tbuckley/cabot-search huggingface dataset:
The Appearance of Disseminated Minute Tumor Nodules in the Chorioallantoic Membrane of the Chick Following Intravenous Inoculation of Ascites Tumor Cells
Authors: Joseph Leighton
Journal: Cancer Research (1963)

Fresh ascites fluid was inoculated into a chorioallantoic vein of 11-day-old chick embryos. The fluid was taken from rats bearing either the Walker carcinosarcoma 256 in ascites form or the Yoshida ascites hepatoma 7974.

The eggs were opened on the 18th day of incubation, 1 week after inoculation. For both tumors, in 90 per cent of the eggs that were viable 1 week after inoculation, a disseminated, fine nodularity was seen in the chorioallantoic membrane, in addition to tumor growth in many organs of the embryos. The architecture of the nodules on the chorioallantoic membrane was characteristic for each type of tumor. The colonies produced by the Walker tumor were dense in their centers, but their margins were indistinct, as numerous tumor cells infiltrated the surrounding connective tissue. The colonies produced by the hepatoma fluid were globular, compact, varied in size, and were clearly delineated from the surrounding connective tissue. A hyperplastic thickening of the ectodermal epithelium over some of the nodules of hepatoma was also found.

The appearance of minute discrete “metastases” in a disseminated pattern suggests that an intravascular “plating out” of cells has occurred.
Abstract 135: Associations between VEGF polymorphisms and clinical outcome in breast cancer
Authors: Jessica Furriol, Hanne E. Puntervoll, Gøril Knutsvik, Monica Mannelqvist, Sura Aziz, Elisabeth Wik, Lars A. Akslen
Journal: Cancer Research (2015)

Abstract Introduction Vascular Endothelial Growth Factor (VEGF) is a key regulator of angiogenesis and is involved in the development and progression of solid tumors. Recent advances in sequencing technologies have allowed the identification of genetic variants associated with development and progression of different diseases including breast cancer. Despite evidence suggesting that these genetic variants can be used for improved risk stratification, results are not conclusive. In this work we have evaluated the relationship between 8 VEGF SNPs (single nucleotide polymorphisms) and survival as well as clinico-pathologic characteristics in breast cancer. Material and Methods In this study 8 VEGF SNPs (rs3025039, rs69947, rs833070, rs2010963, rs3025010, rs25468, rs3025035 and rs833068) were selected. DNA was extracted from non-tumor FFPE-samples from a series of 367 breast cancer patients from a Norwegian population. Associations between SNPs and categorical variables were analyzed by chi-square and Fisher exact tests. We used logistic regression to calculate odds ratios (OR) and 95% confidence intervals (CI). Survival was calculated by the Kaplan-Meier method (log-rank test). Results Our results showed that for a subset of patients, rs3025035 CT and TT were associated with relapse (p = 0.044; OR 3.07, 95%CI 1.08-8.76). Accordingly the rs3025035 CC genotype was related to longer time to recurrence after surgery (p = 0.10). Interestingly, in patients with histologic grade 3, a trend between CC and improved survival was also found in rs3025035 (p = 0.10), whereas the CC genotype in rs3025039 was associated with worse prognosis in this group (p = 0.037). Finally, the haplotype rs3025035T-rs3025039C was associated with relapse (p = 0.015; OR 3.72, 95% CI 1.31-10.62). Conclusions We report for the first time an association of the rs3025035 CC genotype with disease relapse and suggest that it could be a prognostic marker in breast cancer. Independent studies are needed to confirm our result. Citation Format: Jessica Furriol, Hanne E. Puntervoll, Gøril Knutsvik, Monica Mannelqvist, Sura Aziz, Elisabeth Wik, Lars A. Akslen. Associations between VEGF polymorphisms and clinical outcome in breast cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 135. doi:10.1158/1538-7445.AM2015-135
Chimeric NK receptor-bearing murine T cells mediate anti-tumor immunotherapy against lymphoma
Authors: Charles L. Sentman, Bethany A. Gagne, Tong Zhang
Journal: Cancer Research (2006)

621  NKG2D is an activating cell surface receptor expressed on natural killer (NK) cells and some T cell subsets. Its ligands are primarily expressed on tumor cells. The aim of this study was to determine whether chimeric NK receptor bearing T cells would directly kill tumor cells and lead to induction of host immunity against tumors. Chimeric NK receptors were produced by linking NKG2D or Dap10 to the cytoplasmic portion of the CD3ζ chain. Our results showed that chNKG2D-bearing T cells responded to NKG2D ligand-bearing tumor cells (RMA/Rae-1β, EG7) but not to wildtype tumor cells (RMA). This response was dependent upon ligand expression on the target cells but not on expression of MHC molecules, and the response could be blocked by anti-NKG2D antibodies. These T cells produced large amounts of Th1 cytokines and proinflamatory chemokines and killed ligand-expressing tumor cells. Adoptive transfer of chNKG2D-bearing T cells inhibited RMA/Rae-1β tumor growth in vivo. Moreover, mice that had remained tumor-free were resistant to subsequent challenge with the wildtype RMA tumor cells, suggesting the generation of immunity against other tumor antigens. Adoptive transfer of chNKG2D-bearing T cells prevented growth of RMA/Rae1β tumor cells in vivo in B6 and B6.Rag1-/- mice indicating that host T and B cells were not required for the anti-tumor effect. However, only B6 mice were protected from a subsequent challenge with RMA tumor cells, suggesting that development of resistance to RMA tumor cells was dependent upon host lymphocytes and likely due to host T cells. Taken together, our findings indicate that modification of T cells with chimeric NKG2D receptors represents a promising approach for immunotherapy against cancer.
Abstract 2603: Gender Is An Important Determinate For The Predictive Value Of NT-proBNP In Patients Presenting With An Acute Coronary Syndrome
Authors: Michael W Weber, Eva Keil, Michael Stanisch, Holger Nef, Helge Moellmann, Christian Kleine, Bianca Dippel, Albrecht Elsaesser, Christian Hamm
Journal: Circulation (2007)

Background BNP und NT-proBNP provide prognostic information in patients with acute coronary syndromes (ACS). Even though it is generally accepted, that gender, age and atrial fibrillation are important determinants for BNP respectively NT-proBNP values, there is no data available evaluating the impact of those factors on the predictive value of those biomarkers. Therefore it was our aim to evaluate the predictive value of NT-proBNP for mortality after an ACS in association to gender, age and rhythm Methods and results We included 1123 consecutive patients (age 64±12 years; 342 females) with an ACS within the last 48 hours. Follow up data after median of 204 days were available for 1115 (99%) patients. During the follow up 77 (6.8%) patients died. NT-proBNP values on admission were higher in patients who deceased compared to those who survived (2047 (576 –5624) pg/ml vs. 465 (127–1519) pg/ml; p&lt;0,001). The AUC of the ROC curve for NT-proBNP as a predictor for mortality was 0.714 (p&lt;0.001) and an optimised cut-off value of 1815 pg/ml could be calculated. Patients with NT-proBNP above this cut-off had a significantly higher mortality rate (16% vs. 4%; p&lt;0,001; Log Rank 48; p&lt;0,001)). Even though patients with AF had higher NT-proBNP values as those patients with SR (1952 (770 – 4070) pg/ml vs. 452 (121–1492) pg/ml) NT-proBNP at the same cut-off value of 1815 pg/ml was highly discriminative for mortality (27.9% vs. 7.5%; p&lt;0.022; Log Rank 5.7; p=0,017). Patients with an age above 65 years had higher NT-proBNP values as compared to patients younger than 65 years (894 (255–2642) pg/ml vs. 279 (75–945) pg/ml; p&lt;0,001). However the predictive value of NT-proBNP in both age groups was comparable. Women had higher NT-proBNP values as compared to men (966 (237–2549) pg/ml vs. 407 (102–1273) pg/ml; p&lt;0,001). But in dissimilarity, in women NT-proBNP values above 1815 pg/ml were not associated with a higher mortality and thus were without predictive value (10,6% vs. 6,8%; p&lt;0,304; Log Rank 1,556; p&lt;0,212). Conclusion Gender, age and rhythm are important determinants for NT-proBNP values of patients presenting with an ACS. However, only gender had impact on the predictive value of NT-proBNP for mortality. In women cut-off values need to be adopted.
Inactivation of the mouse melanocortin-3 receptor results in increased fat mass and reduced lean body mass
Authors: Airu S. Chen, Donald J. Marsh, Myrna E. Trumbauer, Easter G. Frazier, Xiao-Ming Guan, Hong Yu, Charles I. Rosenblum, Aurawan Vongs, Yue Feng, Linhai Cao, Joseph M. Metzger, Alison M. Strack, Ramon E. Camacho, Theodore N. Mellin, Christian N. Nunes, William Min, Jill Fisher, Shobhna Gopal-Truter, D. Euan MacIntyre, Howard Y. Chen, Lex H.T. Van der Ploeg
Journal: Nature Genetics (2000)
Obesity and cancer
Authors: Donald C McMillan, Naveed Sattar, Mike Lean, Colin S McArdle
Journal: BMJ (2006)

View this table:

 
Percentage of cancer cases attributable to overweight and obesity in countries of the European Union, by cancer site. Adapted from Bergstrom et al (see Further Reading box) 



Obesity is increasing at an alarming rate throughout North America and Europe and is associated with substantial morbidity and mortality. The condition has long been recognised as a risk factor for diabetes and cardiovascular disease, but not for developing cancer. A recent survey of the public by the American Cancer Society found that less than 5% of respondents were aware of the increased cancer risk associated with overweight and obesity. 



Contribution of overweight and obesity to mortality from cancer in the United States, 1982-98. Adapted from Adami H-O et al ( N Engl J Med 2003;348:1623-4) 



A recent meta-analysis showed that more than 70 000 of the 3.5 million new cases of cancer each year in the European Union are attributable to overweight or obesity. This is likely to be a conservative estimate for two reasons. Firstly, only those tumours for which there was existing evidence to suggest a link between obesity and cancer (namely, for breast, colon, endometrium, prostate, kidney, and gallbladder) were included in the study. Secondly, the number of cancers attributable to obesity is likely to have increased because obesity levels have increased substantially since the publication of many of the studies included in this meta-analysis. 

More recently, the American Cancer Society's prospective population based study of about 900 000 subjects confirmed that obesity was directly associated with an increased risk of death from a variety of cancers. 



Mortality from cancer for US men, 1982-98, by body mass index (BMI). For each relative risk, the comparison was between men in the highest BMI category and men in the reference category (18.5 to 24.9). Adapted from Calle et al (see Further Reading …
Isolation of a B-Tropic Type-C Virus From Reticulum Cell Neoplasms Induced in BALB/c Mice by SJL/J Type-C Virus2
Authors: Kenneth S. S. Chang, Tadao Aoki, Lloyd W. Law
Journal: JNCI Journal of the National Cancer Institute (1975)

D1-murine leukemia virus (MuLV), an N-tropic type-C virus isolated from a spontaneous reticulum cell neoplasm, type B (RCN-B) of an SJL/J mouse was propagated in NIH Swiss mouse embryo cell cultures. When injected into BALB/c mice 1 day after neonatal thymectomy, 30% of the inoculated mice developed RCN-B in 5 months, whereas none of the uninoculated controls did. From the spleen and lymph node extracts of all RCN-B-bearing mice tested, B-tropic type-C viruses (designated E1-MuLV) were isolated in high titers (105-106 XC plaqueforming units/ml). Only low titers (101-102 XC plaqueforming units/ml) of N- or B-tropic viruses were isolated from those thymectomized mice, inoculated but nontumorous, whereas only N-tropic viruses were detected in the uninoculated thymectomized mice. No virus was isolated from the nonthymectomized, untreated controls. Antigenically, the viral envelope antigen (VEA) of E1-MuLV was distinct from those of DI-MuLV, xVEA, or Gross-VEA, but some cross-reaction with AKR-MuLV-VEA was observed. The relationship of DI-MuLV to E1-MuLV with respect to oncogenesis and viral genome activation was discussed.
Anthracycline-Induced Cardiomyopathy
Authors: Daniela Cardinale, Alessandro Colombo, Giuseppina Lamantia, Nicola Colombo, Maurizio Civelli, Gaia De Giacomi, Mara Rubino, Fabrizio Veglia, Cesare Fiorentini, Carlo M. Cipolla
Journal: Journal of the American College of Cardiology (2010)
Real-life experience of managing vulval erosive lichen planus: a case-based review and U.K. multicentre case note audit
Authors: R.C. Simpson, S.M. Littlewood, S.M. Cooper, M.E. Cruickshank, C.M. Green, E. Derrick, J. Yell, N. Chiang, H. Bell, C. Owen, A. Javed, C.L. Wilson, J. McLelland, R. Murphy
Journal: British Journal of Dermatology (2012)

There is a lack of published evidence for treatment and outcome measures for vulval erosive lichen planus (ELPV).To conduct a multicentre case note review to examine real-life management of ELPV comparing current U.K. practice against an agreed audit standard.Criteria for standards of care for which to evaluate current service provision were set following communication with experts from the British Society for the Study of Vulval Disease. Participants from 10 U.K. centres included nine dermatologists and one gynaecologist who run specialist vulval clinics. Standards examined the documentation of disease severity/impact measures, the use of diagnostic biopsies, treatments used and assessment of treatment response.Audit data were collected from 172 patients. Documentation of symptoms/clinical findings was excellent (99%, 170/172). A schematic diagram was present in the notes of 87% (150/172). Patient-related disease impact measures including Dermatology Life Quality Index (3%, 6/172) or visual analogue scales (1%, 2/172) were less well documented. Biopsies were performed in 78% (135/172); 71% (96/135) showed histological features consistent with erosive lichen planus. Squamous cell carcinoma developed in four patients (two vulval, two oral) and vulval intraepithelial neoplasia in two further patients. Recommended first-line treatment with a very potent topical steroid was used in 75% (129/172) with improvement in 66% (85/129). Significant variation in second-line therapy was seen.Wide variation in U.K. practice demonstrates the absence of standardized guidance for treating ELPV and the need for vulval-specific outcomes. This audit should act as a framework towards improving ELPV management and to plan future research in this area.
Mechanisms of acquired resistance to iodonium-class NADPH oxidase inhibitors in human colorectal cancer
Authors: James H. Doroshow, Edward Strong, Austin Dulack, Amanda Wood, Jessie Eagleton, Waymee Lwin, Krishnendu Roy
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

4629 

Recent studies suggest that reactive oxygen species (ROS) generated by a membrane-bound, non-mitochondrial flavin dehydrogenase, NADPH oxidase 1 (NOX1), play a critical role in the control of human colorectal cancer growth by modulating signal transduction through the Wnt pathway as well as ROS-mediated angiogenesis (Proc. Amer. Assoc. Cancer Res. 2005; 46: [Abstract # 6108; Abstract # 2283]). We demonstrated previously that the iodonium-class NOX inhibitors diphenylene iodonium (DPI) and Di-2-thienyliodonium (DTI) at their IC50 concentrations downregulate cyclin D1 leading to a G1/S block; drug exposure also produces a significant decrease in ROS production as well as decreased phosphorylation of beta-catenin. To examine the mechanism(s) of action of DPI and DTI further, HT-29, HCT-15, SW-620, and KM-12 human colon cancer lines resistant to these iodonium analogs were developed by stepwise exposure to increasing DPI or DTI concentrations over a period of at least 6 months. Individual DPI- and DTI-resistant variants of each of the four model systems were found to be from 4 to 5-fold resistant to DPI and 4 to18-fold resistant DTI by comparison of their respective IC50 values. Flow cytometric analysis with the fluorescent probe H2DCF revealed that in both DPI- and DTI-resistant variant cell lines baseline levels of reactive oxygen production were increased by > 3-fold compared to parental cells. Furthermore, expression levels of phospho-beta catenin, c-myc, CDK4, cyclin D1, and the transcription factor TCF-4, that are significantly decreased following exposure to DPI and DTI in parental cells, were either unchanged or upregulated in the resistant cell variants. In summary, DPI and DTI resistance in human colon cancer cells is associated with a significant increase in reactive oxygen setpoint, and a compensatory overexpression of oxidant-sensitive signal transduction components of the Wnt pathway. These studies suggest that reactive oxygen homeostasis plays a critical regulatory role in the growth of colon cancer cells, and thus, may be an important target for the development of novel colon cancer therapeutics.
Abstract 4250: Nitric oxide synthase activity and its modulation in the treatment of colorectal cancer
Authors: Asim Alam, Chris Rabender, Li Wang, Sundaresan Gobalakrishnan, Jamal Zweit
Journal: Cancer Research (2014)

Abstract The American Cancer Society estimates more than 141,000 new cases of and about 50,000 deaths from colorectal cancer every year. Treatment options include surgery, radiation therapy and targeted therapies such as anti-angiogenics. However, no therapies address the key driving factor of colorectal cancer: inflammation. It is well known that chronic inflammatory conditions such as Crohn's Disease, ulcerative colitis, diabetes, obesity and cigarette smoking all elevate the risk of developing colorectal cancer. One of the hallmarks of chronic inflammation is the elevated levels of reactive oxygen/nitrogen species (ROS/RNS). A primary source of these ROS/RNS is uncoupled Nitric Oxide Synthase. Under non-inflammatory conditions NOS generates Nitric Oxide. However, in an inflammatory environment, such as the oxidative tumor microenvironment, NOS's cofactor tetrahydrobiopterin (BH4) is oxidized to dihydrobiopterin (BH2). NOS bound to BH2 is said to be uncoupled and produces superoxide O2- and peroxyinitrite (ONOO-). Previous work in our and other's labs have shown that increased production of ROS/RNS leads to the activation of pro-inflammatory/proliferative molecules such as NFκB, Stat3, β-Catenin and Akt. NOS can be re-coupled by supplementing cells and animals with BH4 or its precursor Sepiapterin (SP). Herein Wwe have shownshow that by recoupling NOS with SP in HCT116, Caco-2 and HT29 cells, decreased tumor cell proliferation, increased β-Catenin degradation and decreased Akt activity. We have also seen increased tumor cell death measured via by in vitro clonogenic assays, as well decreased metabolic uptake in AOM/DSS induced colorectal cancer in vivo measured via by F18Deoxy-Glucose PET imaging. We believe by recoupling NOS both in vivo and in vitro we are modulatingion Wnt signaling via Akt and GSK-3β. Further studies are needed to elucidate the mechanism of decreased Akt activity and the downstream effectors of Wnt signaling which are affected by NOS recoupling. Lastly, we wish to combine radiation therapy with Sepiapterin SP to determine if the combination of these therapies can increase tumor cell deathincrease tumor control. Citation Format: Asim Alam, Chris Rabender, Li Wang, Sundaresan Gobalakrishnan, Jamal Zweit. Nitric oxide synthase activity and its modulation in the treatment of colorectal cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4250. doi:10.1158/1538-7445.AM2014-4250
Computed Tomographic Pulmonary Angiography for Pulmonary Embolism
Authors: Grégoire Le Gal, Marc Righini, Philip S. Wells
Journal: JAMA (2015)

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Farming, moisture damage, microbes and development of asthma in childhood: A birth cohort study
Authors: Anne M. Karvonen, Anne Hyvärinen, Helena Rintala, Gert Doekes, Erika von Mutius, Juha Pekkanen
Journal: European Respiratory Journal (2014)

Background : Microbial exposure has been suggested to mediate the protective health effects of farming environments and the adverse health effects of moisture damage buildings.

Objective : To explore, whether microbial exposures mediate the effect of farming and moisture damage on the development of asthma.

Methods: In a birth cohort, 319 children were followed-up with questionnaires until the age of 6 years for asthma (doctor-diagnosed asthma or at least two asthmatic bronchitis, n=46). 32% lived on farms with livestock. Collection of living room floor dust samples and home inspection for moisture damage were performed before the age of 1 year. Concentrations of 3-hydroxy fatty acids (3-OH FAs), muramic acid, ergosterol, endotoxin, EPS, β(1,3)-glucan and two bacterial genera and six fungal species, genera or groups (determined with quantitative polymerase chain reaction, qPCR) were measured in house dust.

Results: Living on a farm decreased the risk of asthma (aOR 0.33, 95%CI 0.14, 0.80), whereas moisture damage was associated with increased risk of asthma. Both farm homes and moisture damaged homes had increased levels of all measured microbial markers, except concentrations of Mycobacterium spp. and Streptomyces spp. were lower on farms. According to the first multivariate analyses, approximately half of the farming effect on asthma was explained by measured microbial exposures, but the proportion explained was much less for moisture damage.

Conclusion: Better markers of microbial exposure are needed to better differentiate between environments with protective or adverse effects on asthma.
Health Effects of Exposure to Low Level Ionising Radiation, by Ed William R Hendee, F Marc Edwards
Authors: C. Bowie
Journal: BMJ (1997)

Ed William R Hendee, F Marc Edwards /IOP Publishing, £125, pp 640 /ISBN 0 750 30349 2

When it comes to radiobiology we–physicians and health physicists–seem to keep getting the theory wrong about the health effects of ionising radiation by using animal models to predict human response. The history chapter in this book reminds us to beware. Despite this, several chapters are about radiation theory based on animal experiments. They can be safely ignored. Two chapters are more interesting.

In a masterly chapter John Boice, chief of the Radiation Epidemiology Branch, …