tbuckley/cabot-search huggingface dataset:
Abstract 257: R4 knock-out mice showed lung hyperplasia and susceptible to urethane-induced lung carcinogenesis
Authors: Ji Won Choi, Il Yong Kim, Jae Hoon Shin, Seo Hyun Lee, Yun Soo Bae, Je Kyung Seong
Journal: Cancer Research (2010)

Abstract Lung cancer is responsible for 1.3 million deaths worldwide annually. There have been several reports on candidate genes driving lung cancers including ras. However still it is needed to find new genes which can cause lung cancers. Recently we developed R4 knock-out (KO) mice which showed larger relative lung weight and volume than age-matched wild-type (WT) mice. Lung hyperplasia was found with increased alveolar thickness in 6, 18 and 40 week-old R4 KO mice. Also, this finding was observed in E16.5 and 18.5 day KO mice. Cell cycle markers including PCNA and cyclinD1 were highly expressed in the lung of R4 KO mice than WT mice. PCNA positive cells were mostly type 2 pneumocytes. To determine the susceptibility of lung cancer in R4 KO mice, we induced lung cancer by the injection of 1g/kg urethane weekly for a total of eight doses. Twenty weeks after the initial injection, mice were sacrificed, and the lungs were fixed, and the number of tumors on the lung surface was assessed. Also lung tumors were scanned by micro-CT at the end of the lung carcinogenesis protocol for measure the tumor diameter. Surface lung tumor number is significantly increased in KO mice. And tumor size is also significantly larger in KO mice than WT. Histological findings showed more severe well differentiated lung adenoma in urethane-injected R4 KO mice. We conclude that R4 KO mice is susceptible to tumorigenesis in the urethane model and the functional loss of R4 gene may cause lung cancer. Therefore, R4 gene has a possibility as a potential target for chemoprevention of lung cancer. 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 257.
AB0266 Baseline CD4+ T Lymphocyte Count Predicts Clinical Response to Rituximab in Rheumatoid Arthritis
Authors: M.H. Stradner, C. Dejaco, K. Brickmann, W.B. Graninger, H.-P. Brezinschek
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> B cell depletion with rituximab (RTX) is an effective treatment strategy for Rheumatoid Arthritis (RA). However, a considerable proportion of patients fail to respond to this treatment, particularly after previous therapy with tumor necrosis factor-α inhibitors. <h3>Objectives</h3> Our study was designed to identify lymphocyte subsets in the peripheral blood of RA patients predictive of clinical response to RTX. <h3>Methods</h3> 52 RA patients receiving RTX for the first time were included in this prospective observational study. Clinical assessment, complete blood count and flow cytometry of lymphocyte subsets were obtained at baseline as well as at weeks 2 and 24 after RTX. Logistic regression and receiving operating characteristic (ROC) curve analyses were conducted to identify predictors for EULAR response at week 24. <h3>Results</h3> Total lymphocyte count (TLC) at baseline was significantly lower in EULAR moderate and good responders compared to non- responders (<i>P</i>=0.007). We also observed a lower T lymphocyte count in moderate and good responders than in non-responders (<i>P</i>=0.008). Among the T-cell subsets we found higher levels of CD4<sup>+</sup>T cells in non-responders compared to moderate and good responders (<i>P</i>=0.024). Multivariate logistic regression indicated that TLC was an independent and significant negative predictor of EULAR response (OR 0.853 [0.737-0.987] per TLC increase of 100 lymphocytes/μl, <i>P</i>=0.033). Also, CD4<sup>+</sup>T cell count was confirmed as an independent and significant negative predictor of EULAR response (OR 0.805 [0.665-0.975] per CD4<sup>+</sup>T cell count increase of 100 cells/μl, <i>P</i>=0.027). A baseline TLC of &lt;1645/μl predicted EULAR response with a high specificity of 91% (sensitivity 40%). A baseline CD4<sup>+</sup>T cell count of &lt;1126/μl predicted EULAR response with a specificity of 91% and a sensitivity 66%. <h3>Conclusions</h3> Baseline TLC and particularly CD4<sup>+</sup>T lymphocyte count reliably predict clinical response to RTX in RA patients. <h3>Disclosure of Interest</h3> M. Stradner: None declared, C. Dejaco Paid instructor for: Speakers fees from Hoffmann-La Roche, Austria, K. Brickmann: None declared, W. Graninger: None declared, H.-P. Brezinschek Grant/research support: Unrestricted research grant by Hoffmann-La Roche, Austria <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3554
Abstract P1-01-09: Which nomograms may be the best for predicting nonsentinel lymph node metastasis in breast cancer patients: a meta-analysis.
Authors: K Chen, L Jin, L Zhu, Q Shan, F Su
Journal: Cancer Research (2012)

Abstract Background: Axillary lymph node dissection (ALND) is the standard treatment for breast cancer patients with positive sentinel lymph nodes (SLNs). Several nomograms were developed to identify SLN-positive patients with low risk of nonsentinel lymph nodes (NSLNs) metastasis. These nomograms were validated in different populations and it is still unknown which is the best. This study is to present a systemic review and perform a meta-analysis to obtained the pooled AUC (Area Under the receiver-operator Curve) value of each models. Methods: This review focused on six models: Cambridge, MSKCC, Mayo, MDA, Tenon and Stanford models. A “Pubmed” search and “Web of science” search were conducted and 35 literatures were ultimately included. AUC and the number of patients with positive NSLNs were extracted. Publication bias and heterogeneity were analyzed. AUCs were converted to odds ratios (ORs) for combination. The combined ORs were converted back to AUCs to represent the integrated discriminative capabilities of each models. Findings: In total, the Cambridge, Mayo, MDA, MSKCC, Stanford and Tenon models were validated in 8, 6, 4, 39, 14 and 15 studies, with 2156, 2431, 843, 8143, 3700 and 3648 patients included, respectively. There were no publication bias or heterogeneity observed in the Cambridge, Mayo, MDA and Tenon models (Table 1). The combined ORs and the corresponding AUCs of each models were listed as follow: Cambridge (OR = 3.86, AUC = 0.71), Mayo (OR = 3.71, AUC = 0.71), MSKCC (OR = 3.47, AUC = 0.70), MDA(OR = 3.44, AUC = 0.70), Tenon (OR = 3.46, AUC = 0.70) and Stanford (OR = 2.92, AUC = 0.67). For each of the predictive models, both fixed and random effect models were used to calculate the combined OR. The presence of larger difference between the fixed and random effect analysis suggests small study effects, rendering the meta-analysis relatively less reliable. The combined ORs were identical when fixed and random effect models were used in the Cambridge and MDA models, suggesting that there was no small study effects in these two models. Conclusions: All of the included models are all better than random chance but not provide excellent discriminative capabilities. The Cambridge and Stanford models were relatively superior and inferior when compared with the other models, respectively. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P1-01-09.
Abstract 2885: Retinoic acid suppressed HEY cell-induced xenograft tumor possibly through reduction of CD133+ cancer stem cells
Authors: Zhong Li
Journal: Cancer Research (2010)

Abstract Ovarian cancer is the most lethal gynecologic cancer with the higher recurrence. Increasing evidence indicates that cancer stem cells plays pivotal role in tumorigenesis and chemoresistance. Retinoic acid (RA), a synthetic derivative of vitamin A, has been used for treatment and chemoprevention of ovarian cancer. But it is not clear if RA affects ovarian cancer stem cells. In this paper, we found that all-trans retinoic acid (RA) treated ovarian cancer cell HEY resulted in the significant smaller xenograft tumor in SCID/NOD mice than untreated HEY cells. To understand if RA inhibition of tumor is involved in dysfunction of cancer stem cells, we detected cancer stem cells in HEY-induced tumors. CD133 positive cells in ovarian cancer were reported to have stem-like features. We found that RA-pretreated HEY cell-induced tumors had less of CD133 positive cells (3.0%) than RA-untreated ones (5.5%). To determine if RA affects status of CD133+ cells, we first cultured HEY cells in spheroid condition. HEY cells formed spheroid in suspend culture in which the percentage of CD133+ cells was increased in analyses by flow cytometry and histochemical staining. A single spheroid of Hey cells was peritoneally injected into mice and induced ovarian tumors. Consequently, treatment of RA in initiating spheroid culture attenuated HEY spheroid formation. In analyzing the molecular mechanism of RA in tumor suppression, we found that RA-treated HEY cells increased phosphorylated PTEN and level of p53 and CRABP II, and reduced expression of CD133 in Hey cells in early period (24-48h). PTEN, a tumor suppressor gene and a PI3K functional antagonist, is widely involved in normal and cancer cell proliferation, migration, drug resistance and stem cell maintenance. We further overexpressed PTEN in HEY cells that dramatically suppressed spheroid formation, suggesting that RA-induced early PTEN activation, increases of p53 and CRABP II may be involved in change of malignancy of HEY cells. These results demonstrate that RA treatment of ovarian cancer cells would alternate the cell features that compromise the change of Cd133+ positive stem-like cells which are important in tumorigenesis. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 2885.
Diagnostic Performance of In-111 Capromab Pendetide SPECT/CT in Localized and Metastatic Prostate Cancer
Authors: William J. Rieter, Thomas E. Keane, Mark A. Ahlman, Clayton T. Ellis, Kenneth M. Spicer, Leonie L. Gordon
Journal: Clinical Nuclear Medicine (2011)

Purpose: To determine the diagnostic performance of In-111 capromab pendetide single photon emission computed tomography/computed tomography (SPECT/CT), in the prostate gland, seminal vesicles, and lymph nodes via correlation to a gold standard of histopathology. Materials and Methods: In this study, we retrospectively reviewed all In-111 capromab pendetide SPECT/CT acquired at our institution for dedicated histopathology within a 4-month period. Statistical measures of performance were calculated in terms of glandular, seminal vesicle, and lymph node activity. The accuracies of glandular and seminal vesicle activity were then correlated to the indices of risk, including the stage, Gleason score, and prostate-specific antigen level, as well as the treatment history. Results: Of the 200 scans meeting the criteria of our study, 197 had prostate gland histopathology, 94 had bilateral seminal vesicle histopathology, and 5 had a total of 43 resected lymph nodes for comparison. The overall accuracies of the scan results were determined to be 77.7% (area under the receiver operating characteristic curve [AUC] = 0.539) for the gland, 67.0% (AUC = 0.510) for the seminal vesicles, and 93.0% (AUC = 0.787) for lymph nodes. For glandular activity alone, scan accuracy was found to significantly improve with increasing Gleason score (P < 0.0001), and in a setting prior to treatment (P = 0.0005). No statistically significant differences were found between different scan groups with regards to seminal vesicle activity. Conclusions: The results of this study provide substantiating evidence In-111 capromab pendetide can be used to accurately diagnose lymph node metastases from primary cancers of the prostate; however, they also suggest the test may have limited utility in diagnosing tumors within the prostate gland and seminal vesicles.
Abstract 5488: The rate of vertical transmission of human papillomavirus from mothers to infants: Relationship between infection rate and mode of delivery
Authors: Tae Jin Kim, Jae Ho Lee, Hyoung S. Jang, Jun S. Kim, In H. Lee, A R. Cho, Jae W. Kim, Jae W. Shim, Ki H. Lee, Kyung T. Lim, Sung R. Hong
Journal: Cancer Research (2012)

Abstract Objectives: To assess the prevalence of human papillomavirus(HPV) infection among pregnant women and to evaluate the rate of vertical transmission of HPVs to their infants. Methods: 491 pregnant women and their infants delivered at Cheil General Hospital &amp; Women's Healthcare Center were prospectively recruited for this study between February 2010 and November 2011. Cervical swabs and blood samples were collected from the women at 32-36 weeks of gestation. Neonatal buccal swabs and cord blood were taken immediately after birth. HPV positive neonates were rechecked HPV DNA at 6 months postpartum. HPV genotyping with HPV DNA chip (MyGene Co., Seoul, Korea) was used to detect the HPV of mothers and neonates. Type specific PCR was performed to see HPV DNA in the maternal and cord blood in cases of mother and infant infected same types of HPV DNA. Results: HPV DNA was positive in 16%(80/500) of mothers and 3.5%(17/491) of neonates. The rate of vertical transmission of HPV to their infant was 21.3%(17/80). HPV DNA type-specific maternal/neonate concordance was 100%. 16 HPV positive infants were delivered vaginally and 1 HPV positive infant was delivered by cesarean section with labor. There is no HPV positive infants delivered from cesarean section without labor. All HPV positive neonates were converted HPV negative at 6 months after birth. There was no viremia in maternal and cord blood in cases of mother and infant infected same type of HPV DNA. Conclusions: Prevalence of HPV DNA in neonates born from HPV positive mothers was significantly high. However, these data suggest that neonatal HPV DNA positive is not true vertical infection but contamination during vaginal delivery. Key words: Human papillomavirus, vertical transmission 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 5488. doi:1538-7445.AM2012-5488
Abstract LB-353: Targeting pancreatic cancer stem cells by epigenetic regulation of miR-34a
Authors: Sharmila Shankar, Rakesh Srivastava
Journal: Cancer Research (2011)

Abstract MicroRNA-34a (miR-34a) is a transcriptional target of p53 that is down-regulated in pancreatic cancer. This study aimed to investigate the functional significance of miR-34a on growth of pancreatic cancer stem cells through its epigenetic restoration by chromatin modulators, demethylating agent 5-Aza-2′-deoxycytidine (5-Aza dC) and HDAC inhibitor Suberoylanilide hydroxamic acid (Zolinza/vorinostat/SAHA). Re-expression of miR-34a in pancreatic cancer stem cells and pancreatic cancer cell lines on treatment with 5-Aza dC and SAHA strongly inhibited the cell proliferation, cell cycle progression, self renewal, epithelial to mesenchymal transition and invasion. miR-34a upregulation of by 5-Aza dC and SAHA in pancreatic cancer stem cells (PCSC's) also induced apoptosis by activating caspase 3/7. Modulation of miR-34a expression inhibited the protein expression of its putative target genes Bcl-2, CDK6, Cdc25, SIRT1, which was rescued by inhibiting miRNA-34a in the presence of miR-34a antagomir. miR-34a upregulation also induced acetylated p53, p21WAF1, p27, and PUMA protein levels in PCSC's. Interestingly treatment of PCSC'c with 5-Aza dC and SAHA resulted in the inhibition of epithelial -mesenchymal transition by downregulating N-Cadherin, Zeb-1, a crucial inducer of EMT, Slug and Snail expression and also by transcriptional upregulation of E-Cadherin. SAHA retards in vitro cancer stem cell migration and invasion by the inhibition of Notch signaling pathway. Inhibition of miR-34a by antogomiR abrogates the effects of SAHA and 5-Aza dC, suggesting that SAHA and 5-Aza dC regulate stem cell characteristics in PCSC's through miR-34a. The present study thus demonstrates the role of miR-34a as a critical regulator of pancreatic cancer progression. The restoration of miR-34a expression by 5-Aza dC and SAHA in human primary pancreatic cancer stem cells and cell lines will not only provide mechanistic insight and therapeutic targets for pancreatic cancer but also promising reagent to boost patient response to existing chemotherapies or as standalone cancer drug by the elimination of the cancer stem cells characteristics. 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-353. doi:10.1158/1538-7445.AM2011-LB-353
Inhibition of Mammary Carcinogenesis Treadmill Exercise
Authors: H J Thompson, K C Westerlind, J R Snedden, S Briggs, M Singh
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article Inhibition of Mammary Carcinogenesis Treadmill Exercise Get access Henry J. Thompson, Henry J. Thompson Search for other works by this author on: Oxford Academic PubMed Google Scholar Kim C. Westerlind, Kim C. Westerlind Search for other works by this author on: Oxford Academic PubMed Google Scholar Jack R. Snedden, Jack R. Snedden Search for other works by this author on: Oxford Academic PubMed Google Scholar Stephanie Briggs, Stephanie Briggs Search for other works by this author on: Oxford Academic PubMed Google Scholar Meenakshi Singh Meenakshi Singh Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 6, 15 March 1995, Pages 453–455, https://doi.org/10.1093/jnci/87.6.453 Published: 15 March 1995 Article history Received: 21 September 1994 Revision received: 14 December 1994 Accepted: 01 January 1995 Published: 15 March 1995
Crisscross anchor-stents to prevent metal stent migration during endoscopic ultrasound-guided hepaticogastrostomy
Authors: Yusuke Shima, Hiroyuki Isayama, Yukiko Ito, Tsuyoshi Hamada, Yousuke Nakai, Takeshi Tsujino, Ryo Nakata, Kazuhiko Koike
Journal: Endoscopy (2014)

Endoscopic ultrasound-guided hepaticogastrostomy (EUS-HGS) has become increasingly utilized to palliate malignant biliary obstruction in patients with inaccessible papillae as a result of duodenal tumor invasion [1] [2]. Although a covered self-expandable metal stent (SEMS) is preferred to a plastic stent in EUS-HGS because of its lower risk of bile leakage [3], SEMS migration can be a fatal complication [4]. Herein, we present a case in which a SEMS at risk of proximal migration was successfully managed by adding plastic stents to serve as an anchor.
Screening for Chronic Obstructive Pulmonary Disease
Authors: Albert L. Siu, Kirsten Bibbins-Domingo, David C. Grossman, Karina W. Davidson, John W. Epling, Francisco A. R. García, Matthew Gillman, Alex R. Kemper, Alex H. Krist, Ann E. Kurth, C. Seth Landefeld, Carol M. Mangione, Diane M. Harper, William R. Phillips, Maureen G. Phipps, Michael P. Pignone
Journal: JAMA (2016)

<h3>Importance</h3> About 14% of US adults aged 40 to 79 years have chronic obstructive pulmonary disease (COPD), and it is the third leading cause of death in the United States. Persons with severe COPD are often unable to participate in normal physical activity due to deterioration of lung function. <h3>Objective</h3> To update the 2008 US Preventive Services Task Force (USPSTF) recommendation on screening for COPD in asymptomatic adults. <h3>Evidence Review</h3> The USPSTF reviewed the evidence on whether screening for COPD in asymptomatic adults (those who do not recognize or report respiratory symptoms) improves health outcomes. The USPSTF reviewed the diagnostic accuracy of screening tools (including prescreening questionnaires and spirometry); whether screening for COPD improves the delivery and uptake of targeted preventive services, such as smoking cessation or relevant immunizations; and the possible harms of screening for and treatment of mild to moderate COPD. <h3>Findings</h3> Similar to 2008, the USPSTF did not find evidence that screening for COPD in asymptomatic persons improves health-related quality of life, morbidity, or mortality. The USPSTF determined that early detection of COPD, before the development of symptoms, does not alter the course of the disease or improve patient outcomes. The USPSTF concludes with moderate certainty that screening for COPD in asymptomatic persons has no net benefit. <h3>Conclusions and Recommendation</h3> The USPSTF recommends against screening for COPD in asymptomatic adults. (D recommendation)
Abstract 5414: Malignant monocytic AML cells trigger apoptosis in anti-leukemic lymphocytes: Role of NADPH oxidase gp91phox expression and PARP-1 activity
Authors: Johan Aurelius, Fredrik B. Thoren, Mats Brune, Lars Palmqvist, Markus Hansson, Kristoffer Hellstrand, Anna Martner
Journal: Cancer Research (2012)

Abstract The dysfunction of natural killer (NK) cells and T cells in acute myeloid leukemia (AML) determines the course of disease, but only limited information is available on the mechanisms of lymphocyte inhibition. This study aimed to evaluate to what extent malignant AML cells utilize NADPH-oxidase derived reactive oxygen species (ROS) as an immune evasion strategy. We report that a subset of genetically defined malignant monocytic AML cells (FAB class M4/M5), recovered from blood or bone marrow of untreated AML patients at diagnosis, express gp91phox, a component of the NADPH oxidase. These AML cells produced large amounts of ROS upon activation and triggered PARP 1-dependent apoptosis in adjacent natural killer (NK) cells, CD4+ T cells, and cytotoxic T cells. In contrast, myeloblastic (FAB class M2) or immature (FAB class M1) AML cells did not express gp91phox, did not produce ROS, and did not trigger NK or T cell apoptosis. Our data are suggestive of a novel mechanism by which monocytic AML cells evade lymphocyte immunity. 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 5414. doi:1538-7445.AM2012-5414