tbuckley/cabot-search huggingface dataset:
PWE-183 Does Insertion of a Gastrostomy Confer any Quality Of Life Benefit to Either Patients or their Carers?
Authors: M Kurien, M E McAlindon, J Grant, E F Wong, A J Johnston, B Hoeroldt, K L Dear, D S Sanders
Journal: Gut (2013)

<h3>Introduction</h3> Gastrostomy feeding is an effective means of providing enteral nutrition to patients who have functionally normal gastrointestinal tracts but who cannot meet their nutritional requirements because of an inadequate oral intake. Whilst improvements in outcome measures such as nutritional status and mortality have been demonstrated in certain patients undergoing gastrostomy insertion, there remains a paucity of work evaluating another important health outcome measure, which is health related quality of life (HRQoL). Furthermore no previous study has looked at the impact on carers’ HRQoL when considering all referral indications for gastrostomy. This prospective, multicenter study evaluates HRQoL in both gastrostomy patients and their carers, with comparisons made with a population control group. <h3>Methods</h3> 61 patients (mean age 68 years) and 58 carers (mean age 65 years) were prospectively recruited from 4 hospitals in South Yorkshire between Feb-Dec 2012. All individuals had HRQoL evaluated prior to gastrostomy insertion, with repeated measurements undertaken at 3 months. Assessment was undertaken using EQ-5D, a validated assessment tool and preferential measure used by NICE, producing scores between 0 for dead and 1 for perfect health. Findings were then compared with a separate cohort of population controls (n = 419), to determine if differences existed in HRQoL. Non-parametric statistical analysis was undertaken using a Wilcoxon Rank test to compare longitudinal paired EQ-5D scores, and a Mann-Whitney test to compare EQ-5D scores between groups, with p values &lt; 0.05 considered significant. <h3>Results</h3> 61 gastrostomy patients have been assessed to date. Of these, 3 died prior the 3 month reassessment post insertion. No significant change was shown in mean EQ-5D scores in either the gastrostomy patients (0.74 versus 0.73, p = 0.11) or their carers (0.96 versus 0.97, p = 0.30) at 3 months following gastrostomy insertion. When compared to population controls, carers had comparable scores to the population controls unlike the gastrostomy patients who had significantly lower mean EQ-5D scores (0.73 versus 0.94, p &lt; 0.0001). <h3>Conclusion</h3> This study demonstrates that HRQoL does not significantly improve for patients or their carers following gastrostomy insertion. Given that gastrostomy feeding has no positive effect on HRQoL, questions must be raised as to the merits of this intervention if it only serves to improve physiological outcomes. <h3>Disclosure of Interest</h3> None Declared.
Abstract 868: Oral SHP-1 inhibitor TPI-1a4 increases TILs in melanoma tumors and interacts positively with CTLA4 antibody for melanoma cure in mice
Authors: Taolin Yi, Daniel Lindner, Ralph Tuthill, Hans Loibner, Ernest Borden
Journal: Cancer Research (2012)

Abstract SHP-1 phosphatase is a promising target for developing inhibitors as novel cancer immune therapeutics given its key role in negative regulation of immune cells. TPI-1a4 is a small molecule SHP-1 inhibitor identified recently and demonstrated activity for melanoma and colon cancer tumors in mice as a tolerated single oral agent. TPI-1a4 has been further evaluated herein for mechanism of action and potential clinical translation. Oral TPI-1a4 increased (up to 8x) in TILs in K1735 melanoma tumors in syngeneic mice in a dose-dependent manner and in correlation with tumor growth inhibition. The growth of 4-day established K1735 tumors (s.c.) in syngeneic C3H/HeJ mice was inhibited 44% (p &amp;lt; 0.05) by TPI-1a4 at 0.4 mg/kg (5 d/wk, gavage) or 90% (p &amp;lt; 0.01) at 0.8 mg/kg (5 d/wk, gavage) during a treatment period of 4 wks. Evaluation of tumor histology (H.E.) revealed increases (2x and 4x for the two treatments) of tumor-infiltrating lymphocytes (TIL). Immunohistochemistry analyses of the tumor samples demonstrate increases (∼3 and 6x) of CD45+ cells (pan-leukocytes), CD3+ cells (T lineage), B220+ cells (B/NK lineages), and Mac3+ cells (myeloid lineages). Oral TPI-1a4 interacted positively with CTLA4 antibody for survival extension and cure in K1735 melanoma tumor mice. TPI-1a4 (1 mg/kg, 5d/wk, gavage) or CTLA4 antibody (9H10, 100 ug x3, ip) as individual agents delayed tumor growth for ∼1-4 wks in C3H/HeJ mice with 4-day established K1735 tumors (s.c.). Their combination delayed tumor growth for 4-14 wks (4/5 mice) or completely blocked tumor growth (1/5 mice) by 20th wk in association with resistance to re-challenging with the melanoma tumor (s.c.). The combination was more effective in C3H/HeJ mice with 1-day established K1735 tumors, blocked tumor growth in most mice (4/5) comparing to mostly delayed tumor growth for several wks by the individual agents. TPI-1a4 in drinking water ad lib with weekly renewal was effective against the melanoma tumors in mice, suggesting chemical stability. Indeed, mass spectrometry verified structural integrity of TPI-1a4 stored as solid compound or in solvent at room temperature for 2 months. These data provide further evidences designate TPI-1a4 as a novel anti-cancer immune agent and a promising candidate for clinical translation. Our studies demonstrate for the first time the potential of TPI-1a4 to improve the clinical efficacy of CTLA4 antibody and other related cancer therapeutics. Future studies of TPI-1a4 analogs and derivatives are warranted and may lead to more refined and effective SHP-1 inhibitors and immune cell activators. 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 868. doi:1538-7445.AM2012-868
Space Imaging Technology Yields Down-to-Earth Cancer Benefits
Authors: Michael E. Newman
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Space Imaging Technology Yields Down-to-Earth Cancer Benefits Get access Michael E. Newman Michael E. Newman Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 14, 17 July 1991, Pages 986–987, https://doi.org/10.1093/jnci/83.14.986 Published: 17 July 1991
What Is PET and How Does It Work?
Authors: T. Reynolds
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article What Is PET and How Does It Work? Get access Tom Reynolds Tom Reynolds Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 4, 15 February 1995, Pages 247–248, https://doi.org/10.1093/jnci/87.4.247 Published: 15 February 1995
Effect of Antiidiotypic Antibodies to HLA on Graft Survival in Renal-Allograft Recipients
Authors: Elaine Reed, Mark Hardy, Alan Benvenisty, Conrad Lattes, Jeffrey Brensilver, Robert McCabe, Keith Reemstma, Donald W. King, Nicole Suciu-Foca
Journal: New England Journal of Medicine (1987)

Although the presence in the recipient of preformed antibodies to HLA antigens in the kidney of a renal-transplant donor may be associated with early graft failure, such grafts are often well tolerated. We have investigated the possibility that anti-anti-HLA (antiidiotypic) antibodies influence the outcome of renal transplantation in recipients with a history of presensitization to their donor's HLA antigens. A retrospective analysis of 20 such cases showed that in 10 patients the transplanted kidney was rejected within one month, whereas in the remaining 10 the graft was tolerated for more than a year. Nine of the 10 patients in whom the graft was tolerated had anti-anti-HLA antibodies at the time of transplantation. Nine of the 10 patients in whom the graft was rejected had antibodies that potentiated, rather than blocked, the cytotoxic activity of anti-donor-HLA antibodies. These results suggest that patients with anti-anti-HLA antibodies specific for a potential donor can safely undergo transplantation, despite a prior history of anti-HLA antibodies. At the time of transplantation, patients who have antibodies that potentiate the cytotoxic activity of a historically positive serum are at high risk of graft rejection within a short period. Taking these considerations into account may improve the reliability of cross-matching in renal transplantation.
The Quality of Life of Patients with End-Stage Renal Disease
Authors: Roger W. Evans, Diane L. Manninen, Louis P. Garrison, L. Gary Hart, Christopher R. Blagg, Robert A. Gutman, Alan R. Hull, Edmund G. Lowrie
Journal: New England Journal of Medicine (1985)

We assessed the quality of life of 859 patients undergoing dialysis or transplantation, with the goal of ascertaining whether objective and subjective measures of the quality of life were influenced by case mix or treatment. We found that 79.1 per cent of the transplant recipients were able to function at nearly normal levels, as compared with between 47.5 and 59.1 per cent of the patients treated with dialysis (depending on the type). Nearly 75 per cent of the transplant recipients were able to work, as compared with between 24.7 and 59.3 per cent of the patients undergoing dialysis. On three subjective measures (life satisfaction, well-being, and psychological affect) transplant recipients had a higher quality of life than patients on dialysis. Among the patients treated with dialysis, those undergoing treatment at home had the highest quality of life. All quality-of-life differences were found to persist even after the patient case mix had been controlled statistically. Finally, the quality of life of transplant recipients compared well with that of the general population, but despite favorable subjective assessments, patients undergoing dialysis did not work or function at the same level as people in the general population.
Abstract 2617: Cytokine and cytokine receptors of adaptive immune response are differentially associated with breast cancer risk in women of African ancestry and European ancestry
Authors: Lei Quan, Song Yao, Zhihong Gong, Elisa V. Bandera, Helena Hwang, Michelle Roberts, Gary Zirpoli, Gregory Ciupak, Warren Davis, Lara Sucheston, Karen Pawlish, Dana Bovbjerg, Lina Jandorf, Christine B. Ambrosone, Chi-Chen Hong
Journal: Cancer Research (2012)

Abstract Disparities in breast cancer biology are evident between women of African ancestry (AA) and women of European ancestry (EA), and may be due, in part, to differences in inflammatory pathway genes. Studies on the relationships between cytokines and breast cancer risk have focused on a small number of genes and have not included AA women. In a large case-control study of 1008 AA (n=547 cases) and 763 EA (n=381 cases) women, we systematically tested the association between risk of breast cancer and single-nucleotide polymorphisms (SNPs) in 22 cytokine and cytokine receptor genes involved in adaptive immune response pathways. Logistic regression was used to estimate odds ratios and 95% confidence intervals in a genotypic (co-dominant) model adjusting for major breast cancer risk factors including age, education, body mass index (BMI), family history of breast cancer and proportion of European ancestry. All analyses were stratified on race. SNPs rs17810546 in IL12A (interleukin 12A), rs1041981 in LTA (lymphotoxin alpha), and rs3135932 in IL10RA, were associated with breast cancer risk in AA but not EA women. When stratifying by menopause and ER status, SNPs rs2070874 in IL4, rs1041981 in LTA and rs2430561 in IFNG (interferon gamma) were associated with breast cancer risk in pre-menopausal AA women, and SNPs rs2243248 in IL4 and rs746868 in LTA were associated with ER-negative breast cancer in EA women. Common variants in inflammatory pathway genes may help to define populations at high risk of breast cancer. Notable differences in distributions of SNPs and associations by ancestry may be related to the differential epidemiology of breast cancer in AA and EA women. 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 2617. doi:1538-7445.AM2012-2617
Case 6-1998
Authors: Bruce M. Ewenstein, Elizabeth Van Cott
Journal: New England Journal of Medicine (1998)

Presentation of CaseA six-year-old boy was admitted to the hospital because of a painful hip.The child had been well until 11 days earlier, when an upper respiratory tract infection developed. Two days later, he fell while playing and noticed mild pain in the right hip. During the night, the pain increased, and the next day a physician prescribed ibuprofen. Radiographs of the hip showed no abnormalities.On the following day, the child was admitted to another hospital because of more severe pain and low-grade fever. The urea nitrogen, creatinine, glucose, and electrolyte levels were normal. Other laboratory findings . . .
Abstract 5297: Dual-modality imaging of hepatocellular carcinoma
Authors: David Corn, Jack Jesberger, Jeffrey Kolthammer, Christopher Flask, Zhenghong Lee
Journal: Cancer Research (2011)

Abstract Choline compounds are linked to malignancy since elevation of the intensity of choline peak reflects increased biosynthesis of membrane phospholipids and can be a marker for cellular proliferation. Positron Emission Tomography (PET) images an injected tracer dose (nM∼pM) of [11C]-choline while Proton MR Spectroscopy (1H MRS) can characterize endogenous choline-containing compounds usually in the mM range. There have been studies on brain and prostate cancers with both imaging modalities although correlation between the results from PET and MRS is inconsistent. The transient radiolabeled choline metabolism measured by PET is different from the relative steady total choline contents measured by MRS. However, it begs the question of whether the two imaging modalities are measuring the same metabolic pathways of choline in cancer. For primary Hepatocellular Carcinoma (HCC), there have been [11C]-choline PET studies, both pre-clinical and clinical, showing focal uptake. Likewise, there have been 1H-MRS studies of choline with animals and humans showing significantly high choline levels in HCC. So far, there is no comparison study reported to link the two measurements in HCC. This study was conducted with a woodchuck model of hepatitis viral infection-induced HCC, which is regarded as a naturally occurring animal model of human HCC with similar pathology and clinical behavior. The original objective of the study was to examine the effects of animals being fed and fasted on PET scans using [11C]-choline. MRI and MRS were added and performed immediately before PET imaging. Experiments were first performed with animals at the fed state using a 4T MR scanner with a human head coil. Dynamic PET images were then generated from a nearby clinical PET/CT scanner right after, spanning 50 minutes starting from [11C]-choline injection. Time-activity curves and tracer contrast uptake between focal uptake in HCC and that in the surrounding hepatic tissues were calculated in liver regions. The same animals were scanned again four days later following the exact same procedure, except that the animals were fasted over night. The results from PET imaging with [11C]-choline showed that the dietary state of fed or fast had little impact on radio-choline uptake in HCC while the results from 1H MRS of choline found similar choline/lipids ratios in HCC regardless of whether the animal was fed or fasted. These results are very promising for correlating the two measurements although further experiments are needed to confirm that the two imaging modalities are measuring related lipid metabolic pathways in HCC involving choline. This work is supported in part by NCI grants R01 CA095307 and U24 CA110943. 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 5297. doi:10.1158/1538-7445.AM2011-5297
RE-EVALUATION OF NITRATE TOLERANCE: A STUDY OF CENTRAL AORTIC PULSE WAVEFORM ANALYSIS
Authors: Michael F. O’Rourke, Xiong Jing Jiang, Wei Ji, Yi-Shi Li, Audrey Adji, Hui Dong, Meng Peng, Lisheng Liu
Journal: Journal of the American College of Cardiology (2016)
314O_PR Second-line afatinib vs methotrexate (MTX) in patients (pts) with recurrent and/or metastatic head and neck squamous cell carcinoma (R/M HNSCC): subgroup/biomarker analysis of LUX-head and neck 1 (LUX-H&amp;N1)
Authors: M. Tahara, E.E.W. Cohen, R.I. Haddad, J. Fayette, L.F. Licitra, P.M. Clement, J.B. Vermorken, T. Gauler, D. Cupissol, J.J. Grau, J. Guigay, J.M. del Campo, K. Okami, S. Takahashi, B. Burtness, X.J. Cong, N. Gibson, F. Solca, E. Ehrnrooth, J.-P.H. Machiels
Journal: Annals of Oncology (2015)
Case 3-2015
Authors: William S. David, Elizabeth S. Temin, Jessica J. Kraeft, David C. Hooper
Journal: New England Journal of Medicine (2015)

A 60-year-old woman was admitted to the hospital because of abdominal pain, dyspnea, and diplopia. Several hours after presentation, she was unable to phonate clearly or protrude the tongue, and proximal weakness of the arms and legs developed. A diagnostic test was performed.
South African health minister wins first round of tobacco battle
Authors: P. Sidley
Journal: BMJ (1998)

South Africa's health minister, Dr Nkosazana Zuma, has won the first round of her battle with tobacco companies over her plan to introduce tough antismoking legislation.

Last week the High Court in Cape Town dismissed an application brought by the tobacco industry to stop Dr Zuma presenting her bill to parliament. The bill will drastically curtail tobacco advertising, virtually end sponsorship of sporting events by tobacco companies, and ban smoking in workplaces and public venues.

The tobacco industry asked the court to force …
Abstract LB-283: Aurora B binds p53 during both interphase and mitosis, phosphorylates it and promotes its degradation
Authors: Enrique Fuentes-Mattei, Christopher Gully, Guermarie Velazquez-Torres, Ji-Hyun Shin, Jiun-Sheng Chen, Hyun Ho Choi, Ping-Chieh Chou, Henry P. Adams, Liem Phan, Tsung-Ying Yang, Sai-Ching J. Yeung, Mong-Hong Lee
Journal: Cancer Research (2012)

Abstract Aurora B (AurB) is a mitotic checkpoint kinase that plays a pivotal role in the cell cycle, ensuring correct chromosome segregation and normal progression through mitosis. Tumor suppressor p53 is a genome guardian and an important negative regulator of the cell cycle. Although overexpression of AurB and loss or degradation of p53 have been described in many types of human cancers, it is not known whether AurB and p53 are coordinately regulated during the cell cycle. Recently has been shown that NIR, which is a transcriptional co-repressor of histone acetyltransferase activity, interact with and suppress p53 via interaction with AurB. Our results show that AurB directly interacts with p53 in a NIR-independent matter. To prove direct molecular interaction between AurB and p53 in whole cells, we employed the method of bimolecular fluorescent complementation (BiFC). AurB-p53 interaction occurs at the nucleus in interphase and at the centromeres in prometaphase of mitosis. We observed that AurB-p53 interaction co-localized with Survivin and CENP-A, suggesting that AurB and p53 interact at the centromeres. Our results also show that Aurora B phosphorylates p53 to accelerate p53's degradation through the polyubiquitination-proteasome pathway, thus functionally suppressing the expression of p53 target genes involved in cell cycle inhibition and apoptosis. Inhibition of Aurora B in cancer cells with wild-type p53 increased p53 protein level and expression of p53 target genes to inhibit tumor growth. Together, these results give a new insight of a novel mechanism of p53 inactivation during the cell cycle and imply that oncogenic hyperactivation or overexpression of AurB may compromise p53's tumor suppressor function. 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 LB-283. doi:1538-7445.AM2012-LB-283
Abstract 2222: Mutational and copy number analysis of the PI3K/Akt/mTOR pathway in oral cavity squamous cell carcinoma
Authors: Luc GT Morris, Ian Ganly, Adriana Heguy, Timothy A. Chan
Journal: Cancer Research (2010)

Abstract The phosphatidylinositol 3-kinase signaling (PI3K) pathway is integral to cell growth, proliferation and survival, and is upregulated in multiple human cancers. Several oncogenes and tumor suppressors within this pathway are altered by mutation, amplification or deletion, and are currently being investigated as therapeutic targets. The pattern of dysregulation in this pathway differs among various cancers, and has not been comprehensively characterized in oral squamous cell carcinoma. After institutional review board approval, fresh frozen tumor and matched normal tissues were obtained from 32 patients treated for oral cavity squamous cell carcinoma, and genomic DNA was extracted. Using high-throughput Sanger sequencing, the 23 component genes of the PI3K/Akt/mTOR pathway were comprehensively sequenced. Putative mutations identified by mutation detection software were validated on a second PCR and sequencing procedure. Array CGH was performed on the Agilent 1M microarray, and data analysis performed using the RAE method. Component genes within the PI3K/Akt/mTOR pathway were comprehensively sequenced, including AKT1, AKT2, AKT3, AKTS1, AXL, AGAP2, MTOR, GBL, GOLPH3, RAPTOR, MUC1, PDPK1, PIK3CA, PIK3CB, PIK3CD, PIK3CG, PIK3R1, PIK3R2, PTEN, RHEB, RICTOR, TSC1 and TSC2. Activating mutations were identified in PIK3CA in 2 of 32 (6.3%) specimens. No other genes harbored somatic mutations. DNA copy number gains and losses are described in detail. In the first comprehensive mutational and copy number analysis of 23 component genes of the PI3K/Akt/mTOR pathway in cancer, we report a low prevalence of somatic mutations, and a higher frequency of copy number alteration in oral cancer specimens. In contrast to colorectal, breast, ovarian, brain and bladder cancers, mutation is not the primary source of activation of this pathway in oral cancers. 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 2222.