tbuckley/cabot-search huggingface dataset:
Abstract P2-13-01: Impact of Body Mass Index (BMI) on the efficacy of aromatase inhibitors to suppress estradiol serum levels in postmenopausal patients with early breast cancer: a prospective proof of principle
Authors: G Pfeiler, R Königsberg, P Hadji, F Fitzal, M Maroske, G Ban, J Zellinger, R Exner, M Seifert, C Singer, M Gnant, P Dubsky
Journal: Cancer Research (2012)

Abstract Background: BMI impacts on the efficacy of aromatase inhibitors (AIs) regarding disease outcome in patients with early breast cancer. We hypothesized that this clinical impact of BMI is driven by the inability of AIs to suppress estradiol (E2) serum levels to the same low level in obese compared to non-obese patients. Methods: 68 postmenopausal ER positive patients with breast cancer, scheduled to receive anastrozole or letrozole as adjuvant endocrine treatment were prospectively included in this study. Serum was taken before (T1) and 3 months after start with aromatase inhibitors (T2). Serum levels of FSH, LH, E2, glucose and insulin were analyzed immediately in the clinical routine lab and in a dedicated central lab able to measure E2 in serum at low concentrations with high sensitivity. Results: 40 patients were normal - or overweight (non-obese; BMI 18.5–29.9 kg/m2) and 28 patients were obese (BMI ≥ 30 kg/m2). A weak non-significant correlation between BMI and baseline E2 serum levels (r = 0.2, p = 0.2) translated into a strong negative, highly significant correlation between BMI and baseline FSH (r = −0.6, p &amp;lt; 0.01). After 3 months of AI treatment, a moderate correlation between BMI and E2 serum levels (r = 0.35, p = 0.05) and a moderate negative correlation between BMI and FSH (r = −0.34, p = 0.05) could be observed. Aromatase inhibitors significantly suppressed E2 serum levels in non-obese (T1: 18.9 pg/ml, T2: 9.0 pg/ml, p &amp;lt; 0.01) as well as in obese patients (T1: 20.2 pg/ml, T2: 12.5 pg/ml, p &amp;lt; 0.05). In addition an increase in FSH serum levels was observed in obese (T1: 50.0 mIU/ml, T2: 65.5 mIU/ml, p &amp;lt; 0.01) but not in non-obese (T1: 84.0 mIU/ml, T2: 84.6 mIU/ml) patients. However, after 3 months of AI treatment, E2 levels of obese patients were not at the same low level when compared to non-obese patients (E2 obese: 12.5 pg/ml vs. E2 non-obese: 9.0 pg/ml, p = 0.1). This difference translated into significantly lower FSH serum levels in obese compared to non-obese patients (FSH obese: 65.5 mIU/ml vs. FSH: 84.6 mIU/ml, p &amp;lt; 0.01). The significant effects of BMI on FSH serum levels could be detected both in the routine - as well as in the dedicated central lab. Conclusion: AIs are less efficient at suppressing E2 serum levels in obese when compared to non-obese women. The observed effect may contribute to the survival disadvantage of obese patients in adjuvant AI trials. FSH serum levels should be validated as high sensitive surrogate parameters for estradiol serum level suppression by aromatase inhibitors in postmenopausal patients with breast cancer. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P2-13-01.
Abstract 1762: Clinical relevance of plasma IL-6 and IL-6 levels in chronic lymphocytic leukemia (CLL)
Authors: James B. Johnston, Ju-Yoon Yoon, Sunjay Lakhi, Brenda Kuschak, Donna Hewitt, Spencer B. Gibson
Journal: Cancer Research (2010)

Abstract It has been suggested that cytokines play an important role in the survival and proliferation of chronic lymphocytic leukemia (CLL) cells and these growth factors may be derived from a variety of cell types, including CLL cells. The plasma levels of the inflammatory cytokines, IL-6 and IL-8, vary in CLL and increased levels have been associated with a poor prognosis. This phenomenon has been related to the inhibition of apoptosis of CLL cells by the cytokines. In the present study, plasma IL-6 levels were measured by an ELISA assay in 193 CLL patients (107 males, 86 females; ages, 37-92 yr (median, 67.6 yr)) and the plasma IL-8 levels in 66 patients (31 males, 35 females; ages, 37-92 yr (median, 69 yr)). Samples were obtained from patients followed in the CLL Clinic at CancerCare Manitoba. Among the patients, plasma IL-6 levels ranged from &amp;lt; 0.01 to 1058 pg/mL, with a median value of 5.23 pg/mL. The median plasma IL-6 level in 37 age- and sex-matched controls was significantly lower at 0.83 pg/mL (range, 0.06-8.11 pg/mL)). Plasma IL-8 levels in the patients ranged from &amp;lt;0.01 to 1058 pg/mL, with a median value of 5.23 pg/mL. There were 22 normal age- and sex-matched controls for IL-8 levels, and the median IL-8 level here was 3.86 pg/mL (range, 1.42-11.60 pg/mL). A significant correlation was observed between plasma levels of IL-6 and IL-8 (Spearman r = 0.4810, p-value &amp;lt;0.0001), and the levels of both cytokines correlated positively with age and β2-microglobulin. There was also a trend between cytokine levels and RAI stage. There was no correlation between cytokine levels and CD38, IgVH mutation status or the Zap-70 level. For patients aged ≥65 yrs, approximately 22% had increased levels of plasma IL-6 (&amp;gt;3 pg/mL, 8% in normals) and 25% had increased IL-8 (&amp;gt;10 pg/mL, 8% in normals). Plasma from CLL patients with high IL-6 levels was able to induce IL-6 expression in CLL cells whereas plasma from CLL patients with low IL-6 levels failed to induce IL-6 expression in CLL cells. This indicates that factor(s) within the microenvironment are contributing to increased IL-6 levels in CLL. We have previously shown that the relative survival decreases in CLL after age 65 yrs. The present study suggests that this may be related to a potentiation in the age-related increase in IL-6/IL-8 that is observed in the normal population. Whether the increase in mortality in elderly CLL patients is related to frailty/cardiovascular disease or to CLL progression is being investigated. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1762.
Inadvertent placement of a palliative colonic stent through a malignant colocolonic fistula, resulting in absolute large bowel obstruction
Authors: N. Ventham, N. Masson, A. McAvoy, S. Boyce
Journal: Endoscopy (2012)

Emergency surgery for malignant large bowel obstruction has high morbidity and mortality [1]. Alternatively, SEMSs may palliate an obstruction or act as a "bridge to surgery" [2]. Stent placement has a complication rate of around 25 % [3]; complications include perforation, migration, and blockage [4] [5].
IMCT-08ReACT: LONG-TERM SURVIVAL FROM A RANDOMIZED PHASE II STUDY OF RINDOPEPIMUT (CDX-110) PLUS BEVACIZUMAB IN RELAPSED GLIOBLASTOMA
Authors: David A. Reardon, Annick Desjardins, James Schuster, David D. Tran, Karen L. Fink, Louis B. Nabors, Gordon Li, Daniela A. Bota, Rimas V. Lukas, Lynn S. Ashby, J. Paul Duic, Maciej M. Mrugala, Andrea Werner, Laura Vitale, Yi He, Jennifer Green, Michael J. Yellin, Christopher D. Turner, Thomas A. Davis, John H. Sampson
Journal: Neuro-Oncology (2015)

BACKGROUND: EGFRvIII, a constitutively active EGFR deletion driver mutation, is associated with poor long-term survival in glioblastoma (GB). The investigational vaccine rindopepimut consists of an EGFRvIII-specific peptide sequence conjugated to keyhole limpet hemocyanin (KLH), delivered intradermally with GM-CSF. Three phase II studies in newly diagnosed, resected, EGFRvIII+ GB demonstrated encouraging progression-free survival (PFS), overall survival (OS) and safety. METHODS: In the Phase II “ReACT” study, 73 bevacizumab (BV)-naive pts in 1st or 2nd relapse with EGFRvIII+ GB were randomized 1:1 to BV plus double-blinded injection of rindopepimut or control (KLH). Endpoints: 6-month PFS (PFS6; primary; target α = 0.2 by 1-sided chi-square test), objective response rate (ORR), PFS, OS and safety. RESULTS: Primary rindopepimut toxicity is Grade 1-2 injection site reaction. For rindopepimut + BV vs. KLH + BV (per centralized review; RANO criteria): PFS6 = 28% (10/36) vs. 16% (6/37) (p = 0.116); ORR = 30% (9/30) vs. 18% (6/34). Cessation of steroids > 2 months: 44% (8/18) vs 21% (4/19), >6 months: 33% (6/18) vs. 0. Median (95% CI) OS = 11.6 (10.0, 16.2) vs. 9.3 (7.1, 11.3) months (HR = 0.57 [0.33, 0.98], p = 0.039). 9 vs 6 pts remain in follow-up; 6 vs. 2 are progression-free. OS analyses adjusted for various prognostic factors consistently favor rindopepimut. Rindopepimut induced robust anti-EGFRvIII titers (1:12,800-1:6,553,600) in 80% of pts. Antibodies, predominantly IgG1 isotype, mediate killing of EGFRvIII+ tumor cells through ADCC and CDCC in vitro. Within the rindopepimut arm, peak titer (≥1:12,800 at any time) and rapid titer generation (≥1:12,800 by Day 57) were associated with prolonged OS (HR = 0.16, p = <0.0001 and HR = 0.59, p = 0.182, respectively). Evaluation of humoral response quality, HLA typing vs. outcome, and survival follow-up continue. In an additional cohort of BV-exposed pts (n = 53), four pts experienced objective tumor response. CONCLUSIONS: Rindopepimut induces potent EGFRvIII-specific immune response and tumor regression, and appears to significantly prolong survival when administered with BV, in pts with relapsed GB.
Infectious colon polyp in patient with human immunodeficiency virus
Authors: Helmut Neumann, Michael Vieth, Klaus Mönkemüller
Journal: Endoscopy (2014)

A 46-year-old Caucasian man was referred to our hospital because of weight loss and fatigue. He had been diagnosed with human immunodeficiency virus (HIV) infection 18 months earlier, and was under highly active antiretroviral therapy (HAART) with darunavir + ritonavir, emtricitabine, tenofovir disoproxil fumarate, and efavirenz.
Abstract 2838: High-throughput genotoxicity screening unlocks chemotherapeutic potential of antioxidants
Authors: Kyungjae Myung
Journal: Cancer Research (2012)

Abstract Human ATAD5 is a biomarker for identifying genotoxic compounds because ATAD5 protein levels increase post-transcriptionally in response to DNA damage. We screened over 4,000 compounds with a novel, cell-based quantitative high-throughput ATAD5-luciferase assay detecting genotoxic compounds. We identified 22 antioxidants, including resveratrol, genistein, and baicalein, that are currently used or investigated for the treatment of cardiovascular disease, type 2 diabetes, osteopenia, osteoporosis, and chronic hepatitis, and for anti-aging. Treatment of dividing cells with these compounds induced DNA damage and resulted in cell death. Despite their genotoxic effects, resveratrol, genistein, and baicalein did not cause mutagenesis, which is a major side effect of conventional anti-cancer drugs. Furthermore, resveratrol and genistein killed multi-drug resistant cancer cells. We therefore propose that resveratrol, genistein, and baicalein are attractive candidates for improved chemotherapeutic agents. 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 2838. doi:1538-7445.AM2012-2838
P04.11 * GENETIC POLYMORPHISMS OF EGF 5'-UTR IN PATIENTS WITH GLIOMA: A POSSIBLE PREDICTIVE MARKER OF OUTCOME
Authors: C. Dealis, G. Cipollini, I. Florio, E. Vattemi, G. Di meglio, C. Graiff
Journal: Neuro-Oncology (2014)

BACKGROUND: Epidermal growth factor (EGF) plays an important role in carcinogenesis. An adenine (A) to guanine (G) single nucleotide polymorphism at position 61 in the 5'-untranslated region (5'-UTR) of the EGF gene has been found to be associated with levels of EGF production and contribute to the risk of glioma. However, published data are contradictory. EGF +61G/A polymorphism may contribute to the risk of glioma in different ethnic group. Patients with glioma and GG genotype have been reported to have a risk of poorer outcome than patients with AA genotype. Purpose of this study is to investigate the potential role of this polymorphism in cancer progression and its role as predictive marker of outcome in glioma caucasian patients. METHODS: The significant SNP rs4444903, EGF 61A/G, was analyzed in glioma patients and was determined by means of Polymerase Chain Reaction and Direct Sequencing method from blood samples. Association of this genetic polymorphism with clinical and pathological data of patients was evaluated. RESULTS: We investigated EGF +61G/A polymorphism in 28 glioma patients. EGF +61G allele has been found in 68% of glioma patients (22% G/G genotype and 46% A/G genotype). In astrocytomas, EGF +61G allele represents a 83% frequency; in glioblastomas and in oligodendrogliomas, EGF +61G allele frequency represents respectively 73% and 54%. In WHO IV gliomas, the EGF +61G allele represents a 72% frequency, (27% G/G and 45% A/G ), in WHO III gliomas a 81% frequency (54% G/G and 27% A/G ) and in WHO II gliomas a 33% frequency (80% A/G ). Median PFS of glioblastoma patients was 9 months. 79% of glioblastoma patients with a relapsing disease showed the G/G and A/G genotype. No difference was detected in the others histotypes. CONCLUSIONS: Our data confirm previous studies which reported G allele as a risk factor for glioma in Caucasian. G/A and G/G genotypes seem to be more rappresentative in high grade gliomas . Despite limited number of patients, our study supports the predictive role of EGF 61 A/G polymorphism in GBM. Additional large studies are warranted to confirm the role of EGF polymorphism as indipendent prognostic factor in glioma.
Case 39-1997
Authors: Tracy T. Batchelor, David N. Louis
Journal: New England Journal of Medicine (1997)

Presentation of CaseA 67-year-old woman was admitted to the hospital because of back pain and weakness of the legs.She had a long history of intermittent lumbar pain, with radiation to both hamstring muscles. During the two months before admission, the back pain worsened and was accompanied by weakness of the legs. Two weeks before admission, she was admitted to another hospital, where an examination showed reduced leg strength, with diminished reflexes. Chest radiographs showed atelectasis or infiltration in the left lower lobe. Radiographs of the spine showed narrowing of the L3–4 and L4–5 disk spaces. Oxycodone–acetaminophen was given . . .
Behavioral Nutrition Interventions Using e- and m-Health Communication Technologies: A Narrative Review
Authors: Christine M. Olson
Journal: Annual Review of Nutrition (2016)

e- and m-Health communication technologies are now common approaches to improving population health. The efficacy of behavioral nutrition interventions using e-health technologies to decrease fat intake and increase fruit and vegetable intake was demonstrated in studies conducted from 2005 to 2009, with approximately 75% of trials showing positive effects. By 2010, an increasing number of behavioral nutrition interventions were focusing on body weight. The early emphasis on interventions that were highly computer tailored shifted to personalized electronic interventions that included weight and behavioral self-monitoring as key features. More diverse target audiences began to participate, and mobile components were added to interventions. Little progress has been made on using objective measures rather than self-reported measures of dietary behavior. A challenge for nutritionists is to link with the private sector in the design, use, and evaluation of the many electronic devices that are now available in the marketplace for nutrition monitoring and behavioral change.
Unique Cancers Surfacing in HIV-Infected Children
Authors: P. Eastman
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Unique Cancers Surfacing in HIV-Infected Children Get access Peggy Eastman Peggy Eastman Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 18, 20 September 1995, Pages 1352–1353, https://doi.org/10.1093/jnci/87.18.1352 Published: 20 September 1995
Soluble factors derived from infrapatellar fat pad adipocytes of oa patients modulate CD4+T cell cytokine production
Authors: A Ioan-Facsinay, J C Kwekkeboom, M Kloppenburg, R E M Toes
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background and objectives</h3> As shown in previous studies, the infrapatellar fat pad (IFP) of OA patients has an inflammatory phenotype and could contribute to the biological processes in the OA knee joint. The authors have previously characterised the immune cell infiltrate in the IFP and have shown the presence of CD4+T cells. Because several studies have shown that the phenotype of CD4+T cells in adipose tissue is changing with the adiposity of the individual, the authors hypothesised that this effect could be due to the modulation of infiltrating T cells by the tissue-resident adipocytes. Therefore, the authors investigated whether adipocytes from IFP can modulate CD4+T cell cytokine production. <h3>Materials and methods</h3> CD4+T cells were purified from peripheral blood mononuclear cells isolated from buffycoats obtained from healthy volunteers. The purity of the CD4+T cells isolated using magnetic beads coated with antihuman CD4 was above 95%. Plate-bound anti-CD3 and soluble anti-CD28 antibodies were used to activate T cells. Adipocytes were isolated from IFP of OA patients by collagenase digestion and were either cultured with purified CD4+T cells or were cultured in vitro for 24 h in DMEM/F12 medium supplemented with 0.5% bovine serum albumin to generate adipocyte-conditioned medium (ACM). Cytokine/adipokine production was measured by intracellular cytokine staining (ICS), ELISA or cytokine multiplex. Lipids were isolated using hapten and lipid profiling was performed by liquid chromatography combined with mass spectrometry. <h3>Results</h3> CD4+T cells produced increased levels of interferon γ (IFNγ) when activated in the presence of adipocytes. This effect is mediated by soluble mediators, as shown in transwell and ACM transfer experiments. Other T cell cytokines, such as tumour necrosis factor α, IL-17 and IL-5 were also modulated by IFP-derived ACM, indicating a general effect on memory T cells. Several cytokines, adipokines and lipid species were detected in ACM and current research aims at identifying the main soluble mediator responsible for T cell modulation. Finally, IFP of OA patients contained more IFNγ-competent CD4+T cells than peripheral blood in three out of three patients tested, suggesting a possible in vivo consequence of our results. <h3>Conclusions</h3> Soluble mediators secreted by IFP of OA patients can modulate cytokine production of CD4+T cells. Although the precise mechanism involved in this modulation is still unknown, in vivo comparison of IFNγ-producing cells in IFP and peripheral blood indicates a possible in vivo relevance of this finding.
Malabsorption in Intestinal Scleroderma
Authors: Ivan J. Kahn, Graham H. Jeffries, Marvin H. Sleisenger
Journal: New England Journal of Medicine (1966)

THE etiology of malabsorption in patients suffering from intestinal scleroderma has been the subject of considerable debate. Impaired intestinal motility, lymphatic obstruction and reduced arterial blood supply, as well as involvement of the intestinal wall by the disease, have all been suggested as possible etiologic factors, without, however, acceptable supporting evidence,1 , 2 The possibility of bacterial overgrowth in atonic loops of bowel has been considered by several observers2 3 4; McBrien and Lockhart Mummery4 reported temporary improvement of intestinal absorption in 1 patient during therapy with a broad-spectrum antibiotic.This report relates our experience with the use of a broad-spectrum antibiotic in . . .
Chew's on First, Dip's on Second: Smokeless Tobacco Use Heavy Among Baseball Players
Authors: K. Smigel
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Chew's on First, Dip's on Second: Smokeless Tobacco Use Heavy Among Baseball Players Get access Kara Smigel Kara Smigel Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 1, January 1989, Pages 7–9, https://doi.org/10.1093/jnci/81.1.7 Published: 01 January 1989
In Search of . . .
Authors: Kyle Brizendine, J. Michael Wells, Scott A. Flanders, Sanjay Saint, Robert M. Centor
Journal: New England Journal of Medicine (2010)

A 61-year-old man was admitted with a week-long history of nausea, vomiting, nocturia, and polyuria. During the previous 6 months, he had noted progressive fatigue and a 7-kg (15-lb) weight loss.
Abstract 2452: Tumor detection and measurement of responses to chemotherapy using human phosphatidylserine targeting antibody fragments
Authors: Jian Gong, Rich Archer, Matthew Peacock, Christopher Hughes, Connie Chang, Bruce Freimark
Journal: Cancer Research (2012)

Abstract Phosphatidylserine (PS) is a phospholipid normally residing in the inner leaflet of the plasma membrane and becomes exposed on tumor vascular endothelial cells and tumor cells in response to chemotherapy, irradiation and oxidative stresses in the tumor microenvironment. Binding of antibodies targeting PS on the tumor endothelial cells and tumors recruit immune cells and engage the immune system to destroy tumor vasculature. The antibodies also enhance anti-tumor immunity by blocking the immunosuppressive action of PS. A chimeric anti-PS antibody, bavituximab, is being used in combination with chemotherapy to treat patients with solid tumors in Phase II trials. In the present study, we characterize the response to chemotherapy of human tumor xenografts in mice using near-infrared dye labeled PGN650, a human F(ab’)2 fragment that targets PS expression. NIR-PGN650 bound human PC-3luc prostate, BT474 breast and A549luc non-small cell lung tumors in SCID or nude mice in the absence of chemotherapy. Docetaxel treatment enhanced tumor targeting of NIR-PGN650 approximately 2-3-fold compared to imaging signals prior to chemotherapy. Peak tumor uptake of NIR-PGN650 was observed when docetaxel was delivered 24 hours prior to injection of NIR-PGN650. Using these parameters, NIR-PGN650 is able to detect responses to chemotherapy in both the primary tumor and metastases. 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 2452. doi:1538-7445.AM2012-2452