tbuckley/cabot-search huggingface dataset:
Induction Chemotherapy (Ict) with Docetaxel/Cisplatin/5-Fluorouracil (T/P/F) Followed By Chemoradiotherapy with Cisplatin (Crtp) Vs Bioradiotherapy with Cetuximab (Rtcx) for Unresectable Locally Advanced Head &amp; Neck Cancer (Ulahnc): Preliminary Results on Toxicity a Ttcc Group Trial
Authors: R. Hitt, R. Mesia, J.J. Grau, J. Rubió, J. Martínez-Trufero, E. Del Barco Morillo, C. Almodóvar Alvarez, M. Taberna-Sanz, C. García-Girón, S. Vazquez, B. Cirauqui, M. Pastor Borgoñón, E. Galve Calvo, O. Juan-Vidal, R. Lopez, J. Martinez-Galan, R. Bastus, A. Berrocal, J.C. Adansa Klain, J.J. Cruz Hernandez
Journal: Annals of Oncology (2014)
Abstract 1641: Complex behavior of ALDH1A1 and IGFBP1 in liver metastasis of colorectal cancer
Authors: Jin Cheon Kim, Ye Jin Ha, Ka Hee Tak, Seon Ae Roh, Chan Wook Kim, Tae Won Kim, Dong-Hyung Cho, Seon-Kyu Kim, Seon-Young Kim, Yong Sung Kim
Journal: Cancer Research (2016)

Abstract The present study aimed to identify upregulated genes associated with colorectal cancer (CRC) liver metastasis (CLM) using our dataset (GSE50760) previously established by RNA sequencing and to verify their biological behavior. Candidate genes were assessed for their role in tumor proliferation, invasion, and the expression of epithelial-mesenchymal transition/CRC stem cell (EMT/CSC)-related molecules. The role of the identified genes in CLM was verified in mice after intrasplenic transplantation of CRC cells. Of nine candidate genes, ALDH1A1 and IGFBP1 were selected and showed few post-translational changes. The upregulation of ALDH1A1 and IGFBP1 significantly and time-dependently decreased cell proliferation (p ≤ 0.001-0.003) and suppressed invasiveness by ≥3 fold over control cells (p &amp;lt; 0.001) in the SW480 cell line, whereas it had a mild effect on reducing SW620 cell proliferation. EMT/CSC-related molecules showed different patterns of expression in CLM tissues and treated CRC cells. The cadherin switch, namely, N-cadherin upregulation with E-cadherin downregulation, was not observed in CLM tissues and treated CRC cells. Persistent overexpression of β-catenin, vimentin, and ZO-1 in IGFBP1-overexpressing SW480 cells may have contributed to CLM development in mice implanted with IGFBP1-overexpressing cells (CLM occurrences: SW480/IGFBP1 transfected mice vs. SW480/vector and /ALDH1A1 transfected mice, 4/8 vs. 0/10, p = 0.023). ALDH1A1 and IGFBP1 were differentially overexpressed in CLM and may play a dual role, functioning as tumor suppressors and metastasis promoting genes in CRC. Unidentified behaviors of these genes may facilitate the reassessment of their potential value as CLM modulators and as therapeutic targets. Citation Format: Jin Cheon Kim, Ye Jin Ha, Ka Hee Tak, Seon Ae Roh, Chan Wook Kim, Tae Won Kim, Dong-Hyung Cho, Seon-Kyu Kim, Seon-Young Kim, Yong Sung Kim. Complex behavior of ALDH1A1 and IGFBP1 in liver metastasis of colorectal cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1641.
Collateral and collateral-adjacent hyperemic vascular resistance changes and the ipsilateral coronary flow reserve Documentation of a mechanism causing coronary steal in patients with coronary artery disease
Authors: M Billinger
Journal: Cardiovascular Research (2001)

The goal of this clinical study was to assess the influence of hyperemic ipsilateral, collateral and contralateral vascular resistance changes on the coronary flow velocity reserve (CFVR) of the collateral-receiving (i.e. ipsilateral) artery, and to test the validity of a model describing the development of collateral steal.In 20 patients with one- to two-vessel coronary artery disease (CAD) undergoing angioplasty of one stenotic lesion, adenosine induced intracoronary (i.c.) CFVR during vessel patency was measured using a Doppler guidewire. During stenosis occlusion, simultaneous i.c. distal ipsilateral flow velocity and pressure (P(occl), using a pressure guidewire) as well as contralateral flow velocity measurements via a third i.c. wire were performed before and during intravenous adenosine. From those measurements and simultaneous mean aortic pressure (P(ao)), a collateral flow index (CFI), and the ipsilateral, collateral, and contralateral vascular resistance index (R(ipsi), R(coll), R(contra)) were calculated. The study population was subdivided into groups with CFI<0.15 and with CFI> or =0.15.The percentage-diameter coronary artery stenosis (%-S) to be dilated was similar in the two groups: 78+/-10% versus 82+/-12% (NS). CFVR was not associated with %-S. In the group with CFI> or =0.15 but not with CFI<0.15, CFVR was directly and inversely associated with R(coll) and R(contra), respectively.A hemodynamic interaction between adjacent vascular territories can be documented in patients with CAD and well developed collaterals among those regions. The CFVR of a collateralized region may, thus, be more dependent on hyperemic vascular resistance changes of the collateral and collateral-supplying area than on the ipsilateral stenosis severity, and may even fall below 1.
The ARVD/C Variome of the Netherlands
Authors: Jan D. Jongbloed, Zahir A. Bhuyian, Paul A. van der Zwaag, Ludolf G. Boven, Jasper J. van der Smagt, Monique G. Cox, Ans C. Wiesfeld, Luz M. Rodriguez, Roselie Jongbloed, Isabelle C. van Gelder, Maarten P. van den Berg, Richard J. Sinke, Robert M. Hofstra, Richard N. Hauer, Arthur A. Wilde, Peter J. van Tintelen
Journal: Circulation (2009)
Hyperglycemia treatment is associated with longer length of hospital stay in colorectal cancer surgery patients
Authors: J. M. Geraci, N. Busaidy, J. Wang, T. P. Lam, J. M. Skibber, J. H. Freeman, J. S. Goodwin
Journal: Journal of Clinical Oncology (2006)

6133 Background: Diabetes mellitus (DM) is associated with longer hospital stays in some medical and surgical inpatient populations. Aggressive control of blood sugar may prevent complications and decrease hospital length of stay (LOS). Methods: We conducted a retrospective study of 519 patients at UT MD Anderson Cancer Center (UTMDACC) who had major surgery for colon or rectal cancer in calendar years 2000–2003. Patient data extracted from the UTMDACC Institutional Database included demographics, admission and discharge dates and diagnoses, surgical procedures, and diabetes medication use during the hospitalization. Known DM was defined as present if the patient had a diabetes diagnosis prior to or at admission; hyperglycemia treatment was defined as receipt of a medication for diabetes (insulin or oral medication) during the index hospitalization. Chi-square and t tests were performed to assess associations between patient characteristics and long LOS, and multiple logistic regression was used to identify independent predictors of hospital LOS at or greater than the 75th percentile for the study population (long LOS). Results: The mean age of the study population was 60.4 years (median 61, range 18–91). Known DM was present in 10.4% of cases; the same percentage received hyperglycemia treatment during their hospital stay, although not all were known diabetics. Mean LOS was 8.9 days; median 7 days and the 75 th percentile 9 days. 50% of patients treated for hyperglycemia had long LOS (27 of 54 cases, p&lt; 0.0005). In a logistic regression model controlling for patient demographic and clinical characteristics and the occurrence of post-operative complications, hyperglycemia treatment was an independent predictor of long LOS (odds ratio 4.1, 95% confidence interval 1.6, 10.3). Conclusions: Hyperglycemia treatment is associated with longer LOS in patients undergoing surgery for colon or rectal cancer at UTMDACC. Further studies should determine whether patients at risk for long LOS can be identified prospectively such that they might benefit from an intervention to reduce their LOS. [Table: see text]
Abstract 2935: Systematic drug testing and RNA-sequencing of tamoxifen resistant breast cancer cell lines
Authors: Susanne Hultsch, Sara Kangaspeska, Matti Kankainen, Vilja Pietiäinen, Olli Kallioniemi
Journal: Cancer Research (2016)

Abstract Tamoxifen, as a standard treatment of estrogen receptor (ER)-positive breast cancer, reduces breast cancer mortality by 31%. In 50% of advanced ER-positive cancers, however, de novo resistance exists and in 40% of patients with initial response acquired resistance frequently evolves. In order to explore mechanisms underlying endocrine therapy resistance in breast cancer and to identify new opportunities to treat patients, we created seven tamoxifen-resistant breast cancer cell line models that represent the luminal A subtype (MCF-7, T-47D, ZR-75-1), which expresses ER, and the luminal B subtype (BT-474), which additionally expresses the HER2 oncoprotein. We then performed drug sensitivity and resistance testing (DSRT), exome-sequencing and network analysis on all these cancer cell lines to determine the molecular and drug response profiles specific to tamoxifen resistance. As the cells became tamoxifen-resistant, we observed increasing sensitivity towards drugs like ERK1/2-, proteasome- and BCL-family inhibitors, but each of the isogenic cell line pairs had its distinct genomic and drug response profile. We then studied the molecular profiles of the 7 drug-resistant variants by RNA-sequencing in comparison to their 4 isogenic parental cells. We could not detect any common significantly differentially expressed genes (more than 2 fold change) across all the cell lines. However, the cell lines could be grouped into two different categories: The ones with low amount of differentially expressed genes, &amp;lt; 800 genes in the BT-474 and ZR-75-1 cell line pairs (with a 1,2% overlap), and the ones with high amount of differentially expressed genes, &amp;gt;1800 genes in T-47D and MCF-7 (with 7,3% overlap). Further analysis with the Ingenuity pathway analysis tool revealed an involvement of “Fatty Acid Activation” as well as “Stearate Biosynthesis I” in this group. Additionally, we discovered that genes involved in iron metabolism (TFRC, IREB2 and FTL) or iron-regulated genes like CP and NDRG1 are deregulated. These genes and pathways thereby provide avenues to identify new drug vulnerabilities for the tamoxifen resistant cancer cells, which we are now investigating at gene and protein level e.g. by image-based phenotyping. In summary, by combining drug testing data with the RNA-sequencing results, we hope to provide a number of potential drugs as well as matching biomarkers for planning clinical trials for patients with tamoxifen-resistant breast cancer. Citation Format: Susanne Hultsch, Sara Kangaspeska, Matti Kankainen, Vilja Pietiäinen, Olli Kallioniemi. Systematic drug testing and RNA-sequencing of tamoxifen resistant breast cancer cell lines. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2935.
Application of recombinant antigen 5 allergens from seven allergy-relevant Hymenoptera species in diagnostics
Authors: M. Schiener, B. Eberlein, C. Moreno-Aguilar, G. Pietsch, P. Serrano, M. McIntyre, L. Schwarze, D. Russkamp, T. Biedermann, E. Spillner, U. Darsow, M. Ollert, C. B. Schmidt-Weber, S. Blank
Journal: Allergy (2016)

Hymenoptera stings can cause severe anaphylaxis in untreated venom-allergic patients. A correct diagnosis regarding the relevant species for immunotherapy is often hampered by clinically irrelevant cross-reactivity. In vespid venom allergy, cross-reactivity between venoms of different species can be a diagnostic challenge. To address immunological IgE cross-reactivity on molecular level, seven recombinant antigens 5 of the most important Vespoidea groups were assessed by different diagnostic setups.The antigens 5 of yellow jackets, hornets, European and American paper wasps, fire ants, white-faced hornets, and Polybia wasps were recombinantly produced in insect cells, immunologically and structurally characterized, and their sIgE reactivity assessed by ImmunoCAP, ELISA, cross-inhibition, and basophil activation test (BAT) in patients with yellow jacket or Polistes venom allergy of two European geographical areas.All recombinant allergens were correctly folded and structural models and patient reactivity profiles suggested the presence of conserved and unique B-cell epitopes. All antigens 5 showed extensive cross-reactivity in sIgE analyses, inhibition assays, and BAT. This cross-reactivity was more pronounced in ImmunoCAP measurements with venom extracts than in sIgE analyses with recombinant antigens 5. Dose-response curves with the allergens in BAT allowed a differentiated individual dissection of relevant sensitization.Due to extensive cross-reactivity in various diagnostic settings, antigens 5 are inappropriate markers for differential sIgE diagnostics in vespid venom allergy. However, the newly available antigens 5 from further vespid species and the combination of recombinant allergen-based sIgE measurements with BAT represents a practicable way to diagnose clinically relevant sensitization in vespid venom allergy.
Abstract 3558: Predicting response to Mcl-1 targeting agents in NSCLC and multiple myeloma
Authors: Kristen McEachern, Greg O’Connor, Justin Cidado, Matthew Belmonte, Evan Barry, Hannah Dry, Paul Secrist, Lisa Drew
Journal: Cancer Research (2016)

Abstract Mcl-1 is an anti-apoptotic member of the Bcl-2 family of proteins and is frequently amplified or over-expressed in both solid tumors and hematological malignancies, suggesting that its activity may be important for the survival of cancer cells. CDK9 inhibition results in the down regulation of Mcl-1 mRNA and subsequent protein levels by inhibiting transcription and represents an indirect approach to targeting Mcl-1. Mcl-1 can also be targeted directly using an inhibitor that disrupts the Mcl-1 complexes to induce apoptosis. Using both molecular and pharmacological approaches, we sought to identify predictive biomarkers of Mcl1 dependency in sensitive NSCLC and multiple myeloma cell lines. Here we demonstrate that NSCLC cell lines lacking MCL1 gene copy number gains are not sensitive to siRNA mediated knockdown of Mcl-1 or Mcl-1 inhibition (cell line sensitivity to CDK9 or Mcl-1 inhibition is defined by potency and extent of caspase activation). However, the presence of a copy number alteration does not predict sensitivity to Mcl-1 inhibition. To better understand what the drivers of sensitivity are, we developed quantitative assays on the Peggy platform (a capillary based immunoassay platform by Protein Simple) to measure both Mcl-1 and Bcl-xL protein levels. Using these assays, we show a correlation between sensitivity to a CDK9 or Mcl1 inhibitor and Mcl-1 levels, as well as to the ratio of Mcl-1 to Bcl-xL protein in a NSCLC cell line panel. These findings were then extended into a panel of multiple myeloma cell lines. While somewhat broad activity for CDK9 or Mcl-1 inhibition is seen across the cell lines tested, a subset of the sensitive lines have MCL1 amplification and express high levels of Mcl-1 protein. Mcl-1 levels alone, however, do not predict for sensitivity across the panel and, similar to NSCLC, the ratio of Mcl1 to Bcl-xL expression has greater positive predictive value. These results provide the rationale for exploring Mcl-1 copy number alterations and Mcl-1 and Bcl-xL protein levels as predictive biomarkers for tumor response when treating with a CDK9 or Mcl-1 inhibitor in both NSCLC and multiple myeloma. Citation Format: Kristen McEachern, Greg O’Connor, Justin Cidado, Matthew Belmonte, Evan Barry, Hannah Dry, Paul Secrist, Lisa Drew. Predicting response to Mcl-1 targeting agents in NSCLC and multiple myeloma. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3558.
7-Year-Old With a Painful Rash
Authors: Julia T. Warren, Christopher P. Miller, Andrew J. White
Journal: JAMA Pediatrics (2016)

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Identification of Novel LNK Mutations In Patients with Chronic Myeloproliferative Neoplasms and Related Disorders
Authors: Stephen T. Oh, Jacob M. Zahn, Carol D. Jones, Bing Zhang, Mignon L. Loh, Hagop Kantarjian, Erin F. Simonds, Robert V. Bruggner, Parveen Abidi, Georges Natsoulis, John Bell, Jason Buenrostro, Garry P. Nolan, James L. Zehnder, Hanlee P. Ji, Jason Gotlib
Journal: Blood (2010)
Pre-Capillary, Combined, and Post-Capillary Pulmonary Hypertension
Authors: Christian F. Opitz, Marius M. Hoeper, J. Simon R. Gibbs, Harald Kaemmerer, Joanna Pepke-Zaba, J. Gerry Coghlan, Laura Scelsi, Michele D’Alto, Karen M. Olsson, Silvia Ulrich, Werner Scholtz, Uwe Schulz, Ekkehard Grünig, Carmine D. Vizza, Gerd Staehler, Leonhard Bruch, Doerte Huscher, David Pittrow, Stephan Rosenkranz
Journal: Journal of the American College of Cardiology (2016)

Pulmonary hypertension (PH) is hemodynamically classified as pre-capillary (as seen in idiopathic pulmonary arterial hypertension [IPAH]) or post-capillary (as seen in heart failure with preserved ejection fraction [HFpEF]). Overlaps between these conditions exist. Some patients present with risk factors for left heart disease but pre-capillary PH, whereas patients with HFpEF may have combined pre- and post-capillary PH. This study sought to further characterize similarities and differences among patient populations with either PH-HFpEF or IPAH. We used registry data to analyze clinical characteristics, hemodynamics, and treatment responses in patients with typical IPAH (<3 risk factors for left heart disease; n = 421), atypical IPAH (≥3 risk factors for left heart disease; n = 139), and PH-HFpEF (n = 226) receiving PH-targeted therapy. Compared with typical IPAH, patients with atypical IPAH and PH-HFpEF were older, had a higher body mass index, had more comorbidities, and had a lower 6-min walking distance, whereas mean pulmonary artery pressure (46.9 ± 13.3 mm Hg vs. 43.9 ± 10.7 mm Hg vs. 45.7 ± 9.4 mm Hg, respectively) and cardiac index (2.3 ± 0.8 l/min/m2 vs. 2.2 ± 0.8 l/min/m2 vs. 2.2 ± 0.7 l/min/m2, respectively) were comparable among groups. After initiation of targeted PH therapies, all groups showed improvement in exercise capacity, functional class, and natriuretic peptides from baseline to 12 months, but treatment effects were less pronounced in patients with PH-HFpEF than typical IPAH; with atypical IPAH in between. Survival rates at 1, 3, and 5 years were almost identical for the 3 groups. Patients with atypical IPAH share features of both typical IPAH and PH-HFpEF, suggesting that there may be a continuum between these conditions.
NHS needs culture shift regarding sleeping at work
Authors: Abi Rimmer
Journal: BMJ (2016)

The NHS needs a sizeable culture shift in its attitude to doctors sleeping during night shifts, Michael Farquhar, a paediatric consultant sleep specialist, has told BMJ Careers.

Farquhar said, “There is still this idea that if you are being paid you must not sleep, and that is fundamentally wrong. Your brain is not meant to be awake at night.”

He continued, “Planning sleep and using sleep in a careful and controlled way to improve the level of care that you are delivering is really important. But there is this blanket …
Abstract 4573: Complex interactions among different types of androgen receptor splice variants and the full-length androgen receptor in mediating castration resistance
Authors: Yang Zhan, Guanyi Zhang, Xiaojie Wang, Yanfeng Qi, Haitao Zhang, Yan Dong
Journal: Cancer Research (2016)

Abstract Androgen receptor splice variants (AR-Vs) have been implicated in the pathogenesis and progression of castration-resistant prostate cancer after androgen-directed therapies. Approximately 20 AR-Vs have been identified to date. When expressed alone in cells, some AR-Vs (e.g., AR-V7 and ARv567es) localize primarily to the nucleus, whereas some others (e.g., AR-V4 and AR-V6) distribute equally between the nucleus and the cytoplasm. Significantly, the latter is often co-expressed with the nucleus-localized AR-Vs and the full-length AR (AR-FL). Thus, an important question that needs to be addressed is whether these different types of AR-Vs interact with each other as well as with AR-FL and the consequence of the interactions. In the present study, we used the bioluminescence resonance energy transfer (BRET) assay to show that both AR-V6 and AR-V4 can heterodimerize with AR-V7 and AR-FL. Consequently, AR-V7 and androgen-bound AR-FL induced nuclear localization of AR-V6 and AR-V4, leading to an increased ability of AR-V6 and AR-V4 to transactivate target genes and to confer castration-resistant cell growth. On the other hand, neither AR-V6 nor AR-V4 affected the subcellular localization of AR-V7 or AR-FL. These findings support the ability of AR-V7 and androgen-bound AR-FL to activate AR-V6 and AR-V4. Since AR-FL and nucleus-localized AR-Vs are the predominant forms of AR expressed in clinical specimens, it is likely that most of the AR-Vs in these cells are in the nucleus and are transcriptionally active. Our data therefore highlight the importance of the complex interactions among different AR-Vs and AR-FL in mediating castration resistance. Citation Format: Yang Zhan, Guanyi Zhang, Xiaojie Wang, Yanfeng Qi, Haitao Zhang, Yan Dong. Complex interactions among different types of androgen receptor splice variants and the full-length androgen receptor in mediating castration resistance. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4573.
Impact of thoracic radiotherapy timing in limited-stage small-cell lung cancer: usefulness of the individual patient data meta-analysis
Authors: D. De Ruysscher, B. Lueza, C. Le Péchoux, D.H. Johnson, M. O'Brien, N. Murray, S. Spiro, X. Wang, M. Takada, B. Lebeau, W. Blackstock, D. Skarlos, P. Baas, H. Choy, A. Price, L. Seymour, R. Arriagada, J.-P. Pignon, D. De Ruysscher, C. Le Pechoux, B. Lueza, E. Paris, J.P. Pignon, M. Pijls-Johannesma, A.S. Veillard, Rodrigo Arriagada, Paul Baas, William Blackstock, Sylvie Chevret, Hak Choy, Jeffrey Crawford, Urania Dafni, Suzanne Dahlberg, Dirk De Ruysscher, Allan Hackshaw, Baktiar Hasan, David H. Johnson, Cécile Le Pechoux, Bernard Lebeau, James Lovato, Béranger Lueza, Nevin Murray, Mary O’Brien, Emmanuelle Paris, Jean-Pierre Pignon, Madelon Pijls-Johannesma, Allan Price, Stephen Spiro, Lesley Seymour, Taro Shibata, Dimosthenis Skarlos, Stephen Spiro, Minoru Takada, Anne-Sophie Veillard, Xiaofei Wang
Journal: Annals of Oncology (2016)