tbuckley/cabot-search huggingface dataset:
Sentinel lymph node biopsy in pure tubular carcinoma of the breast: <i>a retrospective multicentric study of 234 cases</i>.
Authors: M Dejode, F Dravet, C Sagan, S Giard, H Mignotte, G Houvenaeghel, G Ferron, J Leveque, C Tunon de Lara, J Rodier, F Marchal, J Classe
Journal: Cancer Research (2009)

Abstract Abstract #207 BACKGROUND. Pure tubular carcinoma (PTC) is a favourable histologic subtype of breast cancer with a low rate of lymph node involvement. This study was initiated to assess the sentinel lymph node (SLN) detection rate and the rate of axillary involvement.&amp;#x2028; METHODS. Inclusion criteria were a PTC (tubular component &amp;gt;90%) core biopsy diagnosed breast cancer smaller than 20 mm, and a homolateral clinically axilla free of nodal involvement. Patients underwent a SLND alone or with an Axillary level I-II Lymphadenectomy (AL). An AL was performed in the case of the learning curve, or in the case of SLN involvement – macrometastases, micrometastases or isolated cells - or in the case of mapping failure.&amp;#x2028; RESULTS. From January 1999 to December 2006, 234 patients were selected from 9 French Comprehensive Cancer Centers. Median tumour size was 9.59 mm (1-22) . The SLN detection rate was 97.9% (229/234). The median number of SLN harvested was 2.15 (range 0-8). Respectively the frequency of macrometastasis - &amp;gt;2mm - was 2.6% (6/229), micrometastasis was 6.5% (15/229) and isolated cells was 0.8% (2/229). There were no false negative cases among the 24 patients with a systematic complementary axillary lymphadenectomy performed in the case of a learning curve. Axillary macrometastasis were found in non sentinel lymph nodes after completed axillary lymphadenectomy in 3 / 6 patients with macrometastasis, in 1/15 patients with micrometastasis and in 0/2 patients with isolated cells. There was no lymph node involvement for tumour size &amp;lt; 10mm. Pathological tumor size &amp;gt;10 mm was statistically correlated to the risk of axillary involvement (p=0.0223).&amp;#x2028; CONCLUSIONS. This study confirms that in the case of PTC ≤ 20mm SLN detection is feasible and the risk of lymph node involvement very low. In the case of PTC&amp;lt;10 mm our series suggests that a surgical axillary evaluation, even with the SLN technique, is not warranted. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 207.
The Clinical Implications of Spinal-Fluid Lactic Dehydrogenase Activity
Authors: Felix Wróblewski, Barry Decker, Rita Wróblewski
Journal: New England Journal of Medicine (1958)

IN vitro and in vivo experiments suggest that malignant cells impart increased lactic dehydrogenase activity to the fluid mediums that bathe the neoplastic tissues. Cultures of malignant tissue have been shown to manifest increased lactic dehydrogenase activity in the culture mediums that nurture the cancer cells; benign tissue in culture fails to show the same increase in the activity of the culture medium.1 Pleural and peritoneal effusions free of malignant cells have less activity than the serum examined concomitantly. However, when serous effusions contain neoplastic cells, the lactic dehydrogenase activity of the effusion is usually greater than that of the . . .
Registries Keep Track in Spain
Authors: C. Vanchieri
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Registries Keep Track in Spain Get access Cori Vanchieri Cori Vanchieri Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 9, 5 May 1993, Pages 698–700, https://doi.org/10.1093/jnci/85.9.698 Published: 05 May 1993
Endoscopically resected giant esophageal carcinosarcoma
Authors: C. Gubler, P. Bauerfeind
Journal: Endoscopy (2013)

A 79-year-old man presented with dysphagia evolving over months. Notably, he underwent right upper lung lobe resection in his sixties and has emphysema and coronary heart disease. Gastroscopy showed a large, inhomogeneous tumor in the proximal esophagus, with a diameter exceeding 5 cm ([Fig. 1]), which was judged to be unresectable endoscopically. Biopsies revealed stromal cells without definite malignancy. Surgical resection was refused due to comorbidities and localization of the tumor; therefore an endoscopic approach was again discussed.
THE EFFECT OF QUERCETIN ON BLOOD PRESSURE: A SYSTEMATIC REVIEW AND META-ANALYSIS OF RANDOMIZED CONTROLLED TRIALS
Authors: Maria Corina Serban, Amirhossein Sahebkar, Paul Muntner, George Howard, Ali Ahmed, Ian Graham, Nathan D. Wong, Florina Andrica, Diana Antal, Wilbert Aronow, Alberto Zanchetti, Maciej Banach
Journal: Journal of the American College of Cardiology (2016)
Noninvasive Prenatal Diagnosis of a Fetal Microdeletion Syndrome
Authors: David Peters, Tianjiao Chu, Svetlana A. Yatsenko, Nancy Hendrix, W. Allen Hogge, Urvashi Surti, Kimberly Bunce, Mary Dunkel, Patricia Shaw, Aleksandar Rajkovic
Journal: New England Journal of Medicine (2011)

This proof-of-principle study shows that it is possible to detect a genetic microdeletion carried by a fetus through analysis of DNA in circulating maternal blood.
Urinary Concentrations of Phthalate Metabolites and Bisphenol A and Associations with Follicular-Phase Length, Luteal-Phase Length, Fecundability, and Early Pregnancy Loss
Authors: Anne Marie Jukic, Antonia M. Calafat, D. Robert McConnaughey, Matthew P. Longnecker, Jane A. Hoppin, Clarice R. Weinberg, Allen J. Wilcox, Donna D. Baird, Antonia M. Calafat, D. Robert McConnaughey, Matthew P. Longnecker, Jane A. Hoppin, Clarice R. Weinberg, Allen J. Wilcox, Donna D. Baird
Journal: Environmental Health Perspectives (2015)

Certain phthalates and bisphenol A (BPA) show reproductive effects in animal studies and potentially affect human ovulation, conception, and pregnancy loss.We investigated these chemicals in relation to follicular- and luteal-phase lengths, time to pregnancy, and early pregnancy loss (within 6 weeks of the last menstrual period) among women attempting pregnancy.Women discontinuing contraception provided daily first-morning urine specimens and recorded days with vaginal bleeding for up to 6 months. Specimens had previously been analyzed for estrogen and progesterone metabolites and human chorionic gonadotropin. A total of 221 participants contributed 706 menstrual cycles. We measured 11 phthalate metabolites and BPA in pooled urine from three specimens spaced throughout each menstrual cycle. We analyzed associations between chemical concentrations and outcomes using linear mixed models for follicular- and luteal-phase lengths, discrete-time fecundability models for time to pregnancy, and logistic regression for early pregnancy loss.Higher concentrations of monocarboxyoctyl phthalate (MCOP) were associated with shorter luteal phase [2nd tertile vs. 1st tertile: -0.5 days (95% CI: -0.9, -0.1), 3rd vs. 1st: -0.4 days (95% CI: -0.8, 0.01), p = 0.04]. BPA was also associated with shorter luteal phase [2nd vs. 1st: -0.8 days (95% CI: -1.2, -0.4), 3rd vs. 1st: -0.4 days (95% CI: -0.8, 0.02), p = 0.001].BPA and MCOP (or its precursors) were associated with shorter luteal phase. Menstrual cycle-specific estimates of urinary BPA and phthalate metabolites were not associated with detrimental alterations in follicular-phase length, time to pregnancy, or early pregnancy loss, and in fact, DEHP [di(2-ethylhexyl) phthalate] metabolites {MEOHP [mono(2-ethyl-5-oxohexyl) phthalate] and ΣDEHP} were associated with reduced early loss. These findings should be confirmed in future human studies.
A1.07 Reprogramming of metabolic pathways inhibits TLR2-induced inflammation in ra
Authors: T McGarry, M Biniecka, W Gao, DJ Veale, U Fearon
Journal: Annals of the Rheumatic Diseases (2016)

<h3>Background&nbsp;and&nbsp;objectives</h3> Recent studies have emphasised a tight link between the metabolic state and phenotype of immune/inflammatory cells. Metabolic turnover of the inflamed synovium may induce acellular switch in energy production, characterised by a glycolytic flux, suppression of mitochondrial function andpotentiation of inflammation. The role of Toll-like receptors (TLRs) in immune responses is well documented, however emerging evidence suggests they also play a role in metabolism. In this study, we examine mitochondrial function, cellular metabolism and synovial inflammation in response to TLR2 activation. <h3>Methods</h3> RA synovial explant cultures and RA synovial fibroblasts (RASFC) were cultured with TLR2-ligand Pam3CSK4&nbsp;(1&nbsp;µg/ml). Mitochondria DNA (mtDNA) mutations were assessed using a Random Mutation Capture assay andreactive oxygen species (ROS), mitochondrial membrane potential (MMP) and ATP levelswere quantified using fluorescent probes. Mitochondrial and glucose metabolism gene arrays were quantified by RT-PCR and the mitochondrial ultrastructure assessed by transmission electron microscopy (TEM). Surrogate markers of glycolysis PKM2, GLUT1, ATP5B and GAPDH were quantified in RA/OA synovium by immunohistochemistry. PKM2 was alsoassessed by western blotting and immunofluorescence. Finally, we examined the effect of glycolytic inhibitor 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO)&nbsp;(20&nbsp;µM) on TLR2–induced cytokine production, invasion/migration and signalling components NFĸBp65, Notch-1IC and p-STAT3. <h3>Results</h3> Pam3CSK4 significantly induced mtDNA mutation frequency, ROS, and inhibited the MMP. In parallel, Pam3CSK4 differentially regulated key mitochondrial genes SOD2, BNIP3 and BBC3 (all p &lt; 0.05) and markedly altered the ultrastructure of mitochondria. Consistent with this, we demonstrated altered metabolic activity in RASFC, with induced PKM2 nuclear translocation, increased ATP levels and differential regulation of metabolic genes FBP1/2, PGAM2 and ACo2 (all p &lt; 0.05), resulting in metabolic shift in favour of glycolysis. This change in metabolic activity was mirrored <i>in-vivo</i> where expression of PKM2, GLUT1 and ATP5B were significantly higher in RA synovium compared to OA (p &lt; 0.05). Finally, reprogramming of metabolism using 3PO significantly inhibited TLR2-induced cytokine production, cell migration/invasion and transcriptional regulation of NFĸBp65 and p-STAT3. <h3>Conclusion</h3> Reprogramming of metabolic activity in RA resulted in resolution of inflammation. These results show close interactions between innate immunity, metabolism and inflammation, further elucidation of these interactions may provide new insights to new therapeutic approaches in RA.
DETECTION OF RV WALL MOTION ASYNERGY ON 4D CT IMAGES USING RV DIAMETER ON TRANSTHORACIC ECHOCARDIOGRAM AND SERUM BRAIN NATRIURETIC PEPTIDE IN SUBJECTS WITH PULMONARY HYPERTENSION
Authors: Koya Ozawa, Nobusada Funabashi, Hiroyuki Takaoka, Nobuhiro Tanabe, Koichiro Tatsumi, Yoshio Kobayashi
Journal: Journal of the American College of Cardiology (2015)
Low plasma homovanillic acid levels in recently abstinent alcoholic men
Authors: M K Fulton, G Kramer, F G Moeller, Y Chae, P G Isbell, F Petty
Journal: American Journal of Psychiatry (1995)

To explore dopaminergic mechanisms in alcohol dependence, the authors measured plasma homovanillic acid (HVA) in recently detoxified alcohol-dependent men.Plasma HVA was measured in 83 male patients with a diagnosis of alcohol dependence who had maintained documented abstinence for at least 3 weeks and in 69 healthy male comparison subjects.The alcoholic patients as a group had significantly lower levels of plasma HVA than the comparison subjects. This difference was not influenced by any other measured covariate, including a family history of alcohol dependence.These results imply that factors such as alcohol dependence should be taken into account in future studies of plasma HVA.
Abstract 263: Silence of SOX2 induces apoptosis through both mitochondria and death receptor signal pathway by activating the RAS/MAPK signals in human lung cancer cells
Authors: Si Chen, Xuefei Li, Yingxi Xu, Lina Wang, Yanan Chen, Dan Lv, Ralph A. Reisfeld, Na Li, Rong Xiang
Journal: Cancer Research (2012)

Abstract Previous study showed that the stem cell gene-SOX2 plays an important role in the anti-apoptotic property of tumor cells, but the regulatory mechanism of SOX2 in the apoptosis signals is still elusive. In this study we used lentivirus system to deliver the shRNA to human lung cancer cell line- A549 and H460 and found that silencing of SOX2 gene can effectively induce apoptosis. Proteomic array assay and western blotting showed that down-regulation of SOX2 activates both the mitochondria and death receptor signal pathway, which were marked by the overexpression and phosphorylation of p53, overexpression of Bax and Bad, and activation of caspase 3 and 8 in A549 cells with SOX2 silencing. Real-time RT-PCR showed that down-regulation of SOX2 leads to the activation of Ras/MAPK signal pathway, which activated the transcription of two key inducers for apoptosis signals-TNF-α and p53 and also down-regulates the expression of survivin. In vitro and in vivo experiment further showed that this apoptotic effect of SOX2 silencing was compromised by overexpression of survivin. Immunohistochemistry study of human lung tissues showed that the protein expression level of SOX2 is closely correlated with that of survivin. In addition, SOX2 and survivin double positive patients showed worse prognosis, suggesting these two proteins can be used as dual-diagnosis factors to evaluate the clinical progression and prognosis of lung cancer patient. These findings revealed the important mechanism for SOX2 to regulate the apoptosis signals and demonstrated that survivin is one of vital downstream molecules that contribute to the anti-apoptosis property of SOX2. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 263. doi:1538-7445.AM2012-263
SP0091 Vascular Disease Models in Systemic Sclerosis
Authors: B. Maurer
Journal: Annals of the Rheumatic Diseases (2013)

<h3></h3> Systemic sclerosis (SSc) is characterized by widespread vascular changes and progressive fibrosis of the skin and internal organs. Alterations of microvessels, preceded by damage and probably an increased apoptosis of endothelial cells, lead to clinical vascular manifestations such as digital ulcers, scleroderma renal crisis and pulmonary arterial hypertension. Of note, vascular manifestations such as Raynaud’s phenomenon and digital ulcers might occur even before the onset of fibrosis indicating a crucial role of microvascular injury for the overall pathogenesis. With respect to pathophysiology, in SSc, two different types of vascular changes can be observed: 1) a destructive vasculopathy of capillaries with vasodilation and rarefication, and 2) a proliferative vasculopathy of small arteries with intimal thickening. Despite the high morbidity and mortality of vascular complications in SSc, the majority of the currently available animal models only cover the fibrotic aspects of the human disease. To illustrate the importance of vasculopathy and its possible link with onset of fibrosis, within this lecture, animal models which display vascular features of SSc will be discussed with respect to 1) individual pathophysiological aspects, 2) identified potential molecular key molecules, and 3) suitability for interventional proof of concept-studies. <h3>Disclosure of Interest</h3> None Declared
Backward and Feeble-Minded Children.
Journal: JAMA (1913)

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
Heparin-Induced Skin Necrosis
Authors: G C Christiaens, H K Nieuwenhuis
Journal: New England Journal of Medicine (1996)

Figure 1. A 36-year-old woman received prophylactic subcutaneous heparin injections after an elective cesarean section. On the fifth postoperative day, subcutaneous edema, redness, and pain developed at the injection site, and heparin was discontinued. The next day, central necrosis of the lesion developed, with a clear line of demarcation between the affected area and surrounding tissue (the diameter of the lesion was 20 cm). The patient did not have thrombocytopenia or thrombotic complications. She also had normal plasma concentrations of protein C and protein S. The lesion later became bullous, with subsequent necrosis of the entire lesion, and skin grafting . . .
Phase 1b study of ARN-509 with abiraterone acetate (AA) and prednisone (P) in patients (pts) with metastatic castration-resistant prostate cancer (mCRPC).
Authors: Edwin M. Posadas, Kim N. Chi, Ronald De Wit, Maja J. De Jonge, Gerhardt Attard, Terence W. Friedlander, Margaret K. Yu, Peter Hellemans, Caly Chien, Charlene Connelly Abrams, Martha Gonzalez, Geralyn Carol Trudel, Vijay Chauhan, Juhui James Jiao, Fred Saad
Journal: Journal of Clinical Oncology (2015)

5028 Background: ARN-509 and AA target the androgenreceptor (AR) axis via different mechanisms and may have complementary activity in mCRPC. ARN-509, a potent and selective AR antagonist, inhibits AR nuclear translocation and DNA binding without significant AR agonist properties (Clegg. Cancer Res. 2012). AA is a prodrug of abiraterone, a CYP17 specific inhibitor that blocks androgen synthesis. No overlapping toxicities are expected for the combination. This phase 1b study evaluates potential PK drug-drug interaction, antitumor activity, and safety of ARN-509 in combination with AA + P (NCT02123758). Methods: Pts with progressive mCRPC and ECOG PS ≤ 2 received AA (1000 mg/d) + P (5 mg BID) beginning on Cycle 1 Day 1 (C1D1) with the addition of ARN-509 (240 mg/d) on C1D8 in 28-day treatment cycles. Efficacy assessment was based on RECIST and PCWG2 criteria. Results: 29 pts started treatment on study. Median age was 70 years (range 49 - 83) and median PSA was 56.8 µg/L (range 4.1 - 2597.0 µg/L). Bone, nodal, and visceral disease were present in 25 (86%), 17 (61%), and 8 (29%) pts, respectively. 14 (48%) pts were previously treated with docetaxel, 12 (41%) with AA, 12 (41%) with enzalutamide (ENZ). 22 pts are currently on treatment and 7 discontinued for disease progression. Thus far, 41% of pts have had confirmed PSA declines > 50%; 52% had any PSA decline. Confirmed PSA responses > 50% included 3 pts who failed prior ENZ or AA therapy. Most common ( ≥ 3 pts) drug-related adverse events (AEs) were grade 1-2 and included fatigue (n = 8), dysgeusia (n = 5), vomiting (n = 4), anorexia (n = 4), abdominal pain (n = 3), diarrhea (n = 3), nausea (n = 3). Grade 3 drug-related AEs (hyponatremia [n = 1], fatigue [n = 1], increased ALT [n = 1], and urinary tract infection [n = 1]) were managed by drug interruption and supportive measures. Conclusions: Interim data indicate that ARN-509 in combination with AA + P is well tolerated in pts with mCRPC. Further study of the efficacy and safety of ARN-509 and AA + P for mCRPC is warranted. Clinical trial information: NCT02123758.
P01.17 * ROLE OF PHOSPHATYDILCHOLINE-SPECIFIC PHOSPHOLIPASE C IN MODULATION OF CXCL12/CXCR4 AXIS IN A HUMAN GLIOMA CELL LINE
Authors: L. Mercurio, A. Ricci, S. Cecchetti, A. Pacella, F. Podo, E. Iorio, G. Carpinelli
Journal: Neuro-Oncology (2014)

BACKGROUND: The CXCR4 chemokine receptor and its ligand CXCL12 are one of the most well studied chemokine systems in tumor biology. In gliomas CXCL12/CXCR4 axis regulates multiple mechanisms that sustain tumor growth as migration, proliferation, angiogenesis and is emerging as a novel biologically relevant target for brain tumor therapy. Previous studies, in our laboratory highlights a role of the phosphatydilcholine-specific phospholipase C (PC-PLC) in the regulation and expression of growth factor membrane receptors, suggesting a relationship between the metabolism of phosphatydilcholine (PC) and cell receptor status. AIM: Investigate the crosstalk between the chemokine receptor CXCR4 and PC-PLC and its implications in glioma cells growth. MATERIALS AND METHODS: U87MG, a glioblastoma cell line was treated with a conventional CXCR4 antagonist, AMD3100 (10 µM), or with a PC-PLC inhibitor, D609 (Xantate) (100 µM). Confocal Laser Scanning Microscopy (CLSM) and Western Blotting (WB) experiments were performed on cells to investigate protein expression and intracellular localization. Cell metabolism on both treated or untreated U87MG cells was evaluated by in vitro Nuclear Magnetic Resonance Spectroscopy (MRS). RESULTS: CLSM analyses highlighted for the first time an extensive co-localization of CXCR4 and PC-PLC on the plasma membrane of U87MG cells. Furthermore we observed a down-modulation of CXCR4 from cell membrane in response to both inhibitors, AMD3100 and D609, however D609 only induced a decrease in CXCR4 total protein content. Moreover, D609 treatment reduced PC-PLC expression, induced a reduction of pAKT and exerted a significative anti-proliferative effect on U87MG cells (49% inhibition). MRS analyses revealed alterations on U87MG metabolism, showing in D609-treated cells an increase of choline-containing metabolites (Glycerophosphocholine, GPCho; Choline, Cho) (increase of 77%) that could be correlated with activation of lipases and phospholipases that can induce an accumulation of neutral lipids associated with the inhibition of cell proliferation. D609 treatment also induced a significative decrease of intracellular concentration of Lactate (38%), and preliminary analyses on lactate deydrogenase (LDH) showed a decrement of the enzyme activity (30%) suggesting that inactivation of PC-PLC could impaired the glycolysis pathway in U87MG. CONCLUSIONS: In this study we identified for the first time an interaction between the chemokine receptor CXCR4 and the enzyme PC-PLC on a glioma cell line. The specific inhibition of PC-PLC modulates CXCR4 receptor localization on cellular membrane and protein expression. Our findings suggest that the inhibition of PC-PLC could represent a new molecular approach in CXCR4-overexpressing glioma cells.