tbuckley/cabot-search huggingface dataset:
Abstract 1357: Creation and establishment of xenograft model for uterine leiomyoma in immunodeficient mice
Authors: Chi-Heum Cho, So-Jin Shin, Sang-Hoon Kwon, Soon-Do Cha
Journal: Cancer Research (2012)

Abstract Objective: Uterine leiomyomas are the most prevalent benign tumors in women of reproductive age and the leading indication for hysterectomy in premenopausal women. The underlying causes of uterine leiomyomas are poorly understood, as a result, in part, of the absence of a good model system with which to study these tumors. To overcome this problem, this study was undertaken to develop a murine model for human leiomyoma. Study design: Human leiomyoma tissues were cut into small pieces and some of those were cultured. Tissue pieces and cultured cells were inserted subcutaneously in the flank of each severe immunodeficiency (NOD/SCID gamma, NSG) mice (n=6). Estrogen supplement was needed to maintain serum estrogen level 3 days before the tissue or cultured cells transplantation. Xenograft tissues or cells were harvested after 6wks and analyzed. Results: Six uterine leiomyoma xenografts were successfully established with the tumor tissue derived from six patients. The xenografted human uterine leiomyoma tissues retained their gross appearance with small vessels around the implant tissues and did not change in size up to 6wks after implantation. H&amp;E staining showed that xenografts retained major histologic features of the original leiomyoma. The immunohistochemical staining of SMA(smooth muscle actin) revealed strong cytoplasmic and membranous positivity of spindle tumor cells of xenografts.Conclusions: In summary, transplantation of surgical specimens from uterine leiomyoma patients into NSG mice results in an attractive model for the study of the uterine leiomyoma and may also be useful for analysis or new experimental therapeutic approaches for the treatment of this disease. 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 1357. doi:1538-7445.AM2012-1357
Dietary Patterns and Fractures in Postmenopausal Women
Authors: Bernhard Haring, Carolyn J. Crandall, Chunyuan Wu, Erin S. LeBlanc, James M. Shikany, Laura Carbone, Tonya Orchard, Fridtjof Thomas, Jean Wactawaski-Wende, Wenjun Li, Jane A. Cauley, Sylvia Wassertheil-Smoller
Journal: JAMA Internal Medicine (2016)

Considerable efforts have been undertaken to relate single nutrients to bone health. To this point, results are inconsistent. Suboptimal single nutrient intake does not occur in isolation but rather reflects a poor diet quality.
Dietary Supplements Reduce Cancer Deaths in China
Authors: K. Smigel
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Dietary Supplements Reduce Cancer Deaths in China 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 18, 15 September 1993, Pages 1448–1449, https://doi.org/10.1093/jnci/85.18.1448 Published: 15 September 1993
Abstract 707: CD133 is a useful surrogate marker to predict chemosensitivity of neoadjuvant chemotherapy for breast cancer
Authors: Naoki Aomatsu, Masakazu Yashiro, Shinichiro Kashiwagi, Tamami Morisaki, Tatsunari Fukuoka, Tosiki Hirakawa, Tsuyoshi Hasegawa, Junko Matsuoka, Tsutomu Takashima, Hidemi Kawajiri, Naoyoshi Onoda, Tetsuro Ishikawa, Kosei Hirakawa
Journal: Cancer Research (2012)

Abstract Background:Current studies have demonstrated that neoadjuvant chemotherapy (NAC) improves survival outcomes and increases the chance for breast conservation when applied preoperatively. However, no reliable maker to predict chemosensitivity of NAC is not available. CD133 has been considered as a cancer stem cells (CSCs) marker in many kinds of tumors such as breast cancer, colorectal cancer and brain cancer. The aim of this study was to evaluate the value of CD133 as a surrogate maker to predict chemosensitivity of NAC for breast cancer. Experimental Design: A total of 102 patients with breast cancer of stage II and III, as evaluated by core needle biopsy and ultrasonography, was treated with NAC. Expressions of CD133, estrogen receptor, progesterone receptor, and HER2 were assessed by immunohistochemistry. Results: The clinical complete response (CR) rate of all patients was 18% (18/102), partial response (PR) was 61% (62/102), no change (NC) was 20% (20/102), and progressive disease (PD) was 2% (2 /102). The response rate (RR) was 78% (80/102). The pathological complete response rate (pCR) was 29%. The pCR rate and pathological response of CD133-positive cases was significantly lower than that of CD133-negative cases. The recurrence rate of CD133-positive cases was significantly higher than that of CD133-negative cases. CD133 expression showed a poor disease free survival and overall survival time. A multivariate logistic regression analysis showed that CD133 expression was an independent prognostic factor in breast cancers treated with NAC. Conclusion: CD133 is a useful surrogate maker to predict chemosensitivity of NAC chemotherapy for breast cancer. 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 707. doi:1538-7445.AM2012-707
Abstract 4143: <i>microRNA-874</i> as a tumor suppressor in maxillary sinus squamous cell carcinoma based on microRNA expression signature
Authors: Toyoyuki Hanazawa, Nijiro Nohata, Takashi Kinoshita, Naoko Kikkawa, Miki Fuse, Takeshi Chiyomaru, Hirofumi Yoshino, Hideki Enokida, Masayuki Nakagawa, Yoshitaka Okamoto, Naohiko Seki
Journal: Cancer Research (2012)

Abstract (BACKGROUND) Maxillary sinus squamous cell carcinoma (MSSCC) comprises 2-3% of all cancers of head and neck tumor and the annual incidence rate is 0.5-1.0 per 100,000 populations. After introduction of multimodality treatment comprising radiation therapy along with concomitant intra-arterial chemotherapy, rates of local control was improved. However the prognosis of advanced MSSCC is still worse. The 5-years survival rate of T4 tumors is 50% around. Local recurrence is the most common cause of treatment failure and death. Greater understanding of the molecular oncogenic network in MSSCC could help improve diagnosis, therapy, and prevention of the disease. No studies have been carried out for the purpose of identifying specific microRNA (miRNA) alterations in MSSCC. In this study, we focused on the functional siginificance of the most downregulated miRNA in MSSCC on the basis of miRNA expression signature. (METHODS) We used PCR-based methods to investigate the downregulated miRNAs in clinical specimens of MSSCC. Genome-wide gene expression analysis was performed to identify the molecular networks of microRNA-874 (miR-874) by microarray technique. Cell proliferation and invasion assays were performed to investigate the functional significance of miR-874 and its target genes in MSSCC cell lines. (RESULTS) Our miRNA signature identified that 23 miRNAs were significantly reduced in cancer cells. We focused on miR-874 as the most downregulated novel miRNA in our analysis. Ectopic miR-874 overexpression showed potential tumour suppressive functions such as inhibition of cancer cell proliferation and invasion. A molecular target search of miR-874 revealed that protein phosphatase 1, catalytic subunit, alpha isozyme (PPP1CA), proteasomal ATPase-associated factor 1 (PAAF1) and trans-golgi network protein 2 (TGOLN2) were regulated by miR-874. Overexpression of these genes was observed in MSSCC clinical specimens and each gene expression was inversely correlated with miR-874 expression. Moreover, silencing of the PPP1CA gene significantly inhibited cancer cell proliferation and invasion. (CONCLUSION) The downregulation of miR-874 was a frequent event in MSSCC, which suggests that miR-874 functions as a tumour suppressive miRNA, directly regulating PPP1CA that has a potential role of an oncogene. The identification of novel miR-874-regulated cancer network could provide new insights into potential molecular mechanisms of MSSCC oncogenesis. 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 4143. doi:1538-7445.AM2012-4143
THE EFFECT OF ADDING CLOPIDOGREL OR WARFARIN TO THE GOLD STANDARD, ASPIRIN, ON THE RATE OF REPEAT CORONARY ANGIOGRAPHY AND EARLY SAPHENOUS VEIN GRAFT FAILURE
Authors: Dexter Deleon, Fregenet Alemu, Jason Payne, Sulaiman Rathore, Micheal Bentley, Timothy Ball
Journal: Journal of the American College of Cardiology (2015)
11C-Acetate PET/CT in Multicentric Angiomyolipoma of the Kidney
Authors: Chi-Lai Ho, Sirong Chen, Kossen Man Tzit Ho, Wai-Kuen Ng, Yim Lung Leung, Thomas Kam Chau Cheng
Journal: Clinical Nuclear Medicine (2011)

A 35-year-old woman with a left kidney mass was diagnosed on ultrasound and CT; however, the diagnosis was inconclusive and therefore she underwent dual-tracer (11C-acetate and F-18 FDG) PET/CT. 11C-acetate PET/CT identified an exophytic lesion in the left kidney and a chain of left para-aortic nodes from left renal vein level to aortic bifurcation with markedly increased metabolism (11C-acetate lesion-to-kidney SUV ratio (SUVL/K) = 4.8 and 4.9, respectively) but no abnormal F-18 FDG uptake. The diagnosis of “multicentric angiomyolipoma with low-fat content or angiomyolipoma with malignant transformation and metastases” was suggested. The pathologic diagnosis post partial nephrectomy and lymph nodes resection was “angiomyolipoma with lymph node involvement.”
Abstract 3030: Regulation of EGFR in pancreatic cancer.
Authors: Christopher J. Halbrook, Kenneth K. Takeuchi, Howard C. Crawford
Journal: Cancer Research (2013)

Abstract EGFR and EGFR ligand upregulation has been widely seen in both human chronic pancreatitis and pancreatic ductal adenocarcinoma (PDA) for many years; however the role of EGFR in PDA was poorly understood. Recently we and others have shown that genetic ablation of EGFR effectively prevents both spontaneous and cerulein induced tumorigenesis in the pancreas of the LSL-KrasG12D/+;Ptf1aCre/+ (KC) mouse model of pancreatic tumorigenesis. Pockets of EGFR upregulation localized in single acini of KC mice appear to precede pancreatic intraepithelial neoplasia (PanIN) formation in spontaneous tumorigenesis, coupled with a distinct spatially localized immune response. Ubiquitous EGFR upregulation is observed throughout the pancreas upon induction of pancreatitis in wild-type (WT) and KC mice, returning to normal levels in WT mice but continuing to increase along with the widespread tumorigenesis in cerulein treated KC mice. Comparison of cerulein treated KC mice with the EGFRf/f;LSL-KrasG12D/+;Ptf1aCre/+ mice (EKC), which are largely resistant to cerulein induced pancreatitis, offers an opportunity to identify signals in the KC mouse which could be responsible for the upregulation of EGFR and subsequent tumorigenesis. Citation Format: Christopher J. Halbrook, Kenneth K. Takeuchi, Howard C. Crawford. Regulation of EGFR in pancreatic 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 3030. doi:10.1158/1538-7445.AM2013-3030
The Evaluation and Management of Bradycardia
Authors: J. Michael Mangrum, John P. DiMarco
Journal: New England Journal of Medicine (2000)

Bradycardia is a common finding during the clinical evaluation of both healthy patients and those who are ill. Bradycardia may be caused either by intrinsic dysfunction of or damage to the conduction system or by the response of normal tissues to extrinsic factors. In many cases, even profound bradycardia may be asymptomatic and have no immediate or long-term pathologic importance. In this article, we will briefly review the clinical presentation, pathophysiology, diagnostic evaluation, and treatment of patients with bradycardia.Clinical PresentationCardiac output is the left ventricular forward stroke volume multiplied by the heart rate. Patients with bradycardia may be . . .
PREDICTING HEART FAILURE EVENTS WITH HOME MONITORING: USE OF A NOVEL, WEARABLE NECKLACE TO MEASURE STROKE VOLUME, CARDIAC OUTPUT AND THORACIC IMPEDANCE
Authors: Raj M. Khandwalla, Kade Birkeland, Raymond Zimmer, Matthew Banet, Susan Pede, Ilan Kedan
Journal: Journal of the American College of Cardiology (2016)
A Phase Ib Study of Pembrolizumab (Pembro; Mk-3475) in Patients (Pts) with Human Papiilloma Virus (Hpv)-Positive and Negative Head and Neck Cancer (Hnc)
Authors: L.Q. Chow, B. Burtness, J. Weiss, R. Berger, J.P. Eder, E.J. Gonzalez, J. Pulini, J. Johnson, M. Dolled-Filhart, K. Emancipator, J.K. Lunceford, K. Pathiraja, C. Gause, J.D. Cheng, T. Seiwert
Journal: Annals of Oncology (2014)
FRI0431 Venous and Arterial Thrombosis in Sle: Differences in Natural History: Table 1.
Authors: K. Hickman, L. Magder, M. Petri
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Thrombosis is increased in SLE due to disease activity and co-morbid factors including antiphospholipid antibodies. We separately investigated the natural history of venous vs. arterial thrombosis. <h3>Methods</h3> 2250 patients were enrolled in a prospective cohort; 334 had a thrombotic event before cohort entry or diagnosis of SLE. For ALL thrombosis, age over 60 yrs, male gender, African-American ethnicity, SLEDAI greater than 3, and prednisone greater than 0 were risk factors. In general, rates of venous thrombosis were fairly constant, while rates of arterial thrombosis increased with age. <h3>Results</h3> See Table 1. <h3>Conclusions</h3> Prevention of venous thrombosis remains important throughout the course of SLE. Prevention of arterial thrombosis becomes more important later in the disease course. Disease activity is more of a risk factor for arterial thrombosis while prednisone is a risk factor for both venous and arterial thrombosis. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3776
Abstract B12: RB1-mediated regulation of osteoblast migration
Authors: Volkan Gunduz, Pedro Santiago Cardona, Philip W. Hinds
Journal: Cancer Research (2009)

Abstract Alterations involving loss or gain of function of components of the retinoblastoma (RB1) tumor suppressor pathway are observed in a wide range of human cancers. They include loss of p16INK4a expression in melanomas and overexpression of cyclin D1 in breast tumors. RB1 itself, however, is inactivated in a reduced subset of tumors including retinoblastomas, osteosarcomas and small cell lung carcinomas. A common characteristic of these tumors is the lack of well-organized adherens junctions. Thus, in retinoblastoma, the cadherin/catenin complex fails to anchor to the actin cytoskeleton leading to loss of cell-cell contact inhibition. Likewise, osteosarcomas and small cell lung carcinomas show reduced expression of cadherins and beta-catenin. In addition, a strong correlation has been found between abnormal adherens junction structures and the invasive capacity of these tumors. In this study, we aim to investigate the role of RB1 on cell-cell adhesion and migration using calvarial osteoblasts that are deficient in RB1 expression. We observe that RB1-deficient immortal osteoblasts (MC3T3 cells) lack membrane localization of N-cadherin and Beta-catenin and display an increased migratory phenotype compared to the RB1 expressing counterparts. In addition, RB1-deficient MC3T3 osteoblasts express and secrete higher levels of IGF1 leading to the activation of the IGF1 receptor (IGF1R). Interestingly, the opposite pattern of expression/secretion was observed for IGFBP-2, with higher levels observed in RB1-expressing MC3T3 cells. Moreover, activation of the IGF signaling pathway correlated with higher levels of phosphorylated Akt in RB1-deficient MC3T3s and, accordingly, treatment of RB1-deficient MC3T3 osteoblasts with either a neutralizing antibody against IGF1 or an inhibitor of IGF1 receptor led to impaired migration. We have also observed reduced phospho-Akt levels in RB1-deficient MC3T3 osteoblasts that were exposed to the conditioned medium (CM) from RB1 wild type MC3T3 osteoblasts. This reduction in phospho-Akt levels correlated well with a reduced migratory phenotype of RB1-deficient MC3T3 osteoblasts under these conditions. Taken together our data suggest that IGF signaling is one of the mechanisms that might contribute to increased migration in RB1-deficient MC3T3 osteoblasts. Citation Information: Cancer Res 2009;69(23 Suppl):B12.
A phase I study of celecoxib (C) and patupilone (EPO906) in patients (pts) with metastatic colorectal cancer (mCRC).
Authors: S. Iqbal, A. B. El-Khoueiry, D. Yang, S. Cole, W. Boswell, J. Shriki, Y. Ning, R. D. Agafitei, X. Menendez, H. Lenz
Journal: Journal of Clinical Oncology (2010)

2533 Background: Patupilone (EPO906) is an epothilone that stabilizes microtubules leading to cell cycle arrest and apoptosis. Preclinical data reveal regression in colon cancer models resistant to 5-FU. The dose-limiting toxicity (DLT) of EPO906 has been diarrhea in previous studies. Preclinical data suggest an increase in COX-2 expression with EPO906 and reduction in diarrhea when EPO906 is combined with C. Methods: The primary objective of this study was to determine of the maximum tolerated dose (MTD) of EPO906 + C. Secondary objectives were progression-free survival (PFS) and response rate. A standard 3+3 design was used. Pts with mCRC refractory to standard treatment were accrued. The dose of C was fixed at 400 mg bid with EPO906 7 mg/m2 dose escalated to a maximum dose of 13 mg/m2. Pts received C for one week prior to first dose of EPO906. Pts kept a diarrhea diary and were counseled about optimal management of diarrhea. Results: The study accrued 39 pts. Pt characteristics: male/female 6/23; median age 58 (35-84); median number of prior therapies 4 (range 1-9). The MTD was 12 mg/m2. All cycles grade 3/4 toxicities: diarrhea 38%, fatigue 18%, anorexia 15%, nausea 13%, vomiting 7%. Response was evaluable in 32 pts: 3 (9%) partial responses, 13 (41%) stable disease. Median PFS was 3.0 months (95% CI: 1.6-5.7); 4 pts had PFS of ≥ 6 months. Median OS 5.7 months (95%CI: 3.4-7.7). Conclusions: The combination of EPO906 and C is well tolerated with promising activity in heavily pretreated advanced CRC pts. The MTD reported is higher than previous, suggesting a benefit from the addition of C and diarrhea management. A phase II study of this combination in pts with advanced CRC has started. EPO 906 dose level mg/m2 N DLTs 7 3 8 4 9 7 Grade 3 diarrhea, vomiting 10 8 Grade 3 nausea 11 3 12 9 Grade 3 diarrhea 13 5 Grade 3 diarrhea/vomiting Grade 3 diarrhea, anorexia Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Novartis Novartis Novartis
Incidence and significance of cryptic chromosome aberrations detected by fluorescence in situ hybridization in acute myeloid leukemia with normal karyotype
Authors: A Cuneo, R Bigoni, F Cavazzini, A Bardi, MG Roberti, P Agostini, E Tammiso, N Ciccone, M Mancini, M Nanni, R De Cuia, M Divona, R La Starza, B Crescenzi, N Testoni, G Rege Cambrin, C Mecucci, F Lo Coco, G Saglio, G Castoldi
Journal: Leukemia (2002)
Abstract 5091: Proteomic study using a newly established metastatic lung cancer model
Authors: Dongsheng Wang, Zhongliang Hu, Lydia Koenig, Sreenivas Nannapaneni, Dong M. Shin, Zhuo (Georgia) Chen
Journal: Cancer Research (2012)

Abstract To understand metastasis of lung cancer, we established a highly metastatic pulmonary large cell carcinoma cell line (801BL) through 2 rounds of in vivo selection using a nude mouse xenograft model. In the first round, low-metastatic human large cell lung cancer cells (801D cell line) were subcutaneously injected into the flank of the mice. Metastatic tumor cells were collected from mouse brain and re-injected into the mice flank in the second round. A highly metastatic cell line 801BL was established from the metastatic cells in the lung. A PCR-based satellite tandem repeat (STR) analysis confirmed the same genomic background of the newly established metastatic cell line 801BL as the non-metastatic counterpart 801C and low-metastatic counterpart 801D cell lines. A xenografted mouse model showed 100% of the mice (8 out of 8 mice) injected subcutaneously with 801BL developed lung metastatic tumors, while none of the mice injected with 801C cells developed lung metastasis (p&amp;lt;0.0001). The metastatic cells present a different cancer stem cell-like morphological feature compared with the 801C and 801D cell lines. Their invasive capability is also increased by 3.47±0.44 fold compared to the non-metastatic counterpart (801C) in a matrigel invasion assay. A stable isotope labeling by amino acids in cell culture (SILAC)-based quantitative proteomic study was conducted by comparing the isotopic labeled 801BL cells with non-labeled 801C cells. Bioinformatic analysis using Ingenuity software (http://ingenuity.com) revealed significant alterations in several dominant cell signal networks including cell morphology (p-value:2.80E-09 - 6.83E-03), cellular function and maintenance (p-value:1.08E-08 - 6.83E-03), DNA replication, recombination, and repair (p-value:1.08E-08 - 6.83E-03), and cell death (p-value: 1.88E-08 - 6.83E-03), between the highly metastatic cell line (801BL) and its non-metastatic counterpart (801C). Western blot assay of several proteins from each signaling network confirmed the proteomic findings. Since the highly metastatic cell line and its non-metastatic counterpart share the identical genetic background, the model based on this cell line provides a powerful tool for the study of the mechanisms underlying lung cancer metastasis. (This work is supported by grant from DOD W81XWH-07-1-0306). 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 5091. doi:1538-7445.AM2012-5091
926 LONG TERM EFFICACY OF ANTIVIRAL THERAPY IN CHRONIC HEPATITIS C PATIENTS WITH SUSTAINED VIROLOGICAL RESPONSE TO TREATMENT WITH INTERFERON/RIBAVIRIN WITH OR WITHOUT DIRECT ACTING ANTIVIRALS
Authors: K. Rutter, S. Beinhardt, P. Ferenci, P. Rauch, S. Ibrahim, M. Dulic, M. Gschwantler, A. Maieron, H. Laferl, A.F. Stattermayer, T.M. Scherzer, R. Strassl, P. Steindl-Munda, H. Hofer
Journal: Journal of Hepatology (2012)