Mingjun Zhang, Mengxi Sun, Min Cong, Daniel Karin, Kojiro Taura, Chris Benner, Sven Heinz, Tapan Bera, David A. Brenner, Tatiana Kisseleva
Journal: Journal of Clinical Investigation (2017)

Cholestatic liver fibrosis is caused by obstruction of the biliary tract and is associated with early activation of portal fibroblasts (PFs) that express Thy-1, fibulin 2, and the recently identified marker mesothelin (MSLN). Here, we have demonstrated that activated PFs (aPFs) and myofibroblasts play a critical role in the pathogenesis of liver fibrosis induced by bile duct ligation (BDL). Conditional ablation of MSLN+ aPFs in BDL-injured mice attenuated liver fibrosis by approximately 50%. Similar results were observed in MSLN-deficient mice (Msln-/- mice) or mice deficient in the MSLN ligand mucin 16 (Muc16-/- mice). In vitro analysis revealed that MSLN regulates TGF-β1-inducible activation of WT PFs by disrupting the formation of an inhibitory Thy-1-TGFβRI complex. MSLN also facilitated the FGF-mediated proliferation of WT aPFs. Therapeutic administration of anti-MSLN-blocking Abs attenuated BDL-induced fibrosis in WT mice. Liver specimens from patients with cholestatic liver fibrosis had increased numbers of MSLN+ aPFs/myofibroblasts, suggesting that MSLN may be a potential target for antifibrotic therapy.
Sp1 Transcription Factor as a Novel Therapeutic Target in Multiple Myeloma (MM)
Authors: Mariateresa Fulciniti, Pierfrancesco Tassone, Teru Hideshima, Puru Nanjappa, Klaus Podar, Sophia Adamia, Samir B Amin, Rao Prabhala, Rocio Lopez, Kenneth C. Anderson, Nikhil C. Munshi
Journal: Blood (2008)
An Acquired <i>HER2</i> T798I Gatekeeper Mutation Induces Resistance to Neratinib in a Patient with HER2 Mutant–Driven Breast Cancer
Authors: Ariella B. Hanker, Monica Red Brewer, Jonathan H. Sheehan, James P. Koch, Gregory R. Sliwoski, Rebecca Nagy, Richard Lanman, Michael F. Berger, David M. Hyman, David B. Solit, Jie He, Vincent Miller, Richard E. Cutler, Alshad S. Lalani, Darren Cross, Christine M. Lovly, Jens Meiler, Carlos L. Arteaga
Journal: Cancer Discovery (2017)

Abstract We report a HER2T798I gatekeeper mutation in a patient with HER2L869R-mutant breast cancer with acquired resistance to neratinib. Laboratory studies suggested that HER2L869R is a neratinib-sensitive, gain-of-function mutation that upon dimerization with mutant HER3E928G, also present in the breast cancer, amplifies HER2 signaling. The patient was treated with neratinib and exhibited a sustained partial response. Upon clinical progression, HER2T798I was detected in plasma tumor cell-free DNA. Structural modeling of this acquired mutation suggested that the increased bulk of isoleucine in HER2T798I reduces neratinib binding. Neratinib blocked HER2-mediated signaling and growth in cells expressing HER2L869R but not HER2L869R/T798I. In contrast, afatinib and the osimertinib metabolite AZ5104 strongly suppressed HER2L869R/T798I-induced signaling and cell growth. Acquisition of HER2T798I upon development of resistance to neratinib in a breast cancer with an initial activating HER2 mutation suggests HER2L869R is a driver mutation. HER2T798I-mediated neratinib resistance may be overcome by other irreversible HER2 inhibitors like afatinib. Significance: We found an acquired HER2 gatekeeper mutation in a patient with HER2-mutant breast cancer upon clinical progression on neratinib. We speculate that HER2T798I may arise as a secondary mutation following response to effective HER2 tyrosine kinase inhibitors (TKI) in other cancers with HER2-activating mutations. This resistance may be overcome by other irreversible HER2 TKIs, such as afatinib. Cancer Discov; 7(6); 575–85. ©2017 AACR. This article is highlighted in the In This Issue feature, p. 539
Improving Lower Extremity Functioning in Peripheral Artery Disease
Authors: Mary McGrae McDermott, Melina R. Kibbe
Journal: JAMA (2017)

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
<i>Notes from the Field: </i>An Outbreak of<i> Salmonella </i>Typhimurium Associated with Playground Sand in a Preschool Setting — Madrid, Spain, September–October 2016
Authors: Carmen Olmedo Lucerón, Ana Pérez Meixeira, Isabel Abad Sanz, Victoria Cid Deleyto, Silvia Herrera León, Leonor Gutierrez Ruiz
Journal: MMWR Morbidity and Mortality Weekly Report (2017)
Phase II study of arsenic trioxide and temozolomide in combination with radiation therapy in patients with malignant gliomas.
Authors: Priya Kumthekar, Sean Aaron Grimm, MaryAnne H. Marymont, Minesh P. Mehta, James Chandler, Kenji Muro, Borko Jovanovic, Irene B. Helenowski, Katie McCarthy, Jeffrey J. Raizer
Journal: Journal of Clinical Oncology (2014)

2072 Background: Current standard treatment for GBM is radiation (RT) and temozolomide (TMZ). We published phase I data of the addition of arsenic trioxide (ATO) to RT and TMZ. We now present the phase II data. Methods: Patients with newly diagnosed malignant gliomas were eligible for treatment in this single arm phase II. Patients were treated with RT (60GY), TMZ (75 mg/m2 daily x 42 days) and ATO 0.20 mg/kg daily in week 1 then twice a week x 5 weeks. Results: Twenty-five patients (14 M and 11 W) were enrolled with a median age of 56 (28-73). Histology was GBM 18, AA 6 and AO 1. All patients completed RT/TMZ/ATO. Median number of post RT cycles of TMZ was 3 (0-12); 9 patients completed 6 or more cycles. Median PFS was 6 m for GBM and 15 m for AG and median OS was 15 m for GBM and NR for AA. Response was SD in 20, PR in 1 and PD in 4. Conclusions: Adding ATO to RT and TMZ is feasible and tolerable but does not appear to improve outcome compared to RTOG 0525 data where OS is 16.6 months in newly diagnosed GBM. Tissue MGMT status is being analyzed. Clinical trial information: NCT00275067.