tbuckley/cabot-search huggingface dataset:
Recent advances in clinical practice: a systematic review of isolated colonic Crohn's disease: the third IBD?
Authors: Sreedhar Subramanian, Anders Ekbom, Jonathan M Rhodes
Journal: Gut (2016)

The genetics of isolated colonic Crohn9s disease place it approximately midway between Crohn9s disease with small intestinal involvement and UC, making a case for considering it as a separate condition. We have therefore systematically reviewed its epidemiology, pathophysiology and treatment. Key findings include a higher incidence in females (65%) and older average age at presentation than Crohn9s disease at other sites, a mucosa-associated microbiota between that found in ileal Crohn9s disease and UC, no response to mesalazine, but possibly better response to antitumour necrosis factor than Crohn9s disease at other sites. Diagnostic distinction from UC is often difficult and also needs to exclude other conditions including ischaemic colitis, segmental colitis associated with diverticular disease and tuberculosis. Future studies, particularly clinical trials, but also historical cohorts, should assess isolated colonic Crohn9s disease separately.
Distinct Mechanism of Anti-Hemophilic FVIII Activation By Nascent FXa in the Tissue Factor-FVIIa Coagulation Initiation Complex Resistant to FXa-Directed Inhibition
Authors: Yuichi Kamikubo, Grazia Loredana Mendolicchio, Antonella Zampolli, Patrizia Marchese, Andrew J. Gale, Sriram Krishnaswamy, Andras Gruber, Lars Christian Petersen, Wolfram Ruf, Zaverio M Ruggeri
Journal: Blood (2014)
Epidemiology of Adult Acute Lymphoblastic Leukemia in Manitoba, Canada: Does This Approximate Clinical Trial Data?.
Authors: Vi Dao, Morel Rubinger, Eric J. Bow, Brent A. Schacter, Tsiporah B. Shore, Donna Woloschuk, Alain Demers, Xiaoyun Sun, Matthew D. Seftel
Journal: Blood (2005)
Use of complementary and alternative medicine in Korean cancer patients: Results of a survey from the Korean Cancer Study Group (KCSG)
Authors: D. Kim, M. Lee, B. Kim, K. Lee, Y. Hong
Journal: Journal of Clinical Oncology (2007)

17061 Background: The aim of this study was to explore the use of complementary and alternative medicine (CAM) in cancer patients of Korea. This study was performed to identify the prevalence, types, subjective effects, and side effects of CAM use, reasons for CAM use, and patients' expectations of doctors regarding their CAM use among Korean cancer patients. Methods: From August to December, 2006, face to face structured interviews were conducted and the data were analyzed in the KCSG. Results: A total 251 patients were recruited. 84% of patients had used at least one type of CAM since the time of initial diagnosis. The most prevalent types of CAM used by these patients included special diet (60%), ginseong (54%), medicinal mushrooms (50%). Energy therapies, acupuncture and spiritual therapy were used uncommonly. The main reported reason for the use of CAM was to feel hopeful. Patients expected that CAM could cure cancer (64%) and improve immune system (52%). 62 % of patients did not inform their physicians about their CAM use. Patients attributed the reason of nondisclosure that physicians never asked about CAM (43%) and physicians would disapprove the CAM use (23%). 6% of CAM users experienced side effects. Demographic variables were not predictive for the use of CAM. 60% of patients wanted to get more information about CAM with their doctors. Conclusions: More than two-thirds of cancer patients used various kinds of CAM. Physicians treating cancer patients should aware of the frequency of CAM use and should share their opinion about CAM use with cancer patients. In order to help patients make informed decisions, physician should pay more attention to CAM for making appropriate utilization of CAM. No significant financial relationships to disclose.
Effect of Detecting and Isolating Asymptomatic<i>Clostridium difficile</i>Carriers
Authors: Monique J. T. Crobach, Elisabeth M. Terveer, Ed J. Kuijper
Journal: JAMA Internal Medicine (2016)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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 Internal Medicine journal
Predictors of complications after cytoreductive surgery associated with HIPEC in the treatment of peritoneal carcinomatosis.
Authors: Fabio Oliveira Ferreira, Samuel Aguiar, Alessandro Lima, Erika Maria Monteiro Santos, Wilson Toshihiko Nakagawa, Alexsander Kurowa Bressan, Celso Lopes Mello, Ademar Lopes
Journal: Journal of Clinical Oncology (2012)

e14119 Background: A select group of patients with peritoneal carcinomatosis (PC) has been treated with curative intent by cytoreductive surgery (CCS) associated with intraperitoneal hyperthermic chemotherapy (HIPEC). The objective of this study is to identify predictors of postoperative complications in patients undergoing CCS + HIPEC. Methods: We analyzed data from 136 procedures of CCS + HIPEC in 128 patients with PC, from March 2001 to December 2010. Variables clinical, surgical, and the scores obtained by rating scales of risk (ASA, POSSUM and ACE-27), were correlated with scores obtained by rating scales of morbidity and postoperative results (Bennett-Guerrero, NCI and McPeek). Carcinomatosis was caused by tumors of the appendix in 54 cases (39.7%), ovary in 43 (31.6%), colorectal in 22 (16.2%), peritoneal mesothelioma in 14 (10.3%) and others in three (2.2%). All patients were classified as ECOG 0 and 1 and had KPS&gt; 80%. Complete cytoreduction (CC0) was performed in 93 (68.4%), CC1 30 (22.1%) and CC2 or CC3 in 13 (9.5%). Results: The rates of OS and the median follow-up were respectively 79.6% and 102 months for patients with CP of origin in tumors of the appendix, 78.6% and 74.8 months for source of peritoneal mesotheliomas, 73,9% and 55.9 months for ovarian origin and 36.4% and 31.1 months for colorectal origin. The morbidity (serious complications NCI - grade 3, 4, and 5) and postoperative mortality (30 days) were respectively 16.9% and 2.9%. The duration of surgery (&gt; 9 hours) and ASA classification Scale (ASA class III) were the main predictors of postoperative complications in multivariate analysis. Age was a predictor of cardiovascular complications and one of the variables responsible for longer ICU stay. The number of anastomoses performed per procedure (2 or 3) was associated with the occurrence of infectious complications systemic and wound. Conclusions: The duration of surgery, ASA classification in scale, age and number of anastomoses were the factors most often related to the occurrence of severe postoperative complications after cytoreductive surgery associated with intraperitoneal hyperthermic chemotherapy.
Insulin-like growth factor I receptor (IGF-IR) inhibition in trastuzumab (T) resistant HER2+ breast cancer (BrCa) cells
Authors: B. C. Browne, J. Crown, N. Venkatesan, M. Pegram, M. Clynes, M. J. Duffy, D. J. Slamon, N. O’Donovan
Journal: Journal of Clinical Oncology (2007)

14049 Background: IGF-IR signaling interferes with the growth inhibitory action of T in BrCa cell lines and may play a role in clinical resistance to T. We studied the effect of IGF-IR inhibition on T resistance. Methods: HER2 and IGF-IR protein levels were determined by ELISA. T growth inhibition of HER2+ BrCa cell lines was measured by cell counting. HER2 and IGF-IR activity were determined by immunoprecipitation with HER2 and IGF-IR antibodies, followed by western blotting with phospho-tyrosine antibody. The effects of IGF- I/IGF-IR inhibition on proliferation and response to T were investigated. Results: No significant correlation was found between HER2, phospho-HER2 or IGF-IR levels and response to T in 12 HER+ BrCa lines. However, two T-conditioned cell lines show resistance to T (BT474 - 2.6 fold; SKBR3 - 1.8 fold) and have higher levels of phospho-IGF-IR compared to parental cell lines. Neither IGFBP3 nor IGF-IR antibody aIR3 significantly inhibited the growth of T-conditioned cell lines or enhanced the anti-proliferative effects of T. IGF-IR siRNA decreased IGF-IR protein levels and inhibited proliferation (29.8 ± 9.3 %) of T-conditioned SKBR3 cells. IGF-IR siRNA also enhanced T growth inhibition of T-conditioned SKBR3 cells (47.7 ± 13.7 % compared to 17.7 ± 14.8 % for T alone). The small molecule IGF-IR tyrosine kinase inhibitor (TKI), NVP-AEW541, inhibited growth of parental and T-conditioned SKBR3 cells and enhanced response to T (Table). Conclusions: Increased activation of IGF-IR may play a role in resistance to T. Inhibition of IGF-I ligand binding does not appear to alter IGF-IR mediated T-resistance. However, reducing IGF-IR protein levels or blocking IGF-IR TK activity improves response to T in resistant cells. Thus, the combination of IGF-IR TKIs, such as NVP-AEW541, with T may be beneficial for T-resistant HER2+ BrCa. [Table: see text] [Table: see text]
UNG protects B cells from AID-induced telomere loss
Authors: Elena M. Cortizas, Astrid Zahn, Shiva Safavi, Joseph A. Reed, Francisco Vega, Javier M. Di Noia, Ramiro E. Verdun
Journal: The Journal of Experimental Medicine (2016)

Activation-induced deaminase (AID) initiates antibody gene diversification by creating G:U mismatches in the immunoglobulin loci. However, AID also deaminates nonimmunoglobulin genes, and failure to faithfully repair these off-target lesions can cause B cell lymphoma. In this study, we identify a mechanism by which processing of G:U produced by AID at the telomeres can eliminate B cells at risk of genomic instability. We show that telomeres are off-target substrates of AID and that B cell proliferation depends on protective repair by uracil-DNA glycosylase (UNG). In contrast, in the absence of UNG activity, deleterious processing by mismatch repair leads to telomere loss and defective cell proliferation. Indeed, we show that UNG deficiency reduces B cell clonal expansion in the germinal center in mice and blocks the proliferation of tumor B cells expressing AID. We propose that AID-induced damage at telomeres acts as a fail-safe mechanism to limit the tumor promoting activity of AID when it overwhelms uracil excision repair.
Mechanisms of Myocardial Ischemia in Hypertrophic Cardiomyopathy
Authors: Claire E. Raphael, Robert Cooper, Kim H. Parker, Julian Collinson, Vassilis Vassiliou, Dudley J. Pennell, Ranil de Silva, Li Yueh Hsu, Anders M. Greve, Sukh Nijjer, Chris Broyd, Aamir Ali, Jennifer Keegan, Darrel P. Francis, Justin E. Davies, Alun D. Hughes, Andrew Arai, Michael Frenneaux, Rod H. Stables, Carlo Di Mario, Sanjay K. Prasad
Journal: Journal of the American College of Cardiology (2016)

Angina is common in hypertrophic cardiomyopathy (HCM) and is associated with abnormal myocardial perfusion. Wave intensity analysis improves the understanding of the mechanics of myocardial ischemia. Wave intensity analysis was used to describe the mechanisms underlying perfusion abnormalities in patients with HCM. Simultaneous pressure and flow were measured in the proximal left anterior descending artery in 33 patients with HCM and 20 control patients at rest and during hyperemia, allowing calculation of wave intensity. Patients also underwent quantitative first-pass perfusion cardiac magnetic resonance to measure myocardial perfusion reserve. Patients with HCM had a lower coronary flow reserve than control subjects (1.9 ± 0.8 vs. 2.7 ± 0.9; p = 0.01). Coronary hemodynamics in HCM were characterized by a very large backward compression wave during systole (38 ± 11% vs. 21 ± 6%; p < 0.001) and a proportionately smaller backward expansion wave (27% ± 8% vs. 33 ± 6%; p = 0.006) compared with control subjects. Patients with severe left ventricular outflow tract obstruction had a bisferiens pressure waveform resulting in an additional proximally originating deceleration wave during systole. The proportion of waves acting to accelerate coronary flow increased with hyperemia, and the magnitude of change was proportional to the myocardial perfusion reserve (rho = 0.53; p < 0.01). Coronary flow in patients with HCM is deranged. Distally, compressive deformation of intramyocardial blood vessels during systole results in an abnormally large backward compression wave, whereas proximally, severe left ventricular outflow tract obstruction is associated with an additional deceleration wave. Perfusion abnormalities in HCM are not simply a consequence of supply/demand mismatch or remodeling of the intramyocardial blood vessels; they represent a dynamic interaction with the mechanics of myocardial ischemia that may be amenable to treatment.
A phase I, pharmacokinetic and pharmacodynamic study of GSK2256098, a focal adhesion kinase inhibitor, in patients with advanced solid tumors
Authors: J.C. Soria, H.K. Gan, S.P. Blagden, R. Plummer, H.T. Arkenau, M. Ranson, T.R.J. Evans, G. Zalcman, R. Bahleda, A. Hollebecque, C. Lemech, E. Dean, J. Brown, D. Gibson, V. Peddareddigari, S. Murray, N. Nebot, J. Mazumdar, L. Swartz, K.R. Auger, R.A. Fleming, R. Singh, M. Millward
Journal: Annals of Oncology (2016)
Improvement in long-term survival in patients with metastatic colorectal cancer (CRC) after liver resection with modern chemotherapy and hepatic arterial infusion (HAI).
Authors: Nancy E. Kemeny, Joanne F. Chou, Taryn M. Boucher, Marinela Capanu, Ronald P. DeMatteo, William R. Jarnagin, T. Peter Kingham, Peter J. Allen, Yuman Fong, Andrea Cercek, Michael Ian D'Angelica
Journal: Journal of Clinical Oncology (2015)

3563 Background: Hepatic resection of liver metastases from CRC is associated with 5-year (y) and 10-y overall survival (OS) of 30-50% and 20%. The aim of this study was to update OS of 5 consecutive adjuvant (adj) studies using HAI + systemic (sys) after liver resection and to determine effects of clinical factors on long-term OS. Methods: Patients (pts) treated on protocols with HAI FUDR/dexamethasone + sys from 1991 to 2015 with the following inclusion criteria: completely resected hepatic metastases, no extrahepatic disease, bilirubin < 1.5mg/dl, platelet count > 100,000/μL, and no concurrent infection. Pts on studies before 2003 were treated with HAI + sys FU/LV or irinotecan (CPT) and pts on studies after 2003 were treated with HAI + sys oxal/FU/LV or CPT/FU/LV ± molecular targeted therapies. OS was calculated from the time of liver resection until death and was estimated using the Kaplan-Meier method. Using Greenwood’s formula, 95% CI at fixed time points for outcomes were calculated and compared between treatment years (before 2003 vs after 2003). Results: 329 pts were included with a median follow-up of 9.6 y. 5-y OS for those treated before and after 2003 was 56% [95% CI: 49%-63%] and 80% [95% CI: 71%-85%], respectively (p < 0.01). 10-y OS for pts treated before 2003 was 40%, while 10-y OS is not yet obtainable for pts treated after 2003. Various clinical factors and significant p-values (*p) known to influence survival are shown in the table below. Conclusions: Survival for pts undergoing hepatic resection and adj HAI is improving. Pts treated before 2003 with liver resection and adj HAI + sys have a 5-y OS of 56%, while pts treated after 2003 with HAI + modern sys chemotherapy have a 5-y OS of 80%. *p Before/After 2003 Before 2003 n=169 After 2003 n=160 % OS % 5-y OS % 10-y % OS % 5-y Age - / - 22 – 50 27 61 48 38 75 51 – 74 68 55 37 59 81 ≥ 75 5 56 33 3 100 # Hepatic Mets * / * 1 39 71 57 26 87 2 – 4 46 57 35 48 85 5 – 7 11 26 16 15 67 ≥ 8 5 13 0 11 52 Clinical Risk Score * / - 0 – 2 59 64 47 54 85 3 – 5 41 47 30 46 72 Margins (mm) - / * 0 6 50 10 6 40 ≤ 1 50 52 37 63 78 > 1 44 66 48 31 92 Size (cm) - / - < 5 69 58 42 79 81 ≥ 5 31 54 35 21 72 Primary LN * / * Pos 60 52 32 62 73 Neg 40 65 52 38 90 CEA Post op (ng/ml) * / - < 5 ≥ 5 68 32 64 43 44 30 80 20 83 65 KRAS - / * WT MUT - - - 81 19 86 67
Breast cancer outcome and estrogen plus progestin use in postmenopausal women.
Authors: R. T. Chlebowski, G. L. Anderson, M. Gass, D. S. Lane, A. K. Aragaki, L. H. Kuller, J. E. Manson, M. L. Stefanick, J. Ockene, R. L. Prentice
Journal: Journal of Clinical Oncology (2010)

1507 Background: During a mean (SD) 5.6 years (1.3) of intervention, use of estrogen plus progestin in the Women's Health Initiative (WHI) randomized clinical trial increased breast cancer incidence (Chlebowski et al JAMA 2003;289;3243) but breast cancer mortality was not reported. Therefore, we determined combined hormone therapy effects on breast cancer incidence and mortality in the WHI trial over the entire follow-up period (mean [SD] 11.0 [2.7] years) and also in the WHI observational study cohort. Methods: In the clinical trial, 16,608 postmenopausal women with no prior hysterectomy were randomized to conjugated equine estrogens (0.625 mg/d) plus medroxyprogesterone acetate (2.5 mg/d) (estrogen plus progestin) or placebo. In the observational study, 41,449 postmenopausal women with characteristics similar to clinical trial participants were identified at entry as estrogen plus progestin users (n = 16,121) or not users (n = 25,328). Main outcome measures included invasive breast cancer incidence and breast cancer mortality. Results: In the clinical trial, more breast cancers were diagnosed in the estrogen plus progestin group (385 vs. 293; HR, 1.25; 95% CI, 1.07-1.46, p = 0.004) and the breast cancers were more likely to be node positive (p = 0.02). Deaths directly attributed to breast cancer were greater in the estrogen plus progestin group (25 vs. 12 deaths; HR 1.96 95% CI 1.01-4.05, p = 0.048) as were deaths from all causes occurring after a breast cancer diagnosis (49 vs. 31 deaths; HR 1.51 95% CI 0.97-2.39, p = 0.07). Estrogen plus progestin users in the observational study had somewhat more deaths attributed to breast cancer (HR 1.33 95% CI 0.82-2.16, p = 0.26) and more deaths from all causes occurring after a breast cancer diagnosis (HR 1.82, 95% CI 1.33-2.50, p < 0.001) compared to women not using estrogen plus progestin at entry. Conclusions: Estrogen plus progestin use increases breast cancer incidence with cancers more commonly node positive. Mortality from all causes after a breast cancer occurrence was greater and an adverse trend for deaths attributed to breast cancer is seen with combined hormone therapy use. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration AstraZeneca, Lilly, Novartis, Pfizer, Procter and Gamble, Upsher-Smith Laboratories, Wyeth Abraxis BioScience, AstraZeneca, Novartis Amgen, Lilly, Organon, Procter and Gamble, Wyeth
A genomic approach to define important and targetable molecular pathways in brain metastasis arising from solid tumors
Authors: C. K. Anders, D. S. Hsu, C. R. Acharya, R. McLendon, J. H. Sampson, J. J. Vredenburgh, D. Satterfield, N. Spector, A. Potti, K. L. Blackwell
Journal: Journal of Clinical Oncology (2008)

11041 Background: Brain metastasis (BM) is a devastating consequence of aggressive malignancy. Although targeted agents are effective in treating extracranial advanced cancer, optimal targets for preventing and treating BM from solid tumors (ST) remain largely unknown. Methods: Clinically-annotated BM tissues from a variety of ST (melanoma n = 12, lung n = 12, breast n = 4, sarcoma n = 4, colon n = 2, renal n = 2, other n = 4) were sequentially collected from consented patients undergoing a neurosurgical procedure and stored in the Duke Brain Tumor Repository. RNA was extracted, genomic expression data was generated (Affymetrix U133A), and unsupervised hierchical clustering (UHC) was performed prior to investigating differential expression of single genes and oncogenic pathways using class neighbors (GenePattern) and GSEA (Gene Set Enrichment Analysis). Results: UHC of BM revealed two main clusters differentiated by tissue of origin; neuroectodermal (n = 18; melanoma, sarcoma) and ectodermal origins (n = 22; lung, breast, colon). Differential analysis illustrated a significant difference in the top 50 genes expressed between these 2 clusters (p < 0.01). Genes specific to Cluster 1 (neuroectodermal) were related to anti-apoptosis (SNCA), neural crest migration (EDNRB), cell adhesion (PLXNC1, SRPX, CDH19), heat shock protein (HSPA12A); genes specific to Cluster 2 (ectodermal), endothelial cell migration (S100P), cell cycle regulation (SFN, TACSTD2), angiogenesis (KLF5), and cell motility (SPINT2, TSPAN1). GSEA revealed 14 gene sets specific to Cluster 1 and 70 specific to Cluster 2 (p < 0.05). Selected gene sets important to Cluster 1 included HSP27 (p = 0.018) and BAD (p = 0.024); Cluster 2, HDAC (p = 0.01), BRCA1 (p = 0.008) and Myc (p = 0.03). Conclusions: This large-scale genomic analysis of BM arising from ST illustrates an ability to identify targetable pathways, specifically HSP among BM of neuroectodermal origin and HDAC and angiogenesis among BM of ectodermal origin. We will present additional analyses including a comparison amongst tumor primary sites (i.e. lung vs. melanoma, breast vs. lung) and confirmatory protein-expression. Together, study results offer important pathways that may help direct future clinical trials for BM arising from ST. No significant financial relationships to disclose.