tbuckley/cabot-search huggingface dataset:
Annals Story Slam - How to Treat Blue Waffle Disease
Authors: Anita Ravi
Journal: Annals of Internal Medicine (2017)

Web Exclusives7 March 2017Annals On Being a Doctor Story Slam - How to Treat Blue Waffle DiseaseFREEAnita Ravi, MD, MPHAnita Ravi, MD, MPHFrom University of Pennsylvania, Philadelphia, Pennsylvania.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/W17-0027 SectionsAboutVisual Abstract ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Video. Annals Story Slam - How to Treat Blue Waffle Disease "How to Treat Blue Waffle Disease," by Dr. Anita Ravi (Duration 8:09)Building on the popular Annals feature “On Being a Doctor,” storytellers share stories about the experience of doctoring on video.For more videos from and information on Annals Story Slam, visit go.annals.org/StorySlam. Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAffiliations: From University of Pennsylvania, Philadelphia, Pennsylvania.Current Author Address: Anita Ravi, MD, MPH; e-mail, [email protected]com. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 7 March 2017Volume 166, Issue 5Page: SS1 ePublished: 7 March 2017 Issue Published: 7 March 2017 Copyright & PermissionsCopyright © 2017 by American College of Physicians. All Rights Reserved.Loading ...
Establishment and characterization of androgen-independent human prostate cancer cell lines, LN-REC4 and LNCaP-SF, from LNCaP
Authors: Atsushi Mizokami, Yoichi Iwasa, Kazutaka Narimoto, Mikio Namiki, Evan Keller
Journal: Cancer Research (2007)

1004   Aim: To investigate the mechanisms of androgen-independent growth in prostate cancer (PCa), we established two PCa cell lines, LN-REC4 and LNCaP-SF, from the androgen-dependent PCa cell line, LNCaP.  Materials and methods: LN-Pre and LN-REC4 cells were generated from LNCaP tumors grown on intact and castrated scid mouse, respectively. After we cultured LNCaP cells under a steroid-free conditions for 6 months in vitro, LNCaP-SF cells were established. To show the character of LN-REC4 and LNCaP-SF cells, androgen sensitivity was investigated through examination of growth rate, and prostate-specific antigen (PSA), androgen receptor (AR), p21, p27, and cyclin D1 expression were examined by reverse transcription-polymerase chain reaction (RT-PCR). Angiogenesis assay in vitro was carried out using conditioned medium. To examine the expression level of vascular endothelial growth factor (VEGF), RT-PCR and enzyme-linked immunosorbent assay were also done. We also carried out cDNA microarray analysis to compare the differential expression between LNCaP and LNCaP-SF with or without androgen using IntelliGene DNA tip.  Results and conclusions: LN-REC4 cells proliferated better than LNCaP cells in castrated mice and did well irrespective of castration, although responsiveness for androgen of LN-REC4 cells attenuated less than that of LNCaP cells in vitro. LNCaP-SF cells in castrated mice proliferated more rapidly than in normal mice. The PSA expression in LNCaP-SF cells was still induced by androgen. Expression of AR, p21, p27 and cyclin D1 were not changed in LN-REC4 and LNCaP-SF cells. Angiogenesis assay showed that both cells stimulated angiogenesis. LN-REC4 cells induced VEGF more than LNCaP and LN-Pre cells. However, expression of VEGF per cell in LNCaP-SF was lower than LNCaP cells, suggesting that other factors might be involved in angiogenesis. cDNA microarray analysis revealed that more than 200 androgen-regulated genes were up-regulated and down-regulated by androgen in LNCaP and LNCaP-SF cells. These cell lines might be a useful tool for researching androgen-independent growth and treatments of recurred PCa.
HLA-DPB1 mismatch induces a graft-versus-leukemia effect without severe acute GVHD after single-unit umbilical cord blood transplantation
Authors: T Yabe, F Azuma, K Kashiwase, K Matsumoto, T Orihara, H Yabe, S Kato, K Kato, S Kai, T Mori, S Morishima, M Satake, M Takanashi, K Nakajima, Y Morishima
Journal: Leukemia (2017)
Colorectal Cancer Screening: An Opportunity for Training in Colonoscopy?
Authors: A Trifan, C Sfarti, C Cojocariu, G Malgarinos, C Stanciu
Journal: Endoscopy (2006)

Background: Colorectal cancer screening based on colonoscopy has become popular in many countries and it may represent an attractive opportunity for fellows in gastroenterology fellows for training in diagnostic and therapeutic colonoscopy.
VIDEO ANALYSIS OF MATCH INJURIES IN GERMAN MEN'S PROFESSIONAL FOOTBALL
Authors: Christian Klein, Patrick Luig, Hendrik Bloch, Thomas Henke, Petra Platen
Journal: British Journal of Sports Medicine (2017)

Background After description of injury epidemiology the description of injury etiology is the next step to identify relevant preventive approaches. Objective What are common injury situations, mechanisms and characteristics? Design Prospective video-based analysis of match injuries. Setting Two highest German professional leagues in men's football. Participants All first and second division football players who played at least one competitive club match (n=3,747) within the seasons 2010/11, 11/12, 12/13 and 14/15 were included. Interventions Analysis of all moderate and severe match injuries (time-loss&gt;7 days) that were registered by clubs or physicians with the VBG (German statutory accident insurance for the administrative sector) as part of the occupational accident reporting. Main Outcome Measurements A surveillance sheet was evaluated containing six categories and 31 items describing general match and injury information (e.g. date, teams, name of injured player, position on pitch), match situation in moment of injury (e.g. ball possession, movement of injured player, type and direction of possible tackling), mechanism of injury (e.g. type of contact, trigger of injury) and referee's decision. Results 217 moderate or severe match injuries were identified in the video footage. 52.4% of injuries were contact injuries, 20.4% indirect contact and 27.2% non-contact injuries. 17.2% of injuries result from opponent's and 14.3% from own foul play. Injuries mainly occurred during defending actions (sliding 22.1%, tackling 10.6%), shooting (18.6%), heading (13.3), dribbling (11.5%) or passing (11.5%). Moreover, six typical injury situations for thigh, knee, ankle, lower leg and foot injuries were recognized. Conclusions Video analysis of injuries sustained in competition show that the share of injuries effected by irregular actions of the opponents is low. Thus there seems to be a high preventive potential to reduce number and severity of injuries in football. Thus particularly individual intrinsic risk factors needs to be identified within routinely screening measures.
High Generic Drug Prices and Market Competition
Authors: Chintan V. Dave, Aaron S. Kesselheim, Erin R. Fox, Peihua Qiu, Abraham Hartzema
Journal: Annals of Internal Medicine (2017)

Prices for some generic drugs have increased in recent years, adversely affecting patients who rely on them.To determine the association between market competition levels and the change in generic drug prices in the United States.Retrospective cohort study.Prescription claims from commercial health plans between 2008 and 2013.The 5.5 years of data were divided into 11 study periods of 6 months each. The Herfindahl-Hirschman Index (HHI)-calculated by summing the squares of individual manufacturers' market shares, with higher values indicating a less competitive market-and average drug prices were estimated for the generic drugs in each period. The HHI value estimated in the baseline period (first half of 2008) was modeled as a fixed covariate. Models estimated price changes over time by level of competition, adjusting for drug shortages, market size, and dosage forms.From 1.08 billion prescription claims, a cohort of 1120 generic drugs was identified. After adjustment, drugs with quadropoly (HHI value of 2500, indicating relatively high levels of competition), duopoly (HHI value of 5000), near-monopoly (HHI value of 8000), and monopoly (HHI value of 10 000) levels of baseline competition were associated with price changes of -31.7% (95% CI, -34.4% to -28.9%), -11.8% (CI, -18.6% to -4.4%), 20.1% (CI, 5.5% to 36.6%), and 47.4% (CI, 25.4% to 73.2%), respectively, over the study period.Study findings may not be generalizable to drugs that became generic after 2008.Market competition levels were associated with a change in generic drug prices. Such measurements may be helpful in identifying older prescription drugs at higher risk for price change in the future.None.
Estradiol-mediated upregulation of G3BPs results in functional inactivation of p53 in human breast cancer cells
Authors: Mihee M. Kim, Dmitri Wiederschain, Elizabeth Hansen, Derek Kennedy, Zhi-Min Yuan
Journal: Cancer Research (2005)

5248   The majority (75%) of human breast cancers express estrogen receptor (ER). Although ER-positive tumors usually respond to anti-estrogen therapies, 30% of them do not. It is not known what controls the ER status of breast cancers or their responsiveness to anti-hormone interventions. In this report, we document that transgenic expression of  Wnt-1  in mice induces ER-positive tumors. Loss of  Pten  or gain of  Ras  mutations during the evolution of tumors in  Wnt-1  transgenic mice has no effect on the expression of ER, but overexpression of  Neu  or loss of  p53  leads to ER-negative tumors. Thus, our results provide compelling evidence that expression of ER in breast cancer may be influenced by specific genetic changes that promote cancer progression. These findings constitute a first step to explore the molecular mechanisms leading to ER-positive or ER-negative mammary tumors. In addition, we find that ER-positive tumors arising in  Wnt-1  transgenic mice are refractory to both ovariectomy and the ER antagonist tamoxifen, but lose ER expression with either treatment, suggesting that these treatments select for ER -  tumor cells and that the ER +  cell fraction is dispensable for growth of these tumors. This is a first report of a mouse model of anti-estrogen resistant ER +  breast cancers, and could provide a powerful tool to study the molecular mechanisms that control anti-estrogen resistance.
Inhibition of UBE2N As a Therapeutic Approach in Myelodysplastic Syndromes (MDS) and Acute Myeloid Leukemia (AML)
Authors: Laura Barreyro, Avery M Sampson, Lyndsey Bolanos, Madeline Niederkorn, Mario Pujato, Molly A Smith, Muto Tomoya, Wendy D Haffey, Susanne Christie, Xiaona Liu, Matthew Weirauch, Ken Greis, William L Seibel, Daniel T Starczynowski
Journal: Blood (2016)
Neoadjuvant chemotherapy induces breast cancer metastasis through a TMEM-mediated mechanism
Authors: George S. Karagiannis, Jessica M. Pastoriza, Yarong Wang, Allison S. Harney, David Entenberg, Jeanine Pignatelli, Ved P. Sharma, Emily A. Xue, Esther Cheng, Timothy M. D’Alfonso, Joan G. Jones, Jesus Anampa, Thomas E. Rohan, Joseph A. Sparano, John S. Condeelis, Maja H. Oktay
Journal: Science Translational Medicine (2017)

Breast cancer cells disseminate through TIE2/MENA
NICE low back pain guidelines: opportunities and obstacles to change practice
Authors: Kieran O’Sullivan, Mary O’Keeffe, Peter O’Sullivan
Journal: British Journal of Sports Medicine (2017)

The National Institute for Health and Care Excellence recently updated its low back pain (LBP) guidelines,1 with the associated infographic developed to assist interpretation of the recommendations. The guidelines are more consistently aligned with Cochrane systematic reviews than the previous version. The guidelines contain several key directives, which, if widely implemented, could significantly impact on the care of individuals with LBP. Established evidence-based messages, including the need for more cautious referral for some investigations and treatments including imaging, medication and surgery, are reinforced, with a clear emphasis on facilitating self-management strategies. Considering psychosocial factors at an early stage is also advocated, rather than waiting for usual care to fail. There is a timely shift to targeting care based on a person's multidimensional risk profile, rather than merely symptom duration. 1. Which treatment option for whom?
The prevalence and pattern of chemotherapy-induced peripheral neuropathy (CIPN) among women with breast cancer receiving care in a large community oncology practice.
Authors: Natalie Brooke Simon, Michael A. Danso, Thomas Alberico, Ethan M. Basch, Antonia Vickery Bennett
Journal: Journal of Clinical Oncology (2015)

80 Background: CIPN is a common side effect of taxane-based chemotherapy agents. This study examined the prevalence, severity, and risk factors of CIPN and its impact on quality of life (QOL) among women treated for breast cancer in a large U.S. community oncology practice. Methods: In this cross-sectional survey study, women previously treated with taxane-based chemotherapy for early stage breast cancer completed the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ-C30), breast cancer module (QLQ-BR23) and CIPN module (QLQ-CIPN20). Each subscale is scored 0-100 where higher scores indicate better function or greater symptom severity. Clinical data were abstracted from the medical record. Bivariate analyses were conducted to test pre- specified hypotheses. Results: 126 women with mean age 56.7 years (SD = 11.8) were stage I-II (79.4%) or stage III (20.6%) at the time of the survey; 65.1% were White and 27.8% were Black or African American. 73.0% of women reported they had CIPN. The mean time since last taxane chemotherapy cycle was 144.9 weeks (SD = 112.9). The mean (SD) score of QLQ-C30 global health status/QOL was 77.0 (20.3) and physical function was 85.7 (17.1). QLQ-CIPN20 mean scores for the sensory, motor, and autonomic subscales were 18.9 (23.1), 18.6 (18.7), and 17.1 (21.8), respectively. Presence of CIPN was associated with patient referral and visitation to a neurologist or pain specialist (p &lt; 0.05). CIPN symptom severity was negatively correlated with global health status/QOL and physical and role functioning (range of r= -0.46 to -0.72). Further, it was not associated with age, body mass index, diabetes, or cumulative taxane dosage, but was greater for Black or African American patients versus White patients (e.g., sensory: 28.6 vs 14.5, p &lt; 0.002). CIPN sensory impairment was marginally greater for patients treated with paclitaxel compared to docetaxel (23.3 vs 15.6, p &lt; 0.06). Conclusions: CIPN was prevalent in this community oncology practice and significantly impacts function and QOL. These data highlight the importance of developing methods to mitigate CIPN.
Dissecting primary resistance to anti-EGFRs in RAS and BRAF wt metastatic colorectal cancer (mCRC): A case-control study
Authors: Roberto Moretto, Chiara Cremolini, Federica Morano, Rosa Berenato, Elena Tamborini, Federica Perrone, Daniele Rossini, Carlotta Antoniotti, Federica Marmorino, Annunziata Gloghini, Adele Busico, Gemma Zucchelli, Chiara Baratelli, Emiliano Tamburini, Iolanda Capone, Chiara Volpi, Massimo Milione, Massimo Di Maio, Gabriella Fontanini, Filippo de Braud, Alfredo Falcone, Filippo Pietrantonio
Journal: Annals of Oncology (2017)
Microarray analysis to identifiy novel copy number alterations in acute myeloid leukemia.
Authors: Maria Chiara Fontana, Giovanni Marconi, Cristina Papayannidis, Eugenio Fonzi, Emanuela Ottaviani, Eugenia Franchini, Anna Ferrari, Giorgia Simonetti, Antonella Padella, Samantha Bruno, Nicoletta Testoni, Carmen Baldazzi, Andrea Ghelli Luserna di Rorà, Valentina Robustelli, Maria Chiara Abbenante, Stefania Paolini, Jacopo Nanni, Luca Bertamini, Giovanni Martinelli
Journal: Journal of Clinical Oncology (2017)

11622 Background: SNP microarray can detect Copy Number Alterations (CNAs) which could be predictive of response and can help define therapeutic strategies. Our aim is to improve conventional cytogenetic analysis and identify new genetic alterations relevant to leukemogenesis by a SNP array-based genotyping approach. Methods: We performed SNP 6.0/Cytoscan HD (Affymetrix) on 235 Acute Myeloid Leukemia (AML) patients at diagnosis. Seventy-eight/235 samples were also performed by Whole Exome Sequencing, WES (HiSeq,Illumina). SNP Array data were analyzed by Nexus Copy Number (BioDiscovery) and R Core Team. Results: We found several genes preferentially deleted, including MRPS5 (14.8%), PHF6 (9.3%), SCAPER (7.2%), CASK (5.9%), WNK (4.6%), STAG2 (4.2%), LRRK1 (3.4%), PALB2 (3.4%), genes preferentially amplified were RABL2B (16.1%), NF2 (10.2%), NBPF9 (7.6%), JAK2 (6.8%), RB1, NF1 and KMT2A (4.2%), PTEN (3.4%), TP73 and SMAD2 (2.5%). Single-copy losses and deletions were enriched (p &lt; .001) for genes mapping in these pathways: aberrant PD-1 signaling, loss of function of SMAD4 in cancer and SMAD4 MH2 Domain mutants in cancer. The pathways significantly (p &lt; .001) deregulated in our cohort with single copy gain and homozygous amplification were: regulation of transcription and nucleic acid, negative regulation of metabolic processes, constitutive signaling by aberrant PI3K in cancer and PI3K/AKT network. In order to define driver alterations, we correlate deletions and losses with mutational data. We found losses are also targeted by mutations ( BRCA2, LRRK1), while deleted genes, as CASK, CDK6 and MAPT, were involved in pathways affected by genomic mutations ( CASK deletion and MPP6 mutation, CDK6 deletion and PPM1D mutation, MAPT deletion and SPAG5mutation). Conclusions: We have identified new CNAs and pathways involving novel potential leukemia-related genes. The comparison between SNP and WES data could provide important findings on prognosis of AML patients. Minimal deleted regions of genes in deregulated pathways deserve further investigation in order to identify new genes which could be relevant AML biomarkers. Ackn: ELN, AIL, AIRC,prog. Regione-Università 2010-12 (L. Bolondi),FP7 NGS-PTL project,HARMONY.
Re-Evaluation of Age-Related Dysregulation of Hematopoiesis Based on Oxygen Induced Changes Associated with Cell Collection/Processing in Ambient Air
Authors: Hal E. Broxmeyer, Maegan L. Capitano, Heather A. O'leary, Scott Cooper, Hui Lin Chua, Artur Plett, Christie M. Orschell
Journal: Blood (2016)
Response to the combination of thalidomide and capecitabine as second-line therapy in pancreatic carcinoma after treatment and failure with gemcitabine
Authors: S. Beganovic, D. Loesh
Journal: Journal of Clinical Oncology (2006)

14150 Background: A literature search shows only one published case report utilizing the combination of thalidomide and capecitabine as second-line therapy in adenocarcinoma of the pancreas. We report two patients with pancreatic carcinoma treated as second-line therapy with this combination. Methods: CASE #1: Fifty five-year-old female with metastatic pancreatic carcinoma demonstrated clear evidence of progression after 8 months of treatment with gemcitabine At this time, she was started on thalidomide 50 mg at bedtime every other night with capecitabine 1500 mg p.o. b.i.d. for two weeks with one week off. After eight weeks of this regimen, the patient had clinical response with a decrease in abdominal pain, improvement in performance status, and a decrease in her CA 19–9 from 1154 units/mL to 101 units/mL. With this treatment the patient was fully ambulatory and without symptoms for 7 months. CASE #2: The patient is 55-year-old male treated with adjuvant radiation therapy and chemotherapy after surgical resection of his adenocarcinoma of the pancreas. Eight months later, he developed hepatic metastasis and was treated with gemcitabine with progression of disease on that agent. Palliative treatment with capecitabine 1500 mg p.o. b.i.d. for two weeks and one week off was instituted with thalidomide 50 mg at bedtime every other day. After four months of this regimen, the patient had a clinical response with no abdominal pain and decrease in his CA 19–9 from 4647 units/mL to 55 units/mL. Ten months after initiation this regimen patient is asymptomatic, working full time and continues to take thalidomide and capecitabine. Conclusions: Response to second line therapy in adenocarcionoma of pancreas is rare. We are reporting two cases of second-line therapy of adenocarcinoma of the pancreas treated with the combination of thalidomide and capecitabine. Decline in CA 19–9, duration of response, and improvement in functional patient status were unexpected findings. Use of combination of capecitabine and thalidomide in the treatment of the pancreatic adenocarcinoma should be evaluated further in clinical trials. No significant financial relationships to disclose.
Abstract 13927: Allosteric Activation of PP2A Inhibits Experimental Abdominal Aortic Aneurysm
Authors: Chao Zhang, Nianguo Dong, Goutham Narla, Zhiyong Lin
Journal: Circulation (2016)

Introduction: In abdominal aortic aneurysms (AAA), recent studies strongly implicate the kinase, Mitogen-activated protein kinase (MAPK) as an essential contributor to its pathogenesis. Upregulation of Protein phosphatase 2A (PP2A) activity has been shown to be of significant therapeutic value, however pharmaceutically tractable approaches to directly activate PP2A remain elusive in AAA disease. Hypothesis: In light of the potential phosphatase effects PP2A can exert on MAPK protein targets, we hypothesized that PP2A activation by small molecule activators of PP2A (SMAPs) might mitigate AAA progression. Methods: Oral administration of the small molecule activator of PP2A, termed DT-1154, was performed for 4 weeks in apolipoprotein E-null (ApoE-/-) mice concomitant with subcutaneous Angiotensin II infusion. Human abdominal artery tissue as well as abdominal artery tissue from Ang II-infused ApoE-/- mice (+/- DT-1154) were examined by PCR, Western blotting and IHC. Results: To examine its activation state, Phosphorylated-PP2A (Y307) was stained in human and murine AAA tissues, with an increased phospho-PP2A signal indicating less cellular phosphatase activity. Examination of these tissues indeed revealed increased phosphorylation of PP2A compared to control non-AAA tissues indicating a marked reduction of PP2A activation. This strongly suggests that compromised PP2A activation can drive AAA formation. Oral administration of DT-1154 also resulted in significantly reduced AAA incidence and aortic dilation in these pro-AAA ApoE-/- mice. Finally, mechanistic studies indicated that blockade of ERK1/2 and NF-kB signaling by DT-1154 contributed to its effects in ameliorating AAA progression. Conclusions: These studies demonstrate a role of PP2A in AAA etiology and implicate that activation of PP2A may serve as a novel strategy to limit human AAA progression.
Ethical Issues Related to Genetic Testing of Families with Hereditary Non-Polyposis Colorectal Cancer and Familial Adenomatosis Polyposis Syndrome.
Authors: JK Triantafillidis, M Mihalatos, A Apessos, K Petropoulos, I Danielidis, G Nasioulas
Journal: Endoscopy (2006)

Introduction: During the last years, medical ethics has become an important element of the medical studies involving patients and controls, because many bioethical dilemmas could be arise. Screening of relatives with patients with hereditary non-polyposis colorectal cancer syndrome (HNPCC) and familial adenomatosis polyposis syndrome (FAP) for the presence of mutations of relevant genes has become an integral part of our current policy.