tbuckley/cabot-search huggingface dataset:
Abstract 4018: The role of FLI1 in breast cancer development and progression
Authors: Melissa Nicole Scheiber, Patricia M. Watson, Victoria J. Findlay, Tihana Rumboldt, Dennis K. Watson
Journal: Cancer Research (2011)

Abstract Breast cancer is the second most common cancer-related death among women in the US. The majority of the breast cancer-related deaths are due to tumor progression. A multitude of changes in gene expression are required for the cancer cell to acquire the ability to invade and migrate. The transcriptional activation or repression of these cancer-associated genes is not clearly understood, however many ETS family members have been considered good candidates. Friend leukemia virus integration 1 (FLI1) is an ETS protein that is aberrantly expressed in retrovirus-induced hematological tumors, and is found to be rearranged in Ewing's sarcoma and related primitive neuroectodermal tumors characterized by a t(11;22)(q24;q12) translocation. Limited attention has been directed towards elucidating the potential role of FLI1 in epithelial-derived cancers, including breast cancer. Our preliminary immunohistochemical analyses show that FLI1 protein is decreased in human invasive breast tumors compared to normal breast tissue. A decrease of FLI1 mRNA and protein was also demonstrated in breast cell cancer cell lines through Real Time RT-PCR and western blot, respectively. We used adenovirus to examine the effects of FLI1 expression in two invasive breast cancer cell lines (MDA-MB-231 and MDA-MB-157). Re-expression of FLI1 in both MDA-MB-231 and MDA-MB-157 inhibited cell growth, mainly due to a decrease in cellular proliferation. FLI1 expression also inhibited the motility and invasiveness of breast cancer cell lines, determined by the use of Transwell inserts coated with fibronectin or Matrigel, respectively. We hypothesize that the loss of FLI1 is a critical step for breast cancer progression. Loss-of-function studies using shRNA are being performed to complement the above gain-of-function studies. Future studies will investigate potential downstream targets of FLI1. Inhibiting the reduction of FLI1 or regulating its downstream targets may be to be unique targets of breast cancer therapy. 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 4018. doi:10.1158/1538-7445.AM2011-4018
Abstract B35: Amentoflavone inhibits angiogenesis and stimulates apoptosis in cells
Authors: Zhihe Liu, Jinli Zhang, Wenjuan Cao
Journal: Cancer Research (2013)

Abstract Amentoflavone (8-[5-(5,7-dihydroxy-4-oxo-chromen-2-yl)-2-hydroxy-phenyl]-5,7-dihydroxy -2-(4-hydroxyphenyl) chromen-4-one, AF) is a biflavonoid derived from the extracts of Selaginella tamariscina. It has been shown that AF has diverse biological effects including anti-inflammatory, anti-viral, inhibition of fatty acid synthesis, and anti-tumor. It is well known that high cell proliferation and angiogenesis are two key factors in tumorigenesis. In this study, we report that AF inhibited proliferation, and stimulated apoptosis in fibroblasts. Incubation of fibroblast with AF showed inhibitory effect on cell viability and exhibited a series of cellular changes that were consistent with apoptosis. By western blot analysis, our date indicated significant increases in the amounts of cleaved-caspase 3, 8, 9 and Bax, several apoptotic promoters, and a significant decrease in TCTP, an apoptotic inhibitor, in fibroblast treated with AF. Furthermore, AF showed significant inhibitions on the proliferation, migration, and tube formation of endothelial cells, which are associated with angiogenesis. In conclusion, this study suggests that AF stimulates apoptosis in fibroblasts and inhibits angiogenesis of endothelial cells. Therefore, AF is a promising molecule which can be used in cancer treatment. Note: This abstract was not presented at the conference. Citation Format: Zhihe Liu, Jinli Zhang, Wenjuan Cao. Amentoflavone inhibits angiogenesis and stimulates apoptosis in cells. [abstract]. In: Proceedings of the Third AACR International Conference on Frontiers in Basic Cancer Research; Sep 18-22, 2013; National Harbor, MD. Philadelphia (PA): AACR; Cancer Res 2013;73(19 Suppl):Abstract nr B35.
Abstract 293: Characterization of renal tumor-initiating cells in human renal carcinoma cell lines
Authors: Lin Wang, Paul Park, Huina Zhang, Frank La Marca, Chia-Ying Lin
Journal: Cancer Research (2011)

Abstract High aldehyde dehydrogenase activity (ALDH) has been used as a putative marker for the tumor- initiating subpopulation in many cancer types. We previously showed that tumor-initiating cells in human osteosarcoma OS99-1 cell line can be identified using ALDH. In the current study we sought to determine whether ALDH can be also used as a marker to isolate tumor-initiating populations from human renal carcinoma cell lines. By using a xenograft model in which cells from human renal carcinoma cell line ACHN and Caki-2 were grown in NOD/SCID mice, we identified a subset of renal cells that were highly tumorigenic based on the high aldehyde dehydrogenase activity. Isolated cancer cells with relatively high aldehyde dehydrogenase activity (ALDHbr cells) revealed a greater colony-forming efficiency, higher proliferative output, the ability to grow in non-adhesive spheroids, the capability to undergo adipogenic and osteogenic differentiation, and increased expression of stem cell marker genes Oct3/4A, Nanog and Pax-2. In vivo experiments showed that ALDHbr cells were enriched with greater tumorigenicity compared to their counterparts with low ALDH activity (ALDHlo cells), generating new tumors with as few as 25 cells. The isolation of renal tumor-initiating cells by their high ALDH activity may lead to a new insight into the study of how renal cell carcinoma may take place, and may lead to effective prognostic and therapeutic strategies for the treatment of patients with kidney cancer. 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 293. doi:10.1158/1538-7445.AM2011-293
Tracheal Metastasis From Melanoma Detected With 18F-FDG PET/CT
Authors: Trent Shelton, Sword Cambron, Marc Seltzer, Alan Siegel
Journal: Clinical Nuclear Medicine (2013)

A 58-year-old man with a history of stage IIIB melanoma of the right arm initially treated 4 years prior presented with new onset cough and hemoptysis. Bronchial washings were positive for melanoma. The PET/CT study showed a hypermetabolic nodule in the posterior mid-trachea. These findings indicate metastatic melanoma to the trachea. No other metastatic foci were evident. This allowed for endoscopic laser ablation of the metastatic focus.
Absence of Anti-Human Immunodeficiency Virus Types 1 and 2 Seroconversion after the Treatment of Hemophilia A or von Willebrand's Disease with Pasteurized Factor VIII Concentrate
Authors: K. Schimpf, H.H. Brackmann, W. Kreuz, B. Kraus, F. Haschke, W. Schramm, J. Moesseler, G. Auerswald, A.H. Sutor, K. Koehler, P. Hellstern, W. Muntean, I. Scharrer
Journal: New England Journal of Medicine (1989)

Patients with hemophilia A or von Willebrand's disease who are treated with concentrated preparations of human factor VIII made from unscreened pooled plasma are at substantial risk of contracting human immunodeficiency virus (HIV) infection. The purpose of this study was to investigate whether by treating such patients with a pasteurized factor VIII concentrate that had been heated in aqueous solution at 60 degrees C for 10 hours, HIV infection could be avoided. Eleven hemophilia centers in the Federal Republic of Germany and two in Austria identified 155 eligible patients who had been treated exclusively with pasteurized factor VIII concentrate and had not received any other blood products. Between February 1979 and December 1986 they received a total of 15,916,260 IU of pasteurized factor VIII. The United States was the source of 80 percent of the plasma from which the concentrate was made. By September 1988, these 155 patients had been screened for antibody to HIV type 1 (anti-HIV-1) with a total of 657 tests; all were negative. Sixty-seven patients were also tested once for antibody to HIV type 2 (anti-HIV-2); all these tests were negative as well. It appears that pasteurization effectively inactivates HIV, even in plasma that is likely to be highly contaminated with the virus.
Abstract 3943: Oxidatively induced DNA base damage in non-small cell lung cancer
Authors: Ozlem Senol, Halil Resmi, Can Sevinc, Aydin Sanli, Ahmet Onen, Ebru Taylan, Miral Dizdaroglu, Guldal Kirkali
Journal: Cancer Research (2010)

Abstract Non-small cell lung cancer (NSCLC) accounts for 80-85% of all cases of lung cancer and is known to be caused by smoking and other carcinogenic agents. Oxidatively induced DNA damage is involved in multiple modifications and mutations in DNA, thereby in pathogenesis of cancer as well as other diseases. In this study, we compared the tumor tissues to the surrounding healthy tissues obtained from 29 NSCLC patients who had undergone surgical resection. The levels of oxidatively induced DNA lesions such as 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyGua), 8-hydroxyguanine (8-OH-Gua) and (5′S)-8,5′-cyclo-2′-deoxyadenosine (S-cdA) were measured by gas chromatography/isotope-dilution mass spectrometry and liquid chromatography/isotope-dilution mass spectrometry. We found that the level of S-cdA was statistically significantly greater in cancer tissues than that in control tissues (p=0.0063), whereas the levels of FapyGua and 8-OH-Gua showed no significant difference between the two groups. There was no significant correlation between DNA damage and age, smoking or pathological stage. These results provide evidence for significant accumulation of S-cdA in tumor tissues compared to surrounding healthy tissues in NSCLC. The evaluation of the alterations in the levels of DNA lesions may contribute to the elucidation of the DNA repair defects in NSCLC. 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 3943.
LIPID AND LIPOPROTEIN SUBFRACTIONS IN A LARGE CENTENARIAN POPULATION: THE VERY LARGE DATABASE OF LIPIDS STUDY 10C (VLDL-10C)
Authors: Nishant Shah, Renato Quispe, Krishnaji Kulkarni, Seth Martin, Michael Blaha, Roger Blumenthal, Steven Jones, Kristopher Swiger
Journal: Journal of the American College of Cardiology (2016)
Pro and Con Tobacco Forces Face Off Over State Legislation
Authors: E. DeVita
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Pro and Con Tobacco Forces Face Off Over State Legislation Get access Elizabeth DeVita Elizabeth DeVita Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 19, 2 October 1991, Page 1375, https://doi.org/10.1093/jnci/83.19.1375 Published: 02 October 1991
Abstract 2736: Overexpression of L-type amino acid transporter-1 in breast cancer cells and tissues: potential association with growth and progression of tumors
Authors: Zhongxing Liang, Heidi T. Cho, Ke Liang, Aizhi Zhu, Ke Huang, Hui Wu, Samuel Hong, Mark M. Goodman, Hyunsuk Shim
Journal: Cancer Research (2010)

Abstract For a tumor to constantly proliferate, malignant cells require nutrients, especially glucose and amino acids. There is abundant evidence that tumor growth depends heavily on glucose uptake. The L-type amino acid transporter 1 (LAT1) is a major nutrient transport system responsible for the transport of large neutral essential amino acids. In the present study, we analyzed expression levels of LAT1 mRNA and protein with RT-PCR, Western blot and immunohistochemical staining. The results showed that normal breast tissues or low malignant cell lines expressed low levels of LAT1 mRNA and protein, while LAT1 was overexpressed in highly malignant cancer cell lines and high grade breast cancer tissues. In addition, we found higher expression levels of LAT1 in breast cancer tissues were consistent with high stages of breast cancer. Furthermore, we demonstrated that blockade of LAT1 with its inhibitor, 2-amino-bicyclo[2.2.1]heptane-2-carboxylic acid (BCH), or knockdown of LAT1 with transfection of specific siRNA inhibited proliferation of breast cancer cells. A variety of 11C- and 18F-labeled amino acids have been studied for potential use in positron emission tomography (PET) oncology. A non-natural, not-metabolizable leucine analog, anti-1-amino-3-[18F]fluorocyclobutane-1-carboxylic acid ([18F]FACBC), has shown superior tumor/normal brain ratio. We tested whether [18F]FACBC would also be an excellent PET tracer for malignant breast cancer imaging using an orthotopic breast cancer animal model and an experimental animal model of breast cancer metastasis. Our results support that [18F]FACBC could be a useful PET tracer for non-invasive imaging of breast cancer. These findings suggest that overexpression of LAT1 is necessary for proliferation of breast cancer cells and may contribute to progression of tumors. LAT1 may represent a potential target for diagnosis of breast 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 2736.
P122 The Use of Thoracic Ultrasound in Management of Patients with Pleural Disorders
Authors: JA Kastelik, I Aslam, JB Morjaria, AG Arnold
Journal: Thorax (2012)

<h3>Introduction</h3> Pleural diseases are common reason for referral to respiratory specialists. Thoracic ultrasound has become an important tool for investigation and management of patients with pleural diseases. Thoracic ultrasound allows real-time assessment of the pleural space as well as acquired wide use in guiding pleural procedures. Current British Thoracic Society (BTS) guidelines strongly recommend the use of thoracic ultrasound for the investigation and management of patients with pleural disorders. <h3>Aims</h3> To review experience of using thoracic ultrasound by respiratory physicians for investigations and management of patients with pleural disorders. <h3>Methods</h3> Retrospective analysis of thoracic ultrasound procedures performed in a tertiary hospital by respiratory physicians. <h3>Results</h3> Over a period between July 2008 and July 2012 a total of 680 thoracic ultrasound procedures were performed by respiratory physicians in 388 (153 females) patients, mean (range) age 63.4 (17–97) years. The findings of thoracic ultrasound included: 240 cases of pleural effusion, 38 cases of pleural infection including parapneumonic effusion or empyema, 36 cases of consolidated lung, 24 pneumothoraces, 15 cases of pleural thickening, 6 cases of diaphragmatic abnormalities and 6 cases of other abnormalities such as hydropneumothorax, chylothorax or evidence of pleurodesis were recorded. Moreover in 23 cases no anomalies were noted. The most common underlying causes for pleural effusion included malignancy, cardiac failure and infection. Overall 70 pleural procedures such as intercostal chest drain insertion or thoracocentesis were performed. <h3>Conclusions</h3> Thoracic ultrasound performed by respiratory physicians has become a part of routine management of patients with pleural disorders. From our observations the most frequent finding on performing thoracic ultrasound was pleural effusion, however this modality of investigation also enabled identification of other conditions such as consolidated lung or diaphragmatic abnormalities that could on chest radiograph mimic pleural effusion, hence potentially avoiding unnecessary pleural procedures. More importantly thoracic ultrasound was used to guide pleural procedures such as thoracocentesis or intercostal chest drain insertion. Using our findings we recommend the routine use of thoracic ultrasound for the initial investigation and management of patients with pleural disorders as it is a safe, convenient and cost-effective tool.
Abstract B53: Post-translational modification of p53 by HDAC inhibitors leads to selective assembly of transcriptional complexes at the p21 locus
Authors: James Keith, Somdutta Roy, Martin Tenniswood
Journal: Cancer Research (2009)

Abstract CG-1521 is a novel histone deacetylase (HDAC) inhibitor that stabilizes the acetylation of p53 at lysine 373, triggering G2/M phase arrest and apoptosis in LNCaP cells. This is in contrast to the well known HDAC inhibitor trichostatin A (TSA) which stabilizes the acetylation of lysine 382 on p53 and triggers G1/S phase arrest and senesence. The known p53 target gene, p21, contains two p53 response elements (RE) and 6 Sp1 binding sites in its promoter. Previous work in LNCaP cells indicates acetylated p53 isoform-modulated assembly of an active or inactive transcriptional complex at these p53REs in response to CG-1521 or TSA, respectively. Consistent with this finding, p21 mRNA levels were increased only upon treatment with CG-1521. Treatment with either HDAC inhibitor led to the upregulation of p21 protein levels, with a difference in the speed and duration of this increase. A second protein, p21B, coded within the exons and introns of the classical p21 protein, has been implicated in the apoptotic response, should the cellular DNA repair machinery fail to resolve a genomic insult. p21B appears to be controlled by a p53RE within the first intron of p21. This RE exhibits the same qualitative loading characteristics of the classical p21 p53RE in response to cellular stress and the acetylation state of p53, yet is temporally expressed later than p21. Using chromatin immunoprecipitation assays at narrow timepoints, we have determined the temporal loading characteristics of this region upon treatment with the HDAC inhibitors CG-1521 and TSA. Our results demonstrate a clear difference in the components of the basal transcriptional complex depending on the HDAC-stabilized acetylation state of p53. This indicates the acetylation state of the p53 protein is an important regulator of the cellular response to stress and suggests HDAC inhibitors may have an important role as cancer therapeutics beyond their traditional role in histone modification. Citation Information: Cancer Res 2009;69(23 Suppl):B53.
The case for continuity
Authors: Rochel Gelman
Journal: Behavioral and Brain Sciences (2011)

Abstract This article defends a continuity position. Infants can abstract numerosity and young preschool children do respond appropriately to tasks that tap their ability to use a count and cardinal value and/or arithmetic principles. Active use of a nonverbal domain of arithmetic serves to enable the child to find relevant data to build knowledge about the language and use rules of numerosity and quantity.
Note on the extravascular component of coronary resistance to blood flow.
Authors: J Grayson, F Heineman, I Sherman
Journal: Circulation Research (1980)

Note on the Extravascular Component of Coronary Resistance to Blood FlowThis comment was prompted by the article, "Characterization of the Extravascular Component of Coronary Resistance by Instantaneous Pressure-Flow Relationships in the Dog" (Panerai et al., 1979).We have conducted similar investigations of the coronary pressure-flow relationships, including direct measurements of intramyocardial pressure (Heineman et al., 1979) and critical closing pressure (Sherman et al., 1980).While our observations agree with those of Panerai et al., in particular that coronary blood flow ceases at diastolic perfusion pressure of approximately 15 mm Hg, our measurements of IMP do not support their conclusion that this flow cessation phenomenon is attributable to diastolic intramyocardial pressure.We have found diastolic IMP to be 2.7 ± 2.2 mm Hg (mean ± SD, n = 15) at all depths in the myocardial wall, whereas the systolic IMP is a function of the depth from the epicardial surface.A factor which the authors (and other workers estimating diastolic IMP from the coronary pressure-flow curve intercept) failed to consider was the possibility of critical closing being involved in the phenomenon they observed.Although maximal vasodilation with adenosine is likely to eliminate active arteriolar constriction [a mechanism of critical closure suggested by Burton (1951)], other factors may still lead to critical closing in the vessels.Our most recent work (Sherman et al., 1979) proposed that interfacial forces acting between vascular endothelium and blood may arrest flow even in the presence of a positive perfusion pressure.Calculated values for these interfacial forces predict flow cessation at pressures less than approximately 11 mm Hg (Sherman et al., 1979).It has been suggested (Alexander, 1977) that the rheological properties of blood, a factor which would also be independent of vascular tone, may account at least in part for critical closure, although we have obtained flow arrest at positive perfusion pressure with non-cellular perfusates.On the basis of these observations, we submit that the estimation of IMP from coronary pressureflow curves will be in error unless critical closing pressure is taken into account.Not to do so assumes erroneously that the only impedance to diastolic coronary blood flow other than the vascular dimensions is the extravascular resistance in the form of intramyocardial pressure.