tbuckley/cabot-search huggingface dataset:
The role of lymphatics in removing pleural liquid in discrete hydrothorax
Authors: T Nakamura, Y Tanaka, T Fukabori, Y Iwasaki, M Nakagawa, S Kira
Journal: European Respiratory Journal (1988)

The thoracic duct and right lymphatic duct of the dogs in the experimental group were ligated at the neck. Saline labelled with Evans blue was injected (10 ml.kg-1) into the pleural cavity. The colloid osmotic pressure of the saline was adjusted to be exactly equal to that of normal pleural liquid. The change in the volume of the liquid and the decrease of the marker were studied for 3 h. The dynamics of the pleural liquid were investigated. In the control group, the volume of the pleural liquid decreased at the rate of 1.31 ml.h-1.kg-1 body weight and 87% of it left via the lymphatics. With the ligation of the bilateral lymphatic ducts, the lymphatic removal rate decreased to about one tenth. This result shows that the hydrothorax leaves the pleural cavity mainly via the lymphatics.
Identification of Candidate Biomarkers of Therapeutic Response to Docetaxel by Proteomic Profiling
Authors: Liangli Zhao, Brian Y. Lee, David A. Brown, Mark P. Molloy, Gavin M. Marx, Nick Pavlakis, Michael J. Boyer, Martin R. Stockler, Warren Kaplan, Samuel N. Breit, Robert L. Sutherland, Susan M. Henshall, Lisa G. Horvath
Journal: Cancer Research (2009)

Docetaxel chemotherapy improves symptoms and survival in men with metastatic hormone-refractory prostate cancer (HRPC). However, approximately 50% of patients do not respond to Docetaxel and are exposed to significant toxicity without direct benefit. This study aimed to identify novel therapeutic targets and predictive biomarkers of Docetaxel resistance in HRPC. We used iTRAQ-mass spectrometry analysis to identify proteins associated with the development of Docetaxel resistance using Docetaxel-sensitive PC3 cells and Docetaxel-resistant PC3-Rx cells developed by Docetaxel dose escalation. Functional validation experiments were performed using recombinant protein treatment and siRNA knockdown experiments. Serum/plasma levels of the targets in patient samples were measured by ELISA. The IC(50) for Docetaxel in the PC3-Rx cells was 13-fold greater than the parent PC-3 cell line (P = 0.004). Protein profiling identified MIC-1 and AGR2 as respectively up-regulated and down-regulated in Docetaxel-resistant cells. PC-3 cells treated with recombinant MIC-1 also became resistant to Docetaxel (P = 0.03). Conversely, treating PC3-Rx cells with MIC-1 siRNA restored sensitivity to Docetaxel (P = 0.02). Knockdown of AGR2 expression in PC3 cells resulted in Docetaxel resistance (P = 0.007). Furthermore, increased serum/plasma levels of MIC-1 after cycle one of chemotherapy were associated with progression of the cancer (P = 0.006) and shorter survival after treatment (P = 0.002). These results suggest that both AGR2 and MIC-1 play a role in Docetaxel resistance in HRPC. In addition, an increase in serum/plasma MIC-1 level after cycle one of Docetaxel may be an indication to abandon further treatment. Further investigation of MIC-1 as a biomarker and therapeutic target for Docetaxel resistance in HRPC is warranted.
THE VALUE OF MUCH'S GRANULES AND THE ANTIFORMIN METHOD IN DETERMINING THE AETIOLOGY OF THE SO-CALLED TUBERCULIDES, WITH ESPECIAL REFERENCE TO LUPUS ERYTHEMATOSUS
Authors: D. FRIEDLANDER
Journal: British Journal of Dermatology (1912)

ANTIl!ORMlN METHOD.18 tophytes.I have found, however, in some experiments not yet completed, that by the use of a suitable sugary medium the pigment of my cultures of Trichophyton rosaceum early diffuses into the medium and colours it a rich murexide tint.Investigation of the contact of my patients with various animals has not resulted in any light on the subject of origin.I have examined horses, dogs, cats, and pigeons where it has been possible that these were sources of infection, but in no instance was any relationship eshblished.Contagion from man to man seems clearly proved by the clinical stories of several cases, and it is usual to find that the beard cases are either accustomed to be shaved by a barber, or, if ordinarily shaving themselves, have noted the outbreak of the disease after a casual visit to a barber, or after having a razor set in such an establishment .The matter calls for further investigation, and I hope to make a commuuication at a future date on some points in the mycology and inoculation features of this parasite.
Prostate-Specific Antigen Modulates Genes Involved in Bone Remodeling and Induces Osteoblast Differentiation of Human Osteosarcoma Cell Line SaOS-2
Authors: Nagalakshmi Nadiminty, Wei Lou, Soo Ok Lee, Farideh Mehraein-Ghomi, Jason S. Kirk, Jeffrey M. Conroy, Haitao Zhang, Allen C. Gao
Journal: Clinical Cancer Research (2006)

Abstract Purpose: The high prevalence of osteoblastic bone metastases in prostate cancer involves the production of osteoblast-stimulating factors by prostate cancer cells. Prostate-specific antigen (PSA) is a serine protease uniquely produced by prostate cancer cells and is an important serologic marker for prostate cancer. In this study, we examined the role of PSA in the induction of osteoblast differentiation. Experimental Design: Human cDNA containing a coding region for PSA was transfected into human osteosarcoma SaOS-2 cells. SaOS-2 cells were also treated with exogenously added PSA. We evaluated changes in global gene expression using cDNA arrays and Northern blot analysis resulting from expression of PSA in human osteosarcoma SaOS-2 cells. Results: SaOS-2 cells expressing PSA had markedly up-regulated expression of genes associated with osteoblast differentiation including runx-2 and osteocalcin compared with the controls. Consistent with these results, the stable clones expressing PSA showed increased mineralization and increased activity of alkaline phosphatase in vitro compared with controls, suggesting that these cells undergo osteoblast differentiation. We also found that osteoprotegerin expression was down-regulated and that the receptor activator of NF-κB ligand expression was up-regulated in cells expressing PSA compared with controls. Conclusions: Modulation of the expression of osteogenic genes and alteration of the balance between osteoprotegerin–receptor activator of NF-κB ligand by PSA suggests that PSA produced by metastatic prostate cancer cells may participate in bone remodeling in favor of the development of osteoblastic metastases in the heterogeneous mixture of osteolytic and osteoblastic lesions. These findings provide a molecular basis for understanding the high prevalence of osteoblastic bone metastases in prostate cancer.
Individual and Combined Effects of Age, Breast Density, and Hormone Replacement Therapy Use on the Accuracy of Screening Mammography
Authors: Patricia A. Carney, Diana L. Miglioretti, Bonnie C. Yankaskas, Karla Kerlikowske, Robert Rosenberg, Carolyn M. Rutter, Berta M. Geller, Linn A. Abraham, Steven H. Taplin, Mark Dignan, Gary Cutter, Rachel Ballard-Barbash
Journal: Annals of Internal Medicine (2003)

Background: The relationships among breast density, age, and use of hormone replacement therapy (HRT) in breast cancer detection have not been fully evaluated. Objective: To determine how breast density, age, and use of HRT individually and in combination affect the accuracy of screening mammography. Design: Prospective cohort study. Setting: 7 population-based mammography registries in North Carolina; New Mexico; New Hampshire; Vermont; Colorado; Seattle, Washington; and San Francisco, California. Participants: 329 495 women 40 to 89 years of age who had 463 372 screening mammograms from 1996 to 1998; 2223 women received a diagnosis of breast cancer. Measurements: Breast density, age, HRT use, rate of breast cancer occurrence, and sensitivity and specificity of screening mammography. Results: Adjusted sensitivity ranged from 62.9% in women with extremely dense breasts to 87.0% in women with almost entirely fatty breasts; adjusted sensitivity increased with age from 68.6% in women 40 to 44 years of age to 83.3% in women 80 to 89 years of age. Adjusted specificity increased from 89.1% in women with extremely dense breasts to 96.9% in women with almost entirely fatty breasts. In women who did not use HRT, adjusted specificity increased from 91.4% in women 40 to 44 years of age to 94.4% in women 80 to 89 years of age. In women who used HRT, adjusted specificity was about 91.7% for all ages. Conclusions: Mammographic breast density and age are important predictors of the accuracy of screening mammography. Although HRT use is not an independent predictor of accuracy, it probably affects accuracy by increasing breast density.
Specific Mutations in<i>KRAS</i>Codons 12 and 13, and Patient Prognosis in 1075<i>BRAF</i>Wild-Type Colorectal Cancers
Authors: Yu Imamura, Teppei Morikawa, Xiaoyun Liao, Paul Lochhead, Aya Kuchiba, Mai Yamauchi, Zhi Rong Qian, Reiko Nishihara, Jeffrey A. Meyerhardt, Kevin M. Haigis, Charles S. Fuchs, Shuji Ogino
Journal: Clinical Cancer Research (2012)

To assess prognostic roles of various KRAS oncogene mutations in colorectal cancer, BRAF mutation status must be controlled for because BRAF mutation is associated with poor prognosis, and almost all BRAF mutants are present among KRAS wild-type tumors. Taking into account experimental data supporting a greater oncogenic effect of codon 12 mutations compared with codon 13 mutations, we hypothesized that KRAS codon 12-mutated colorectal cancers might behave more aggressively than KRAS wild-type tumors and codon 13 mutants.Using molecular pathological epidemiology database of 1,261 rectal and colon cancers, we examined clinical outcome and tumor biomarkers of KRAS codon 12 and 13 mutations in 1,075 BRAF wild-type cancers (i.e., controlling for BRAF status). Cox proportional hazards model was used to compute mortality HR, adjusting for potential confounders, including stage, PIK3CA mutations, microsatellite instability, CpG island methylator phenotype, and LINE-1 methylation.Compared with patients with KRAS wild-type/BRAF wild-type cancers (N = 635), those with KRAS codon 12 mutations (N = 332) experienced significantly higher colorectal cancer-specific mortality [log-rank P = 0.0001; multivariate HR, 1.30; 95% confidence interval (CI), 1.02-1.67; P = 0.037], whereas KRAS codon 13-mutated cases (N = 108) were not significantly associated with prognosis. Among the seven most common KRAS mutations, c.35G>T (p.G12V; N = 93) was associated with significantly higher colorectal cancer-specific mortality (log-rank P = 0.0007; multivariate HR, 2.00; 95% CI, 1.38-2.90, P = 0.0003) compared with KRAS wild-type/BRAF wild-type cases.KRAS codon 12 mutations (in particular, c.35G>T), but not codon 13 mutations, are associated with inferior survival in BRAF wild-type colorectal cancer. Our data highlight the importance of accurate molecular characterization in colorectal cancer.
Survivin Expression in Sentinel Lymph Nodes From Melanoma Patients
Authors: Maria González Cao, Susana Puig, Begoña Mellado
Journal: Journal of Clinical Oncology (2004)

of the Journal of Clinical Oncology.It provides evidence about the correlation of survivin expression in melanoma sentinel lymph nodes and patients' clinical outcome.Gradilone et al included 36 patients with different melanoma American Joint Committee on Cancer (AJCC) stages, from stage IA to III.Patients with sentinel nodes, in which survivin expression was detected, had a worst outcome: 72% of the samples were positive for survivin, and among these patients, 61.5% died or progressed versus 0% among survivin-negative patients.Although we congratulate the original finding, we believe that some considerations must be taken into account.First, although a role of apoptosis for melanoma genes (including the survivin gene) has been poorly studied in primary and metastatic melanoma, the authors started investigating their role as a prognostic marker in melanoma sentinel nodes, furthermore including hematoxylin and eosin-negative lymph nodes in their analyses.Although tyrosinase was positive in all cases tested, this does not mean that melanoma cells were present in all nodes.Tyrosinase containing nevocytes that have migrated from cutaneous nevi are found in the capsule of the lymph nodes of 24% of patients undergoing lymphadenectomy.Schwann cells of nerves that traverse lymph nodes could also express tyrosinase.Additionally, macrophages that have scavenged partially melanized melanosomes from melanoma cells disrupted in tissues peripheral to the lymph nodes or within the node itself may contain detectable m-tyrosinase.For these reasons, the finding of an enhanced signal for m-tyrosinase after reverse transcriptase polymerase chain reaction (RT-PCR) of a lymph node does not guarantee that the source of this signal is a metastatic melanoma cell.Immunohistochemical staining was carried out to identify the cell histotypes within the metastatic lymph nodes that were positive for survivin, bax, and bcl-2.Authors found that all three proteins were positive, corresponding with the infiltrating cells, whereas lymphocytes were totally negative.It is not clear, in our opinion, how this could be so, since Table 1 of the Gradlione et al 1
Cancer Statistics, 2010
Authors: A. Jemal, R. Siegel, J. Xu, E. Ward
Journal: CA A Cancer Journal for Clinicians (2010)

Each year, the American Cancer Society estimates the number of new cancer cases and deaths expected in the United States in the current year and compiles the most recent data regarding cancer incidence, mortality, and survival based on incidence data from the National Cancer Institute, the Centers for Disease Control and Prevention, and the North American Association of Central Cancer Registries and mortality data from the National Center for Health Statistics. Incidence and death rates are age-standardized to the 2000 US standard million population. A total of 1,529,560 new cancer cases and 569,490 deaths from cancer are projected to occur in the United States in 2010. Overall cancer incidence rates decreased in the most recent time period in both men (1.3% per year from 2000 to 2006) and women (0.5% per year from 1998 to 2006), largely due to decreases in the 3 major cancer sites in men (lung, prostate, and colon and rectum [colorectum]) and 2 major cancer sites in women (breast and colorectum). This decrease occurred in all racial/ethnic groups in both men and women with the exception of American Indian/Alaska Native women, in whom rates were stable. Among men, death rates for all races combined decreased by 21.0% between 1990 and 2006, with decreases in lung, prostate, and colorectal cancer rates accounting for nearly 80% of the total decrease. Among women, overall cancer death rates between 1991 and 2006 decreased by 12.3%, with decreases in breast and colorectal cancer rates accounting for 60% of the total decrease. The reduction in the overall cancer death rates translates to the avoidance of approximately 767,000 deaths from cancer over the 16-year period. This report also examines cancer incidence, mortality, and survival by site, sex, race/ethnicity, geographic area, and calendar year. Although progress has been made in reducing incidence and mortality rates and improving survival, cancer still accounts for more deaths than heart disease in persons younger than 85 years. Further progress can be accelerated by applying existing cancer control knowledge across all segments of the population and by supporting new discoveries in cancer prevention, early detection, and treatment. CA Cancer J Clin 2010;60:277-300. © 2010 American Cancer Society, Inc.
Dickkopf-1 is a master regulator of joint remodeling
Authors: Danielle Diarra, Marina Stolina, Karin Polzer, Jochen Zwerina, Michael S Ominsky, Denise Dwyer, Adelheid Korb, Josef Smolen, Markus Hoffmann, Clemens Scheinecker, Desiree van der Heide, Robert Landewe, Dave Lacey, William G Richards, Georg Schett
Journal: Nature Medicine (2007)
IDH2 R172 mutations define a unique subgroup of patients with angioimmunoblastic T-cell lymphoma
Authors: Chao Wang, Timothy W. McKeithan, Qiang Gong, Weiwei Zhang, Alyssa Bouska, Andreas Rosenwald, Randy D. Gascoyne, Xiwei Wu, Jinhui Wang, Zahid Muhammad, Bei Jiang, Joseph Rohr, Andrew Cannon, Christian Steidl, Kai Fu, Yuping Li, Stacy Hung, Dennis D. Weisenburger, Timothy C. Greiner, Lynette Smith, German Ott, Eleanor G. Rogan, Louis M. Staudt, Julie Vose, Javeed Iqbal, Wing C. Chan
Journal: Blood (2015)
Cytoplasmic Domain of proEGF Affects Distribution and Post-Translational Modification of Microtubuli and Increases Microtubule-Associated Proteins 1b and 2 Production in Human Thyroid Carcinoma Cells
Authors: Janette Pyka, Aleksandra Glogowska, Henning Dralle, Cuong Hoang-Vu, Thomas Klonisch
Journal: Cancer Research (2005)

Abstract We studied the distribution of transcripts encoding the cytoplasmic domain of the membrane-anchored precursor epidermal growth factor (proEGFcyt) and a novel cytoplasmic proEGF splice isoform with a deleted exon 23 and an out-of-frame fusion of exon 24 (proEGFdel23) in human normal and neoplastic thyroid tissues. In papillary thyroid carcinoma (PTC), coexpression of transcripts encoding for both proEGFcyt and proEGFdel23 correlated with poor differentiation of PTC. To determine potential roles of the cytoplasmic proEGF domain in human thyroid cells, we generated stable transfectants of the human follicular thyroid carcinoma cell line FTC-133 overexpressing the normal cytoplasmic domain proEGFcyt, a truncated proEGFcyt composed of the peptide sequence encoded by exons 22 and 23 (proEGF22.23) and proEGFdel23. The proEGFcyt and proEGF22.23 transfectants displayed significantly reduced proliferation rates, an enlarged cellular phenotype, and alterations in the distribution and post-translational modification of the microtubular system. These transfectants also displayed increased production of microtubule-associated proteins 1b and 2c, which was absent in FTC-133-proEGFdel23 or FTC-133-empty plasmid transfectants. This is the first evidence of an involvement of proEGF cytoplasmic domain in microtubular stability in the human thyroid carcinoma cell line FTC-133 and may suggest a specific role for the cytoplasmic domain of membrane-anchored proEGF, particularly exon 23, in thyroid carcinoma. The up-regulation of proEGFdel23 in poorly differentiated PTC and the exclusive detection of both proEGF isoforms in undifferentiated thyroid carcinoma may indicate an involvement of this novel truncated proEGFdel23 cytoplasmic domain during dedifferentiation processes of human thyroid cells.
Left main stem coronary artery disease. Retrospective review of 26 patients treated surgically or medically.
Authors: L J Day, H O Vallin, E Sowton
Journal: Thorax (1976)

The clinical, angiographic, exercise testing, operative, and follow-up data of 26 patients found at angiography to have left main stem coronary artery stenosis, defined as a reduction in the lumen diameter of 50% or more, are reviewed. There was a high incidence of significant proximal stenosis in the branches of the left main stem. No clinical features were found to distinguish patients with left main stem stenosis. All patients were considered for saphenous vein bypass grafting, selection being based upon the severity of symptoms, left ventricular function, and suitability of the coronary vessels for grafting. Two patients died within 24 hours of coronary angiography. Nine patients were operated on with no mortality. There has been one late cardiac death during a mean follow-up time of 13 months. All patients were symptomatically improved with a significant (P less than 0-01) increase in exercise ability postoperatively. Fifteen patients were not operated on. Six of these patients were regarded as operable but surgery was deferred; five have died at a mean time of 7-2 months. Five of the nine patients regarded as inoperable have died at a mean follow-up time of 14-8 months. The five non-surgical survivors remain symptomatic with no significant change in exercise ability. Recently reported surgical and medical series of patients with left main stem stenosis are reviewed.
Former NHS chief criticises private health insurance "lottery"
Authors: A. O'Dowd
Journal: BMJ (2010)

The former head of the NHS, Nigel Crisp, has attacked private health insurers for their policies, which he claims are arbitrary and sometimes leave patients with cancer without the care they need.

Lord Crisp said that private health insurance policies had a worrying lack of transparency, which was creating a “private healthcare lottery.”

But representatives for the industry have rejected the claim, saying that private health insurance works well and that companies often consulted the public to ensure transparency in their policies.

Speaking during a House of Lords debate on 11 November on measures to improve the quality and quantity of life of people with cancer, Lord Crisp called on the Financial Services Authority …
Multivariate analysis of prognostic factors in fulminant hepatitis B
Authors: Jacques Bernuau, Alain Goudeau, Thierry Poynard, Frederic Dubois, Gerard Lesage, Bernard Yvonnet, Claude Degott, Annie Bezeaud, Bernard Rueff, Jean-Pierre Benhamou
Journal: Hepatology (1986)

We assessed prognostic factors in 115 patients with serologically defined fulminant hepatitis B. The diagnosis in each case was based on the finding of IgM antibody to the hepatitis B core antigen in serum. Multivariate analysis showed that factor V level (p less than 0.001), patient's age (p = 0.001), absence of detectable HBsAg by radioimmunoassay (p = 0.06) and serum alpha-fetoprotein concentration (p = 0.07) were independent predictors of survival. The survival rate in the 21 patients in whom HBsAg was not detected was 47%, which was significantly higher than the survival rate of 17% observed in the 94 HBsAg-positive patients (p = 0.006). In patients with fulminant hepatitis B, the absence of HBsAg in serum as detected by radioimmunoassay has an independent, favorable prognostic value.
Investigation of Idiopathic Pleural Effusions by Thoracoscopy
Authors: S. J. Fleishman, A. I. Lichter, G. Buchanan, R. J. S. Sichel
Journal: Thorax (1956)

Previously, we have shown that antigen-specific CD8<sup>+</sup> T cell expansion following TLR agonist/anti-CD40 immunization is dependent on the enhanced expression of CD70 on dendritic cells. The dependence on CD27-CD70 interactions was confirmed by using a blocking anti-CD70 antibody. We now show that in CD27<sup>-/-</sup> mice, the antigen-specific CD8<sup>+</sup> T cell response to TLR agonist/anti-CD40 immunization is intact. However, administration of a blocking anti-OX40L antibody during immunization attenuates the CD8<sup>+</sup> T cell expansion. Thus, similar to the wild-type C57BL/6 mice, the enhanced primary expansion of antigen-specific CD8<sup>+</sup> T cells in response to TLR agonist/anti-CD40 vaccination is dependent on TNF receptor (TNFR) - TNF ligand (TNFL) superfamily interactions. Furthermore, TLR agonist/anti-CD40 vaccination is not affected by depletion of IL-12 using a neutralizing anti-IL-12p40 antibody in either wild-type or CD27<sup>-/-</sup> mice. Together, these data suggest that TNFR-TFNL interactions, facilitated by combined TLR agonist/anti-CD40 vaccination, can act as Signal 3 for CD8<sup>+</sup> T cell immunity in the absence of IL-12. This research is supported by a grant from the NIH.