tbuckley/cabot-search huggingface dataset:
Abstract 1125: The insulin-like growth factor (IGF) axis is involved in normal prostate differentiation and downregulated in local prostate cancer
Authors: Petra Massoner, Michael Ladurner Rennau, Isabel M. Heidegger, Anita Kloss-Brandstätter, Georg Schäfer, Christof Seifarth, Helmut Klocker
Journal: Cancer Research (2011)

Abstract Introduction and Objectives: Clinical trials targeting the insulin-like growth factor 1 receptor (IGF1R) in different tumors, including breast cancer, colorectal cancer, leukemia (ALL, CML), non-small-cell lung cancer (NSCLC), ovarian cancer, pancreatic cancer, prostate cancer and sarcomas are underway. Encouraging data from phase II studies in NSCLC and sarcomas led to rapid development of phase-III studies. However, a phase-III study with an anti-IGF1R antibody combined with erlotinib in advanced NSCLC was terminated recently for safety reasons and lack of efficiency (ClinicalTrials.gov Identifier: NCT00673049). Have we possibly moved to early to clinical trials without entirely understanding the role of the IGF axis in normal and cancer development? The IGF1R is part of a tightly regulated molecular network named IGF axis. The IGF axis is implicated in tumor development and progression, but also exerts essential functions in normal tissues, including control of growth processes, tissue homeostasis, differentiation and metabolism. Methods: Here we analyzed the mRNA expression level of the all members of the IGF axis, including IGF1, IGF2, IGFBP1-IGFBP6, IGF1R, IGF2R and INSR in microdissected tissue specimens of local prostate cancer. We compared IGF expression levels in malignant and benign prostate areas in both, the epithelial and the stromal compartment. Furthermore we investigated whether IGF expression levels are changed during normal prostate differentiation and describe a novel cellular model for prostate differentiation. Results: We show that the IGF axis is not up- but downregulated in local prostate cancer, in both the epithelial and the stromal compartment. Using cellular models we demonstrate that the IGF axis is induced during normal prostate epithelial differentiation and confirm herewith that the IGF axis is required for tissue homeostasis and normal epithelial differentiation in the prostate. Conclusions: Our data confirm a pivotal role of the IGF axis during normal prostate differentiation, which may overcomes its pro-oncogenic effect in local prostate cancer. Treatments of local prostate cancer with IGF1R inhibitors cannot be advised based on these data. Source of Funding: COMET center Oncotyrol and Tyrolean Cancer Foundation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1125. doi:10.1158/1538-7445.AM2011-1125
AB0561 Risk of HBV infection reactivation in patients with rheumatoid arthritis undergoing treatment with ANTI-CD20 (RITUXIMAB)
Authors: M. Covelli, E. Lanciano, A. Notarnicola, L. Coladonato, G. Lopalco, C. Scioscia, M.G. Anelli, G. Lapadula
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background</h3> Hepatitis B virus reactivation is an emerging cause of liver disease in patients undergoing treatment with biologic agents. In particular, the risk of reactivation increases in anti-CD20 (Rituximab) and anti-TNF-alpha therapy. In patients affected by lymphoma and treated with Rituximab, HBV infection is the most common viral infection. In these patients several guidelines recommend strictly monitoring of ALT and serum HBV DNA. However other Authors recommend prophylactic therapy with antiviral agents and show that risk of reactivation is greatly reduced by the identification of high-risk patients and by using lamivudine. These guidelines are extended to patients affected by rheumatoid arthritis and treated with Rituximab. We've studied the risk of reactivation of Hepatitis B in our rheumatoid arthritis patients treated with Rituximab, refractory to one or more anti-TNF alpha blockers. <h3>Objectives</h3> To evaluate risk of HBV infection reactivation in patients with rheumatoid arthritis undergoing treatment with ANTI-CD20 (RITUXIMAB). <h3>Methods</h3> Occult HBV infection (HBsAg negative, anti-HBcAg positive with or without anti-HBsAg and undetectable HBV-DNA) has been observed in 218 patients; 16 of them were undergoing treatment with Rituximab from 2007 to 2010 without prophylactic therapy with antiviral agents. These patients received intravenous rituximab (mean 4 courses, consisting of 2 infusions of 1000 mg each separated by 2 week every 6 months). <h3>Results</h3> In whole 16 patients HBV-DNA was negative before starting therapy and now it still remains undetectable. Finally there wasn't any increase of AST or ALT. <h3>Conclusions</h3> Prophylactic therapy with antiviral agents is recommended in occult HBV infection patients treated with rituximab. However our patients undergoing rituximab not in combination with prophylactic therapy with lamivudine before 2010, didn't present reactivation of HBV infection. Therefore, according to data of our experience, Rituximab appears to be a safe treatment in patients with occult HBV infection too. Further studies are necessary to confirm our experience data. <h3>Disclosure of Interest</h3> None Declared
FRI0300 A large randomised, controlled trial comparing the efficacy and safety of topical ketoprofen in transfersome gel with oral celecoxib for osteoarthritis knee pain
Authors: P.G. Conaghan, J.D. Dickson, W. Bolten, G. Cevc, M. Rother
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> IDEA 033 is a topically applied osteoarthritis (OA) treatment that uses novel Transfersome (TM IDEA AG) – an aqueous dispersion of ultra-deformable carriers – to deliver ketoprofen to soft tissue. <h3>Objectives</h3> To evaluate the efficacy and safety of 2 doses of IDEA 033 in people with OA knee pain and to compare the efficacy with celecoxib. <h3>Methods</h3> A multicentre, randomised, double-blind, placebo- and active-controlled study in pts with ACR criteria OA knee with moderate pain at baseline (rating of ≥4 for question 1 WOMAC 3.1 and total average WOMAC pain subscale &lt;7). Pts received 12 wks twice daily of 50mg or 100mg ketoprofen in Transfersome or matched placebo (gel without ketoprofen; TDT 064); 100mg celecoxib or oral placebo. WOMAC pain and function were assessed at baseline and wks 2, 6, 9 and 12. Pts’ global assessment of response was measured on a Likert scale at wk 12. Primary outcome was change in WOMAC pain subscale score at wk 12 for 100mg ketoprofen in Transfersome vs matching placebo. <h3>Results</h3> The intent-to-treat and safety populations comprised 1395 patients. Throughout the treatment period, all study arms displayed a decrease in pain (Table 1). Treatment with 100mg ketoprofen in Transfersome was non-inferior to celecoxib (Mann–Whitney Estimator=0.4468; predefined benchmark of test for non-inferiority=0.4), and was not superior to topical placebo. Both doses of ketoprofen in Transfersome and matching placebo groups were superior to oral placebo at a magnitude comparable to celecoxib. All groups reported a considerable improvement in physical function. No treatment-related serious AEs were reported. <h3>Conclusions</h3> Treatment for 12 wks with topically applied ketoprofen (50mg and 100mg) in Transfersome was not statistically superior to treatment with matching NSAID-free Transfersome gel. However, there was significant superiority for all Transfersome applications and celecoxib vs oral placebo. All treatments were well tolerated. Investigation of the beneficial effects of the NSAID-free Transfersome gel (TDT 064) is ongoing. <h3>Disclosure of Interest</h3> P. Conaghan Consultant for: Servier, Speakers Bureau: AstraZeneca, Servier, J. Dickson: None Declared, W. Bolten: None Declared, G. Cevc Employee of: Past employee of IDEA AG, M. Rother Shareholder of: IDEA AG (sponsor of the trial), Employee of: IDEA AG (sponsor of the trial) at the time of trial conduct
Incidental Finding of a Large Renal Mass on Tc-99m MDP Bone Scintigraphy
Authors: CHRISTINA FRAGKAKI, PHIVI RONDOGIANNI, IRENE HOUSIANAKOU
Journal: Clinical Nuclear Medicine (2002)

FRAGKAKI, CHRISTINA M.D.; RONDOGIANNI, PHIVI M.D., Ph.D; HOUSIANAKOU, IRENE M.D. Author Information
Breast Cancer Screening: Evidence of Benefit for Women 40 to 49
Authors: C. Vanchieri
Journal: JNCI Journal of the National Cancer Institute (1988)

Journal Article Breast Cancer Screening: Evidence of Benefit for Women 40 to 49 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 80, Issue 14, 21 September 1988, Pages 1090–1092, https://doi.org/10.1093/jnci/80.14.1090 Published: 21 September 1988
Survey Shows: American Women Favor Mammography
Authors: K. Smigel
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Survey Shows: American Women Favor Mammography 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 85, Issue 6, 17 March 1993, Page 439, https://doi.org/10.1093/jnci/85.6.439 Published: 17 March 1993
Abstract 70: A role for the chromatin remodeling protein CHD3 in ovarian cancer therapy response
Authors: Noelle Cutter, Nila Banerjee, Michele Vigliotti, Angel Janevski, Douglas Levine, Nevenka Dimitrova, Robert Lucito
Journal: Cancer Research (2011)

Abstract Carboplatin and cisplatin are chemotherapeutic agents that are used extensively for treating epithelial ovarian cancer. These drugs can be highly effective, yet tumors are frequently refractory to treatment or become resistant upon tumor relapse. Epigenetic silencing, particularly at promoter regions of genes regulates important cell function and has been associated with all stages of tumor formation and progression and may contribute to therapy response. We analyzed the epigenome of 50 primary ovarian tumors and 12 normal ovarian samples using an array based method previously developed in our lab and associated Affymetrix U133 expression data. We then identified gene candidates that segregate patients based on platinum sensitivity and patient survival. These candidates were then pooled into a genome-wide RNAi-based screen where we validated a gene encoding a chromatin remodeling protein, CHD3, a member of the Mi-2 NuRD complex, and show that it is linked to chemoresistance. CHD3 is silenced through an epigenetic mechanism in both ovarian cancer cell lines and primary ovarian tumors. When ovarian cancer cell lines that are transcriptionally silenced for CHD3 are challenged with carboplatin they display a striking slow growth phenotype as well as increased resistance to the chemotherapy drugs carboplatin and cisplatin. Taken together, we provide the first evidence for a role for CHD3 as an important mediator of chemoresistance in ovarian cancer. Furthermore, CHD3 might represent a response predictor and potential therapeutic target for predicting chemoresistance in this disease. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 70. doi:10.1158/1538-7445.AM2011-70
Hyperbaric-Oxygen Therapy
Authors: Patrick M. Tibbles, John S. Edelsberg
Journal: New England Journal of Medicine (1996)

Hyperbaric oxygen — 100 percent oxygen at two to three times the atmospheric pressure at sea level — can result in arterial oxygen tension in excess of 2000 mm Hg1 and oxygen tension in tissue of almost 400 mm Hg.2,3 Such doses of oxygen have a number of beneficial biochemical, cellular, and physiologic effects, and today there are 259 hyperbaric facilities in the United States with 344 single-occupant ("monoplace") hyperbaric-oxygen chambers.4 In this article, we review the mechanisms of action, evidence of clinical efficacy, and risks of therapy with hyperbaric oxygen.Physiologic EffectsFor hyperbaric oxygen, pressure is expressed . . .
Epithelial calcineurin controls microbiota-dependent intestinal tumor development
Authors: Kenneth Peuker, Stefanie Muff, Jun Wang, Sven Künzel, Esther Bosse, Yvonne Zeissig, Giuseppina Luzzi, Marijana Basic, Anne Strigli, Andrea Ulbricht, Arthur Kaser, Alexander Arlt, Triantafyllos Chavakis, Gijs R van den Brink, Clemens Schafmayer, Jan-Hendrik Egberts, Thomas Becker, Marco E Bianchi, André Bleich, Christoph Röcken, Jochen Hampe, Stefan Schreiber, John F Baines, Richard S Blumberg, Sebastian Zeissig
Journal: Nature Medicine (2016)
胸痛-贫血-高钙血症
Authors: 朱卫国, 王望, 王玉, 刘巍, 曾学军
Journal: BMJ (2009)

患者男,70岁,因乏力、间断胸痛6个月,加重1 d于2008年7月25日入院. 患者6个月无诱因出现乏力、活动耐力下降,进行性加重.间断胸痛,心前区闷痛为主,无放射;因乏力较少活动,胸痛多在休息时发作,发作后服用速效救心丸3～5 min可缓解.后发作次数渐频,由每个月发作1～2次,增加到每周发作2～3次.在当地医院查超声心动图:左室壁轻度增厚,舒张功能减低,运动试验心肌灌注显像未见异常,建议常规口服速效救心丸。
Abstract 5209: The roles of Notch signaling in the development of non-small cell lung cancer
Authors: Joyce O. Osanyingbemi-Obidi, Charles M. Rudin
Journal: Cancer Research (2011)

Abstract Lung cancer is the most common cause of cancer related deaths in the United States, accounting for 29% of all cancer deaths. Approximately 85% of all lung cancers are of non-small cell histology. Although current therapies have marginally improved survival and quality of life for patients with Non-Small Cell Lung Carcinoma (NSCLC), this remains a nearly universally fatal disease. New approaches to drug development and further studies of the biology of this disease are critically needed. We hypothesized that high level Notch signaling would define a subpopulation of NSCLC cells with markedly elevated clonogenic potential, and that inhibition of Notch signaling could inhibit NSCLC tumorigenesis. To test these hypotheses and to define the potential utility of Notch inhibitors in NSCLC, we have evaluated the temporal and spatial activation of Notch signaling in a murine model of NSCLC tumorigenesis, evaluated a dominant negative transgenic mouse model, and are assessing whether Notch activation correlates with clonogenic and tumorigenic potential in human NSCLC lines. Down regulation of Notch signaling using a selective γ-secretase inhibitor (Mrk 003; Merck) was evaluated in three NSCLC cell lines (NCI-H1299, and -H1435). Cells were incubated for 96 hours with Mrk 003 at concentrations ranging from 0.1uM to 10.0μM. After 96 hours, a 60% suppression of Hes 1 expression was observed. In conjunction with these studies we have created a double transgenic model, LSL-K-rasG12D × DNMAML (dominant negative mastermind) mice. Expression of the DN-MAML gene results in inhibition of the Notch pathway. We administered adenoviral CRE intranasally to these mice and generated intraparenchymal lung tumors in both KRAS and KRAS/DN-MAML mice. Surprisingly, and in contrast to our hypothesis, tumor burden was not decreased in the double transgenic model relative to the Kras control group. Mastermind-1 may have effects other than regulation of Notch signaling, including a possible interaction with p53 that is being currently explored, and which may explain these surprising findings. Characterization of highly clonogenic progenitor populations in NSCLC, and definition of the roles of Notch pathway regulators in tumorigenesis, may aid in the development of more effective therapeutics. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5209. doi:10.1158/1538-7445.AM2011-5209
A phase III trial of carboplatin, paclitaxel, and thoracic radiation therapy with or without thalidomide in patients with stage III non-small cell carcinoma of the lung (NSCLC): E3598
Authors: J. H. Schiller, S. E. Dahlberg, M. Mehta, D. H. Johnson
Journal: Journal of Clinical Oncology (2009)

7503 Background: Thalidomide (T) is an oral angiogenesis inhibitor with anti-tumor activity in hematological malignancies. Given that antiangiogenic drugs such as bevacizumab have proven activity in advanced NSCLC, ECOG conducted a phase III study to compare the effects of the addition of thalidomide to paclitaxel/carboplatin/radiation therapy (PC/RT) on overall survival (OS) in pts with newly diagnosed stage III NSCLC. Secondary endpoints included time to progression (PFS) and toxicity. Methods: Pts were required to have inoperable stage IIIA or IIIB (no pleural effusion) NSCLC and a PS of 0 or 1. Pts were randomized to receive 2 cycles of P (225 mg/m2)+ C (AUC=6) every 3 wks or PC + thalidomide starting at 200 mg daily with the possibility of dose escalation. This was followed by weekly C (AUC=2), P (45 mg/m2) and concurrent RT (60 Gy) ± T. Pts on PC/RT + T continued thalidomide for 24 mo. or until disease progression. Results: 277 eligible pts were randomized to PC/RT and 272 pts to PC/RT + T. Median age was 63; 61% of pts had stage IIIB disease, 35% had squamous histology, and 46% were PS 0. The third planned interim analysis was conducted with 403 of 506 planned deaths (73.9%) for full analysis and the trial was stopped early by the ECOG Data Monitoring Committee for futility. The median overall survival for the no T arm was 15.3 mo. (12.4–20.2 mo.) compared to 16.0 mo for the T arm (14.4–18.3 mo.); hazard ratio = 0.985 (0.81–1.19); p = 0.88. Median PFS for the no T arm was 7.6 mo. (6.6–8.7 mo.) compared to 8.0 mo. for the T arm (7.1–9.1 mo.), p&gt;0.05. The most common toxicity on both arms was myelosuppression. 11% of pts on the T arm had a grade 3–5 thrombosis/embolism, compared to &lt;3% on the no T arm. Conclusions: The addition of thalidomide to PC/RT in pts with stage III NSCLC does not provide a clinically significant benefit. [Table: see text]
Extrarenal Collection of Tc-99m MAG3 Mimicking a Urinary Leak in a Patient Who Underwent Partial Nephrectomy
Authors: KAZUYOSHI SUGA, NORIHIKO KUME, AYAMI HIRABAYASHI, KEIKO KISHIMOTO, NAOFUMI MATSUNAGA
Journal: Clinical Nuclear Medicine (1998)

Tc-99m DMSA imaging was performed after a Tc-99m MAG3 study in a patient who showed an elevated serum creatinine after partial nephrectomy due to renal cancer. Tc-99m MAG3 imaging showed a bowel collection mimicking a urinary leak. Because biliary excretion of Tc-99m MAG3 is enhanced in the presence of decreasing renal function and because bowel accumulation of this tracer increases with time, the incidence of bowel visualization may increase in patients with poor renal function when Tc-99m DMSA imaging is performed after a Tc-99m MAG3 study. Unexpected extrarenal collections of Tc-99m MAG3 must be carefully interpreted to prevent an erroneous diagnosis of a urinary leak.
Cavernous Angioma Mimicking a Differentiated Thyroid Carcinoma Brain Metastasis
Authors: Daniel Bulzico, Fernanda Vaisman, Cencita H. Cordeiro de Noronha Pessoa, Rossana Corbo
Journal: Clinical Nuclear Medicine (2010)

A 30-year-old man diagnosed with follicular thyroid carcinoma treated previously with total thyroidectomy was referred to radioiodine treatment. Post-therapy scan performed 10 days after a 150 mCi 131NaI revealed radioiodine uptake in left temporal region. To elucidate the abnormal head uptake, Tc-99m MDP bone scan and head magnetic resonance image was performed. No anomalous uptake was observed in the bone scan. Head magnetic resonance image found a well-circumscribed lesion in temporal was compatible with a vascular malformation. Angioresonance confirmed the diagnosis of cavernous angioma, a benign vascular tumor.
Abstract LB-113: Non-small cell lung cancer cells with high ALDH1 activity display cancer stem cell properties and show chemoresistance
Authors: S Wong, E Leung, V Tin, M Wong
Journal: Cancer Research (2011)

Abstract Introduction Cancer stem cells (CSC) are believed to possess tissue stem cell-like properties such as self-renewal and toxicity resistance. These characteristics would facilitate tumor propagation and development of chemoresistance. The biology and regulation of CSC have mostly been studied in acute leukemia and certain solid tumors such as breast cancer. Relatively little data are available regarding CSC in non-small cell lung cancer (NSCLC) due to the lack of a specific CSC marker. This study aims to analyze the applicability of candidate CSC markers by utilizing chemotherapy treatment to enhance CSC proliferation in NSCLC cells. Methodology The expression or activity of 4 putative stem cell markers, CD24, CD44, CD133 and aldehyde dehydrogenase (ALDH1) were measured by flow cytometry in the NSCLC cell lines H1650, HCC827 and H358 before and after chemotherapy treatment for 24 hours. Tumor cells with enhanced marker expression after treatment were regarded as potential CSC, and were selected by fluorescence-activated cell sorting (FACS). Functional analysis was used to test for CSC properties in the marker+ and marker-subpopulations of untreated cells. The expression of genes involved in tissue stem cell functions were also compared by quantitative RT-PCR. Results Flow cytometry analysis showed amongst the 4 markers, only ALDH1+ subpopulation was significantly enhanced by chemotherapeutic treatment, suggesting ALDH1 could be a CSC marker. Untreated ALDH1+ cells formed significantly higher numbers and larger cell spheres in non-adherent culture medium than ALDH1− cells. Likewise, ALDH1+ cells formed significantly more and larger colonies in colony formation assay. Furthermore, MTT assay demonstrated higher resistance to cisplatin and etoposide treatments in ALDH1+ than ALDH1− cells. In addition, ALDH1+ cells showed more prominent tumorigenicity than ALDH1− cells in vivo; as few as 500 ALDH1+ cells formed xenograft tumor in SCID mice which were serially transplantable to 2nd and 3rd recipients, while no tumor was formed from ALDH− cells. Finally, expression analysis of sorted cells revealed higher expression of the pluripotency genes, OCT4, NANOG, BMI1 and SOX9, in ALDH1+ cells. Conclusion NSCLC cells expressing ALDH1 displayed higher capacity for cell renewal, tumorigenecity and drug resistance, as well as showed higher expression of pluripotency genes, suggesting that ALDH1 could be a useful CSC marker in NSCLC. Pathways mediated by the differentially expressed genes studied could be involved in CSC maintenance and/or chemoresistance in NSCLC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-113. doi:10.1158/1538-7445.AM2011-LB-113
The Role of 18F-Flourocholine PET/CT in Biochemically Relapsed Prostate Cancer
Authors: Amir Iravani Tabrizipour, Marina Dunne
Journal: Clinical Nuclear Medicine (2015)

We present the case of a 60-year-old male patient with T3b-N1, Gleason score 8, adenocarcinoma prostate with biochemical relapse (prostate-specific antigen, 5.2 μg/L) 1 year after radical treatment with 50.4-Gy 3-dimensional conformal radiotherapy and androgen deprivation therapy. Conventional imaging including contrast-enhanced abdominal CT and whole-body bone scintigraphy did not reveal any local recurrence or distant metastases. F-flourocholine PET/CT demonstrated a solitary, intensely avid (SUVmax, 9.2) osteolytic metastasis in the manubrium. Histopathology confirmed metastatic prostate adenocarcinoma.