tbuckley/cabot-search huggingface dataset:
Abstract 5354: HPV-16 E7 oncoprotein induces centriole multiplication through deregulation of PLK4, a master regulator of centriole biogenesis
Authors: Nina Korzeniewski, Anette Duensing, Stefan Duensing
Journal: Cancer Research (2010)

Abstract Human papillomavirus (HPV)-associated neoplasms exhibit abnormal centrosome and centriole numbers that can cause mitotic defects, chromosome missegregation and aneuploidy. Centrosomes are the major microtubule-organizing centers in most mammalian cells and orchestrate the formation of mitotic spindle poles. The centrosome consists of a pair of centrioles that normally duplicate precisely once prior to mitosis. The HPV-16 E7 oncoprotein has been found to rapidly stimulate centriole overduplication within a single cell division cycle, thereby increasing the risk for cell division errors. We discovered that this activity of the HPV-16 E7 oncoprotein involves the concurrent formation of multiple daughter centrioles at single maternal centrioles (centriole multiplication). We found that deregulated cyclin E/cyclin dependent kinase 2 (CDK2) activity, as occurs following HPV-16 E7 oncoprotein expression, leads to the aberrant recruitment of polo-like kinase 4 (PLK4) to maternal centrioles, which is subsequently degraded by the SCF ubiqutin ligase complex. These and several other results underscore that the level of PLK4 at maternal centrioles is rate-limiting for centriole multiplication. Hence, we asked whether the HPV-16 E7 oncoprotein can alter PLK4 expression and/or localization. We found aberrant PLK4 protein expression at maternal centrioles in primary human keratinocytes engineered to stably express HPV-16 E7. Real-time quantitative RT-PCR revealed an increase in PLK4 transcription in keratinocytes stably expressing HPV-16 E7. The ability of HPV-16 E7 to upregulate PLK4 mRNA was found to depend on its ability to degrade the retinoblastoma (pRb) protein, suggesting a role of E2F-mediated gene transcription in deregulation of PLK4. Collectively, these results highlight the critical role of PLK4 as a regulator of centriole biogenesis and identify PLK4 as a novel target for small molecules to prevent centriole abnormalities, mitotic infidelity and malignant progression in HPV-associated neoplasms. 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 5354.
FINAL FIVE-YEAR FOLLOW-UP OF POLYMER-FREE SIROLIMUS- AND PROBUCOL-ELUTING STENTS VERSUS NEW GENERATION ZOTAROLIMUS-ELUTING STENTS IN PATIENTS WITH CORONARY ARTERY DISEASE
Authors: Robert A. Byrne, Sebastian Kufner, Jonas Sorges, Janika Repp, Salvatore Cassese, Stefanie Schulz, Massimiliano Fusaro, Ilka Ott, Tareq Ibrahim, Karl-Ludwig Laugwitz, Adnan Kastrati
Journal: Journal of the American College of Cardiology (2015)
Abstract 4494: Preoperative serum levels of matrix metalloproteinase-2 (MMP-2) and survival of breast cancer among Korean women
Authors: Nan Song, Hyuna Sung, Sujee Jeon, Yunhee Lee, Ji-Yeob Choi, Sue K. Park, Kyoung-Mu Lee, Keun-Young Yoo, Dong-Young Noh, Se-Hyun Ahn, Sang-Ah Lee, Daehee Kang
Journal: Cancer Research (2012)

Abstract Objective: We evaluated whether preoperative serum levels of matrix metalloproteinase-2 (MMP-2) work as a prognostic biomarker in breast cancer prognosis. Methods: Three hundred and three women with histologically confirmed breast cancer were recruited. The follow-up time for all patients was 4.24 years. The MMP-2 levels were quantitatively measured by enzyme-linked immunosorbent assay (ELISA) using the preoperative serum. The relationship of MMP-2 to survival was investigated using Cox's proportional hazard model adjusted for the TNM stage and estrogen receptor (ER) status. Results: In the multivariate analysis, disease-free survival (DFS) was worse among patients with the third tertile of MMP-2 compared to the first tertile of MMP-2 (hazard ratio (HR)=1.80, 95% confidence interval (CI)=1.04-3.11, P=0.04). Furthermore, when the patients were stratified by histological grade and nuclear grade, the worse DFS was predicted by high levels of MMP-2 (HR=2.90 and 95% CI=1.42-5.92 in histological grade III vs. I-II and HR=2.61 and 95% CI=1.26-5.39 in nuclear grade III vs. I-II). In ER negative patients, high levels of MMP-2 also tended to have a worse prognosis (HR=2.75 and 95% CI=1.32-5.73). Conclusions: Our results suggest that the preoperative serum levels of MMP-2 were associated with the survival of breast cancer as a potential prognostic biomarker. 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 4494. doi:1538-7445.AM2012-4494
Abstract 2086: Regulation of Axl receptor tyrosine kinase expression, invasion and metastasis by miR-34a and mir-199a/b
Authors: Giridhar Mudduluru, Paolo Ceppi, Kumarswamy Regalla, Heike Allgayer
Journal: Cancer Research (2010)

Abstract Axl is a receptor tyrosine kinase over-expressed in different human cancers which induces proliferation, migration and invasion. In this study, we show that specific microRNAs (miR) can target the 3’-UTR of Axl and can modulate its expression. By a bioinformatics approach, we found conserved target sites for miR-34 and miR-199 within the Axl-3’-UTR at 31-49 nt and 29-56 nt, respectively. Luciferase-reporter assays with wild-type and deleted miR-34 and −199 seed sequences of Axl-3′UTR confirmed the specificity of targeting. An inverse correlation between Axl protein and miR-34a expression in a panel of non-small cell lung cancer (NSCLC), colorectal (CRC) and breast cancer (BRC) cell lines was observed, while no miR-199a or 199b expression was detected. Transient transfection of antagonist-miR or pre-miR for miR-34a and 199a significantly induced and reduced Axl-protein levels, respectively. Pre-miR transfection was able to inhibit in vitro migration and invasion of H1299 and RKO cells and, in vivo, to reduce the number of distant lung- or liver-metastasis in a chicken-embryo-metastasis assay. Moreover, methylation specific PCR on bisulfite-converted DNA obtained from the cell lines showed that the miR-34a promoter methylation status was significantly correlated with Axl expression, and that miR-199a/b promoter regions were methylated in all the cell lines tested. These results suggest that Axl receptor, together with its role in cancer cell growth, invasion and metastasis formation, can be regulated by miR34a and 199a/199b, and that one of the reasons for its over-expression in tumors can be the methylation of DNA that encodes these specific miRs which target Axl expression. 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 2086.
Heavy Tobacco Use In High Schools Needs to be Addressed
Authors: N. Berreth, K. N. Williams
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Heavy Tobacco Use In High Schools Needs to be Addressed Get access Nowell Berreth, Nowell Berreth Search for other works by this author on: Oxford Academic PubMed Google Scholar Kymber N. Williams Kymber N. Williams Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 22, 20 November 1991, Pages 1615–1616, https://doi.org/10.1093/jnci/83.22.1615 Published: 20 November 1991
Abstract 5330: Leukemia initiating cells are frequent and oligoclonal in de novo resistant ALL
Authors: Beat Bornhauser, Maike Schmitz, Petra Breithaupt, Nastassja Scheidegger, Paulina Mirkowska, Barbara Meissner, Laura Bonapace, Joelle Tchinda, Gunnar Cario, Andre Schrauder, Martin Stanulla, Martin Schrappe, Bourquin Jean-Pierre
Journal: Cancer Research (2011)

Abstract Xenotransplantation of primary leukemia cells constitutes an attractive strategy to model disease for translational research, but the consequences of selective pressure on leukemia cells need to be clarified. Here we evaluate the phenotypic and genetic stability of primograft samples that were established by xenotransplantation of ALL cells from a group of patients with very high-risk precursor B-cell ALL, characterized by the persistence of minimal residual disease (VHR-ALL by MRD) after an intensive induction and consolidation therapy. Phenotypic properties remained unchanged, with concordant immunophenotypes in 9-10/10 leukemia-associated markers after up to 5 passages in Nod/scidIL2Rgammanull (NSG) mice and with stable drug response profiles in vitro on bone marrow stroma co-cultures. In 4/6 cases, 100 unsorted ALL cells were sufficient to reconstitute the leukemia. From up to 5 recurrent copy number abnormalities (CNA) detected in diagnostic samples, most were maintained in primografts. Changes in CNAs upon transplantation in NSG mice were few with 0-2 new lesions per case, mostly occurring during the first xenotransplantation. At the single cell level, the pattern of deletions in the CDKN2A/B locus revealed distinct subsets of ALL cells, which could reproducibly be tracked in primografts. These results provide unequivocal data for the existence of clonally closely related but distinct subsets of leukemia initiating cells in ALL, which has important implications for the use of this model for translational research. 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 5330. doi:10.1158/1538-7445.AM2011-5330
Abstract 836: <i>In vivo</i> PET imaging of MET receptor in human cancer using [11C]SU11274
Authors: Patrick C. Ma, Chunying Wu, Zhe Tang, Weiwen Fan, Wenxia Zhu, Changning Wang, Edurado Somoza, Norbert Owino, Ruoshi Li, Yanming Wang
Journal: Cancer Research (2010)

Abstract The mesenchymal-epithelial transition (MET) receptor plays prominent role in human tumorigenesis, tumor progression and metastasis. Overexpression or mutation of MET results in activation of oncogenic signaling pathways and leads to upregulation of diverse tumor cell functions. Mounting evidence has validated MET receptor as novel target for anticancer therapy. For efficacy evaluation of various MET-targeted anticancer therapies currently under development, it is critical to develop an imaging tool that permits detection and quantification of MET expression in vivo. To date, a number of small molecule MET inhibitors have been developed, including SU11274, which is a specific, reversible MET inhibitor that induces apoptosis in cells transformed by activated MET kinase. Here, we report the radiosynthesis and evaluation of a molecular imaging probe, [11C]SU11274, for quantification of MET receptors in human cancers in vivo. The radiolabeling with C-11 was accomplished through radiomethylation using 3-[3,5-Dimethyl-4-(piperazine-1-carbonyl)-1H-pyrrol-2-ylmethylene]-2-oxo-2,3-dihyro-1H-indole-5-sulfonic acid (3-chlorophenyl)-methyl amide hydrochloride as a key precursor. Following the synthesis of the precursor that was achieved in 10 steps with a total yield of 9.7%, [11C]SU11274 was obtained through radiomethylation in a range of 5-10 % radiochemical yield and over 95% radiochemical purity. For in vivo PET studies, two human lung adenocarcinoma cancer xenograft models were established using MET-positive H1975 and MET-negative H520 cell lines. The time-radioactivity curves showed that the uptake of [11C]SU11274 in the H1975 xenograft was significantly higher than in the H520 xenograft (p = 0.00019). Compared to H520, the H1975 xenograft mice exhibited an increased tumor uptake of [11C]SU11274 throughout the entire measurement period of 90 min. At 65 min post-injection, the radioactivity concentration ratio of H1975/H520 reached a statistically significant and enhanced ratio of 2.1, and peaked at 2.6 at 80 min. The PET imaging results were consistent with their corresponding immunohistochemical tissue staining patterns of MET receptors from the same animals. Hence, our results suggest that [11C]SU11274-PET is a specific imaging marker that can differentiate and quantify MET receptor expression in vivo. These studies demonstrated that [11C]SU11274-PET can facilitate the clinical development of MET-targeted cancer therapeutics. 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 836.
HTLV-II–Associated Cutaneous T-Cell Lymphoma in a Patient with HIV-1 Infection
Authors: Bernard Poiesz, Dipak Dube, Syamalima Dube, Jayne Love, Lawrence Papsidero, Aysegul Uner, Robert Hutchinson
Journal: New England Journal of Medicine (2000)

Patients infected with human immunodeficiency virus type 1 (HIV-1) are susceptible to neoplasms, including Kaposi's sarcoma, non-Hodgkin's lymphoma, and anal and cervical carcinoma.1–5 Some of these neoplasms have been associated with oncogenic infectious agents such as human herpesvirus 8 (HHV-8), Epstein–Barr virus (EBV), human T-cell leukemia–lymphoma virus type I (also known as human T-cell lymphotropic virus type I; HTLV-I), and the human papillomavirus (HPV).1–5 Presumably, the immunosuppression caused by HIV-1 allows for the expansion of virally transformed cells and the development of cancer. HTLV-I and human T-cell lymphotropic virus type II (HTLV-II) are oncogenic retroviruses.6,7 HTLV-I infects . . .
SP0048 Focus Transition? - Supporting Teenagers with Rheumatic or Musculoskeletal Disease into Adulthood
Authors: K. Minden
Journal: Annals of the Rheumatic Diseases (2013)

<h3></h3> Adolescence is a life phase with tremendous biological changes and social-role transitions. This unique developmental stage is characterized by pubertal maturation, individuation from parents and peer group identification. In this sensitive period both normative and maladaptive patterns of adult health are established. Sexual health, tobacco use, substance misuse, mental health, obesity, and injuries become major health categories. Adolescents have particular patterns of rheumatic diseases. Adolescents are not only medically, but also developmentally and psychologically distinct from children and from adults. Knowledge of adolescent health and normal adolescent development is pivotal for clinicians to provide developmentally appropriate care for adolescents with rheumatic diseases. The period of transition from adolescence to adulthood presents particular challenges for young people with rheumatic diseases (as for those with other chronic diseases). These patients have not only to cope with their illness, but also with common tasks of adolescence. Young people with a chronic illness may face barriers in achieving autonomy and independence or finding a vocation. Also, they are “doubly disadvantaged” by the higher attributable risk from risk taking behavior (e.g., smoking, substance use) in the context of the underlying chronic disease or its treatment. Therefore, they need support, information and advice on their disease, but also on generic and sexual health, educational/vocational and psychosocial issues. Since rheumatic diseases continue in approximately half of all patients into adulthood, transitional care is an important consideration for adolescents. It is essential to provide the young people with educational resources to help them develop skills they need to manage their care and develop routes of communication to facilitate the transfer from paediatric to adult care provider. Key elements of transitional care include among others a written transition policy, a preparation period, an education programme for patient and parent addressing medical, psychosocial and educational/vocational aspects of care, and a network of relevant local agencies and health care provider (1). The latter should have expertise in rheumatic diseases and special problems of those young people whose illness began in childhood. A close collaboration between health care providers will bridge the gap between pediatric and adult rheumatology. Due to the holistic nature of transition, care requires a multidisciplinary and multiagency approach. McDonagh JE. Young people first, juvenile idiopathic arthritis second: transitional care in rheumatology. Arthritis Rheum 2008;59:1162-70. <h3>Disclosure of Interest</h3> None Declared
A Hereditary Factor in Chondrodystrophia Calcificans Congenita
Authors: F. Clarke Fraser, Jessie Boyd Scriver
Journal: New England Journal of Medicine (1954)

CHONDRODYSTROPHIA calcificans congenita is a rare congenital condition diagnosed by the radiologic demonstration of multiple punctate calcine epiphysial deposits in an infant who may also have one or more of a variety of other defects. The observation of this rare disease in 2 siblings led us to consider the possibility that it was hereditary, and an analysis of the available family data in the literature was therefore undertaken from this point of view.CharacteristicsThe disease was first described by Conradi,1 who considered it a form of chondrodystrophia fetalis hypoplastica. It was named chondrodystrophia calcificans congenita by Hünermann2 and has . . .
Abstract LB-281: The role of POU5F1B in prostate cancer.
Authors: Hongmei Jiang, Man-Tzu Wang, Daotai Nie
Journal: Cancer Research (2013)

Abstract POU5F1B is the one of the pseudogenes of POU5F1 (also known as Oct3, Oct4) with protein-coding potential. It is localized on chromosome 8q24.21, inside of the 1.2 Mb “gene desert” between the FAM84B and the c-MYC gene, which is closely associated with prostate cancer risk. Recent studies showed that POU5F1B, but not POU5F1, is expressed in prostate tissue and is overexpressed in prostatic carcinoma, compared to normal prostatic tissue surrounding the carcinoma. However, the role of POU5F1B in prostate cancer is still unknown. Through in silico analysis of dataset HG-U95A, we found that POU5F1B expression is increased in prostate tumor and markedly increased in metastatic tumors. Western blot analysis revealed a marked increase in POU5F1B expression in prostate cancer cells when compared to non-tumorigenic RWPE-1 cells. To study the role of POU5F1B in prostate cancer, we cloned POU5F1B from prostate cancer cells, sequenced the amplicons, and found several polymorphism. We made pCDH-myc-POU5F1B constructs and expressed POU5F1B in prostate cancer cell lines LNCaP, DU145, and PC-3. Overexpression of POU5F1B in LNCaP, DU145 and PC3 cells can increase cell invasion using Boyden chamber assay. Overexpression of POU5F1B in LNCaP cells also promotes colony formation in soft agar. We also found that DU145 cells with POU5F1B overexpression lost cell-cell contact, compared to DU145-pCDH vector cells, and further found that CDH1 expression is downregulated in DU145-POU5F1B cells. Depletion of POU5F1B reduced the tumor forming ability of LNCaP cells in vivo. The data collectively suggest an important role of POU5F1B in prostate tumor formation and progression. Citation Format: Hongmei Jiang, Man-Tzu Wang, Daotai Nie. The role of POU5F1B in prostate cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-281. doi:10.1158/1538-7445.AM2013-LB-281
Myocarditis Associated with Rabies
Authors: Eugene Ross, Steven A. Armentrout
Journal: New England Journal of Medicine (1962)

ACUTE myocarditis of considerable clinical and pathological significance has been described in a variety of viral infections.1 It is the purpose of this paper to present a case of human rabies with an associated myocarditis, because of its clinical and pathological rarity. A search of the literature and personal communication with the Armed Forces Institute of Pathology did not reveal any report of a similar lesion occurring in a case of rabies.Case ReportA 19-year-old woman (753–858) sustained a superficial laceration of the right hand when bitten by a cat in Guatemala. The cat, not previously known to be . . .
NATIONWIDE DIFFERENCES IN THE UTILIZATION OF MECHANICAL CIRCULATORY SUPPORT AS BRIDGE TO TRANSPLANTATION IN THE UNITED STATES
Authors: Sadeer G. Al-Kindi, Mahmoud Farhoud, Chantal Elamm, Mahazarin Ginwalla, Michael Zacharias, Rudolfo Benatti, Benjamin Medalion, Salil Deo, Soon Park, Guilherme Oliveira
Journal: Journal of the American College of Cardiology (2016)
1035 HEAT SHOCK FACTOR 1 ACCELERATES HEPATOCELLULAR CARCINOMA DEVELOPMENT BY ACTIVATING NUCLEAR FACTOR κB/MITOGEN-ACTIVATED PROTEIN KINASE
Authors: M. Chuma, N. Sakamoto, S. Hige, M. Nakanishi, M. Natsuizaka, G. Suda, T. Sho, S. Maeda
Journal: Journal of Hepatology (2013)
RAPID ESCALATION OF CARDIOVASCULAR RISK FACTOR BURDEN IN RURAL AREAS OF NATIONAL CAPITAL REGION OF DELHI OVER TWENTY YEARS
Authors: Ambuj Roy, P A Praveen, R. Lakshmy, R. Gupta, K. Srinath Reddy, D. Prabhakaran, Anand Krishnan
Journal: Journal of the American College of Cardiology (2015)
Abstract 2591: Folate receptor alpha: A promoter of cancer cell proliferation that is independent of folate
Authors: Katherine A. Rybinski, Brian E. Tomkowicz, Barton A. Kamen, Luigi Grasso, Nicholas Nicolaides, Philip Sass, Yuhong Zhou
Journal: Cancer Research (2011)

Abstract Folate receptor alpha (FRα) is over-expressed in malignant tumors of epithelial origin, particularly in ovarian cancer, but largely absent in normal tissue. High levels of protein expression in tumor cells are associated with increased proliferative capacity and enhanced chemo-resistance to Cisplatinum (CP). However, the underlying mechanism remains unclear. We sought to evaluate the biological function of FRα in CP-resistant cancer and hypothesized that alterations of FRα expression levels in drug CP-resistant cancers would result in the re-sensitization of tumor cells to CP. We first developed a human ovarian cancer cell line, IGROV-1, with increased CP resistance and found that these cells also showed an increase in FRα expression over parental IGROV-1 cells. Then, we used FOLR1 specific siRNA to completely knock-down FRα expression. Surprisingly, ablation of FRα expression did not restore sensitivity to CP but had a substantial negative impact on proliferation in both parental and CP-resistant cells. Similar phenomena were also observed when FRα was knocked-down in 786-0 cells, a human renal carcinoma line that expresses robust levels of FRα. In contrast, when we applied FRα knock-down to the normal human kidney cells HK-2 (FRα+), we observed no impairment on proliferation. One explanation of these results is that removal of FRα in cancer cells impairs the ability of these cells to uptake reduced folates, a requirement for nucleic acid synthesis and other methylation reactions. However, even pharmacological concentrations of 5-methyltetrahydrofolate, provided only partial restoration of proliferation in these cells. Taken together, these results suggest that FRα plays an essential role in the proliferation of tumor cells, but not in normal cells via a yet undefined pathway. 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 2591. doi:10.1158/1538-7445.AM2011-2591