tbuckley/cabot-search huggingface dataset:
Unusual and memorable
Authors: G. D Wright
Journal: Annals of the Rheumatic Diseases (1999)

Identification of crystals in synovial fluidSynovial fluids can contain a number of crystals and other particulate matter.Some of these, particularly monosodium urate monohydrate (MSUM) and calcium pyrophosphate dihydrate (CPPD) crystals, are pathogenic; others, including cholesterol and other lipid particles and the basic calcium phosphates (BCPs), including apatites, are of doubtful significance.Table 1 lists the main forms of particulate matter that have been identified in synovial fluids.In the case of MSUM and CPPD crystals it is clear that the identification of these crystals in a synovial fluid that also has a high polymorphonuclear cell count (indicative of acute inflammation) is the only certain way to diagnose an attack of gout or pseudogout respectively. 1Furthermore, this is one of the few tests that has been shown to change clinical practice in rheumatology, 2 and it is apparent that the consequences of getting the diagnosis wrong can be severe. 3Therefore, accurate identification of MSUM and CPPD is important.
Impact of Adjuvant Chemotherapy (Ac) on Relapse-Free Survival (Rfs) is Different According to Post-Chemoradiation Pathologic Stage (Ypstage) in Rectal Cancer
Authors: S.Y. Kim, J.Y. Baek, E.K. Shim, H.M. Kim, M.S.I. Chang, J.Y. Ku, M.J. Kim, S.C. Park, D.Y. Kim, H.J. Chang, J.H. Oh
Journal: Annals of Oncology (2014)
Abstract 4072: Molecular cytogenetic characterization of HPV types 16 and 18 cervical cancers: Acquired genomic instability by E6 and E7 oncoproteins
Authors: Karen Tate, Lucy Tran, Melanie Baker, Kamilah Evans, Mechelle Rouse, Seyung Chung, Duy Nguyen, Juri Kim, Enijah Smith-Joe, Jay Vadgama, Mengtao Li, Yu-Ling Lin, Roland Patillo, Eva McGhee
Journal: Cancer Research (2016)

Abstract Human Papillomavirus (HPV) high-risk types 16 and 18 are directly associated with approximately 90% incidence of invasive cervical carcinoma. Epithelial cells infected with HPV become transformed and acquire genomic instability. As a result of this transformation, E6 and E7 oncogenes are perpetually expressed. E6 degrades the tumor suppressor p53; E7 inhibits tumor suppressor pRB, leading to disproportionate target cell growth and proliferation. While there have been studies exploring genomic instability induced by HPV oncoproteins E6/E7, the full scope of the genomic damage has not been clearly characterized. Three HPV positive cervical cancer cell lines, HeLa (HPV18), SiHa (HPV16) and CaSki (HPV16), were studied using Spectral Karyotyping (SKY) and Giemsa banding (G-banding). Our results using SKY and G-banding analysis showed HeLa cells exhibited frequent translocations on chromosomes 4 and 11, and deletions on chromosomes 11 and 20. The SiHa cells exhibited translocations primarily on chromosomes 9 and 20, with deletions on chromosome 10. CaSki revealed translocations on chromosomes 10 and 4, with deletions on chromosome 21. All three cell lines gained copies on chromosome 5. The aforementioned aneuploidy is demonstrative of the induced genomic instability acquired from HPV infection, which include tumor suppressor genes; p53 and pRB disruptions caused by E6 and E7 oncoproteins. HeLa cells showed extensive genomic instability on chromosome 11q22-23, where the ATM gene is located. Acquired genomic instability to the ATM chromosome region may further increase the rate of cervical cancer. Citation Format: Karen Tate, Lucy Tran, Melanie Baker, Kamilah Evans, Mechelle Rouse, Seyung Chung, Duy Nguyen, Juri Kim, Enijah Smith-Joe, Jay Vadgama, Mengtao Li, Yu-Ling Lin, Roland Patillo, Eva McGhee. Molecular cytogenetic characterization of HPV types 16 and 18 cervical cancers: Acquired genomic instability by E6 and E7 oncoproteins. [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 4072.
Genomic evolution in muscle-invasive bladder cancer resistant to neoadjuvant chemotherapy.
Authors: David Liu, Philip Abbosh, Diana Miao, Mariel Elena Boyd, Jean H. Hoffman-Censits, Gopa Iyer, Sara M. Tolaney, Kent William Mouw, Scott L. Carter, Joaquim Bellmunt, Elizabeth R. Plimack, Jonathan E. Rosenberg, Eliezer Mendel Van Allen
Journal: Journal of Clinical Oncology (2016)

4518 Background: The majority of patients with muscle-invasive bladder cancer (MIBC) treated with neoadjuvant cisplatin-based chemotherapy (NAC) have residual disease at time of cystectomy. Changes in the tumor genomic landscape after NAC may inform genetic resistance patterns and treatment strategies. Methods: Matched pre- and post-NAC tumor samples were obtained from 31 patients with MIBC who had gross residual disease (≥ pT2) at cystectomy, followed by whole exome sequencing of these “trios” (pre- and post-NAC tumor with matched germline samples). Linear regression was used to adjust for differences in sample purity and predict changes in mutation and neoantigen burden from pre- to post-NAC. Phylogenetic analysis of serial tumor biopsies was performed to identify alterations gained or lost after treatment. Results: A wide proportion of mutations (5-81%, median = 31%) and neoantigens (4-77%, median = 32%) in the post-NAC tumor were not seen in the matched pre-NAC tumor. After adjusting for differences in sample purity, there was no statistically significant overall change in the mutational or neoantigen burden post-NAC (mean = -0.67 mut/Mb [p = 0.06] and -0.88 neoantigens/Mb [p = 0.10] respectively), but the change was strongly associated with pre-NAC mutation and neoantigen levels (R2= 0.44, p < 0.0001; R2= 0.40, p = 0.0002 respectively): tumors with higher baseline levels experienced greater decreases. While no single gene was significantly enriched for nonsynonymous mutations exclusively in pre- or post-NAC samples, 32% (10/31) of patients had either a gain or loss of alterations in potentially actionable genes, including PIK3CA and MTOR. Four post-NAC tumors harbored focal E2F3 amplification, including one acquired after NAC. Conclusions: These results suggest that NAC decreases pre-existing mutation and neoantigen burden while simultaneously revealing new mutations and neoantigens. This may occur by elimination of less fit subclones and induction of new mutations from DNA damage. Further, potentially targetable mutations are lost and acquired after NAC; this heterogeneity suggests that rebiopsy in metastatic/recurrent settings after NAC may be necessary to accurately inform clinical management.
Impact Of CMV Reactivation On Relapse In Patients With Acute Leukemia Who Received Allogeneic Stem Cell Transplantation In First Remission: Possible GVL Effect In CMV Seropositive Population
Authors: Jae-Ho Yoon, Seok Lee, Hee-je Kim, Jung-Ho Kim, Young-Woo Jeon, Seung-Hwan Shin, Sung-Eun Lee, Ki-Seong Eom, Yoo-Jin Kim, Chang-Ki Min, Seok-Goo Cho, Dong-Wook Kim, Woo-Sung Min, Chong-Won Park, Jong-Wook Lee
Journal: Blood (2013)
Abstract 2700: Transcriptome analyses reveal fusion transcripts and transcript variants that are recurrent across sample series of testicular germ cell tumors
Authors: Andreas M. Hoff, Sen Zhao, Bjarne Johannessen, Rolf I. Skotheim
Journal: Cancer Research (2016)

Abstract Testicular germ cell tumors (TGCT) are the most frequently diagnosed solid tumors in young men. Embryonal carcinoma (EC) comprises a histological subgroup of TGCT that exhibits pluripotent characteristics similar to embryonic stem (ES) cells. The genetic drivers underlying malignant transformation of TGCT, including ECs, are unknown. To elucidate the abnormal genetic events potentially contributing to TGCT malignancy, such as the formation of fusion genes or expression of aberrant transcript variants, we have previously performed RNA sequencing of EC cell lines and their non-malignant ES cell line counterparts. From this dataset, we identified and characterized eight novel fusion transcripts and one gene with alternative promoter usage, ETV6. These were the first fusion genes to be shown in TGCT (Hoff et al., Cancer Research, in press). To search for recurrence of the originally nominated TGCT specific fusion transcripts and other transcript variants in an external sample series, we have here parsed raw RNA sequencing data from 102 primary TGCTs obtained from The Cancer Genome Atlas (TCGA; unpublished). In this process, we have evaluated multiple fusion finder algorithms and approaches to determine the optimal method, on the basis of sensitivity and specificity, to query specific transcript variants and breakpoints in RNA sequencing datasets. We were able to detect the recurrent fusion transcripts; RCC1-ABHD12B, RCC1-HENMT1, CLEC6A-CLEC4D and the transcript variant of ETV6, which was previously detected from our in-house RNA sequencing dataset from EC cell lines. We also demonstrate that expression of several fusion transcripts correlate significantly with the histological subtype. In conclusion, the novel fusion transcripts and ETV6 transcript variant are expressed from a high fraction of primary TGCTs with low differentiation grade, as detected across independent sample series. Citation Format: Andreas M. Hoff, Sen Zhao, Bjarne Johannessen, Rolf I. Skotheim. Transcriptome analyses reveal fusion transcripts and transcript variants that are recurrent across sample series of testicular germ cell tumors. [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 2700.
The Prothrombin C&gt;T Mutation at Position 20209 (F2 20209*T) Promotes 3′end mRNA Processing and Thus Contributes to Thrombophilia through Gain-of-Function.
Authors: Sven Danckwardt, Kathrin Hartmann, Ofira Ben-Tal, Matthias W. Hentze, Andreas E. Kulozik
Journal: Blood (2005)
Wet sputum as an objective outcome in a randomized crossover trial in NCF-BE: Reliability and responsiveness
Authors: Beatriz Herrero, Eva Polverino, Marta SanMiguel, Victoria Alcaraz, Dani Marti, Jordi Vilaro, Antoni Torres
Journal: European Respiratory Journal (2014)

AIM: To analyze reliability and responsiveness of wet sputum as an outcome measure in a trial related with bronchial drainage (BD) in stable non-cystic fibrosis bronchiectasis (NCFBE)

METHODS: Randomized crossover trial in NCFBE with chronic sputum production.3 different BD techniques were compared:Autogenic Drainage(AD),Slow expiration with glottis opened in lateral posture(ELTGOL),and temporary positive expiratory pressure(TPEP).Each technique was applied on 3 sessions.Sputum quantity was evaluated at:1) Baseline(24h spontaneous sputum production;2)during BD session;3) post-BD session:24h spontaneous sputum production.The amount of wet sputum samples (without split)were measured in grams.Intra-class correlation coefficient (ICC) and Friedman´s test were used to assess reliability and responsiveness(p<0.05) RESULTS: We recluited 31 patients (29%male) with a mean(SD) age of 59.5 (±18.09) years and a mean(SD) FEV1% of 63%(±23).ICC of baseline wet sputum measures was 0.98(CI95%0.97-0.99; p<0.001).ICC for sputum measures obtained during BD sessions for the 3 techniques were:AD 0.80(CI95%0.68-0.89);ELTGOL 0.96(CI95%0.93-0.98);T-PEP 0.81(CI95%0.68-0.9).ICC for sputum measures obtained post-BD sessions for the 3 techniques were:AD 0.72 (CI 95%0.56-0.84);ELTGOL 0.79(CI95%0.66-0.88);T-PEP 0.96(CI 95%0.92-0.98).All correlation rates were significant (p<0.001).All techniques achieved a reduction in 24h sputum production from baseline to post-BD,9,89g(13.46 – 5.39; p< 0.001)

CONCLUSION: Wet sputum quantity was a reliable and responsiveness outcome measure in order to analyze the efficacy of these 3 BD techniques in stable NCFBE.An analytical study should be performed to confirm our results.
Microrna Mir-21 Is Upregulated after Different Microenvironmental Stimuli and Controls Proliferation, Chemotaxis and Chemoresistance in Chronic Lymphocytic Leukemia
Authors: Marta Crespo, Júlia Carabia, Noelia Purroy, Cecilia Carpio, Pau Abrisqueta, Carles Palacio, Francesc Bosch
Journal: Blood (2014)
Abstract 4400: Hematopoietic age at onset of breast cancer dictates disease aggressiveness and progression
Authors: Jaclyn Sceneay, Timothy Marsh, Irene Wong, Yuanbo Qin, Andreas Sjödin, Björn Nilsson, Sheila A. Stewart, Sandra S. McAllister
Journal: Cancer Research (2016)

Abstract Aging is strongly associated with increased risk of developing breast cancer. Young age at diagnosis is typically associated with more aggressive disease, while breast cancer is generally more indolent in older women. Among the different breast cancer subtypes, triple negative breast cancer (TNBC) accounts for ∼15% of invasive breast cancer cases and TNBC patients have a poor prognosis due to lack of targeted therapies and limited sensitivity to chemotherapy. Emerging studies indicate that older women with TNBC have a better outcome than younger women for reasons that are unclear. Nevertheless, older patients tend to suffer co-morbidities associated with chemotherapy and often forego treatment, resulting in disease recurrence and a poor outcome for these patients. Treatment of TNBC therefore presents age-specific challenges. Here, we investigated how age affects the composition and function of pro-tumorigenic bone marrow cells using TNBC models that enable us to interrogate the impact of bone marrow derived cells on both tumor cells and the tumor microenvironment. Consistent with clinical observations, we found that disease progression was significantly more aggressive in young mice relative to aged mice. We identified age- and tumor-dependent molecular and functional changes to bone marrow derived hematopoietic cells that impact TNBC progression. A specific population of Sca1+/cKit- bone marrow cells that expresses CSF1R and secretes the growth factor granulin to support stromal activation and robust tumor growth in young mice, fails to promote tumor outgrowth in aged mice, resulting in maintenance of disease indolence. Importantly, bone marrow cells from young mice are sufficient to activate a tumor-supportive microenvironment and rescue tumor progression in aged mice. The results presented here indicate that hematopoietic age is an important determinant of TNBC aggressiveness and provide rationale for investigating age-stratified therapies designed to prevent activation of tumor-promoting bone marrow cells. Citation Format: Jaclyn Sceneay, Timothy Marsh, Irene Wong, Yuanbo Qin, Andreas Sjödin, Björn Nilsson, Sheila A. Stewart, Sandra S. McAllister. Hematopoietic age at onset of breast cancer dictates disease aggressiveness and progression. [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 4400.
Abstract 227: Leptin induces a fibroblast and endothelial cell crosstalk in tumor stroma
Authors: Viola Lanier
Journal: Cancer Research (2016)

Abstract Background: The tissue microenvironment plays a major role in tumor development and recurrence. It is known that leptin secreted by cancer and adipose cells can modify the tumor stroma, which is composed of immune, fibroblast, and endothelial cells (EC). Leptin affects both normal and cancer associated fibroblasts. We have previously shown that leptin can modify EC directly via an increase of angiogenic features; which was linked to VEGFR signaling and Notch expression independent of VEGF. It is hypothesized that leptin induces a communication between fibroblast and endothelial cells via induction of Notch signaling, which may be related to exosome production. Methods: Non-expressing Ob-R fibroblasts, and fibroblasts transfected with Ob-R plasmid, were used to investigate leptin's actions on Notch activation. Fibroblasts were challenged with leptin (0.6, 1.2, 6.2 nM) and an inhibitor of Notch signaling activation (DAPT). Fibroblast culture supernatants were added to and human umbilical vein endothelial cells (HUVEC) cultures. Notch proteins and RNA expression and molecular markers of activated fibroblasts and derived exosomes were determined via Western blot, RT-PCR, and multiplex analyses, respectively. EC angiogenic features were also determined. Results: Our findings suggest that leptin induces fibroblast activation, which triggers the expression of Notch and the development of angiogenic features by EC. Conclusions: A novel mechanism is proposed by which leptin promotes tumor stroma development via Notch activation and a crosstalk between fibroblasts and EC. Cancer therapies targeting leptin signaling could be a new strategy for interfering with cellular processes that promotes changes of tumor stroma towards a more aggressive tumor environment. Citation Format: Viola Lanier. Leptin induces a fibroblast and endothelial cell crosstalk in tumor stroma. [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 227.
Miscarriage Associated with Zika Virus Infection
Authors: Annemiek A van der Eijk, Perry J van Genderen, Rob M Verdijk, Chantal B Reusken, Ramona Mögling, Jeroen J A van Kampen, Widagdo Widagdo, Georgina I Aron, Corine H GeurtsvanKessel, Suzan D Pas, V Stalin Raj, Bart L Haagmans, Marion P G Koopmans
Journal: New England Journal of Medicine (2016)

A 31-year-old woman who was 10 weeks pregnant contracted Zika virus infection in Suriname; this led to fetal loss. ZIKV was detected in the woman's blood for at least 21 days.
Intratumoral and Intertumoral Genomic Heterogeneity of Multifocal Localized Prostate Cancer Impacts Molecular Classifications and Genomic Prognosticators
Authors: Lei Wei, Jianmin Wang, Erika Lampert, Simon Schlanger, Adam D. DePriest, Qiang Hu, Eduardo Cortes Gomez, Mitsuko Murakam, Sean T. Glenn, Jeffrey Conroy, Carl Morrison, Gissou Azabdaftari, James L. Mohler, Song Liu, Hannelore V. Heemers
Journal: European Urology (2016)
Abstract 1775: Differential expression of exosomes-associated onco-microRNAs in African Americans with prostate cancer
Authors: Ahmed A. Moustafa, Andrew B. Sholl, Koji Tsumagari, Mohamed Hassan, Emad Kandil, Asim B. Abdel-Mageed, Zakaria Y. Abd Elmageed
Journal: Cancer Research (2016)

Abstract Background: The mortality rate of prostate cancer (PCa) is two times higher in African American (AA) than Caucasian American (CA) men. The molecular mechanisms underlying these health disparities among AA men have yet to be fully elucidated. Our study aimed to evaluate the role of exosomes-associated onco-microRNAs (miRs) as biological determinant for the racial disparity of PCa patients. Methods: Exosomes were isolated from the conditioned medium of MDA-PCa-2b (AA-origin), PC-3 (CA origin), C4-2B and RWPE-1 (non-tumorigenic) cell lines to study the endogenous expression of a number of onco-miRs and their anticipated target genes using Real-Time PCR and Western blot analyses. The potential candidates were validated in exosomes procured from plasma of human AA PCa patients and their counterparts. Onco-miRs target genes such as Lats-2, PDCD4, and SMEK1 were validated on cellular and exosomes derived from cells and human specimens. Onco-miRs and their targets were correlated with age and Gleason score of the disease. Results: Not only onco-miR-125b, miR-155, and miR-3613 were upregulated in PCa versus normal RWPE1 cells but also in AA versus CA PCa cells. Onc-miR-3613 and miR-3680 were 3-4 times upregulated in cells and in C4-2B-derived exosomes compared to RWPE-1-derived vesicles. Also, these miRs were upregulated (∼2.5 fold) in MDA-PCa-2b versus PC-3 cells. The expression of tumor suppressor genes, such as Lats2, PDCD4, and SMEK1, were downregulated in PCa cells compared to normal cells. Differential expression of PCa exosomes-associated onco-miRs was also demonstrated in AA PCa patients compared to CA PCa and their age-matched normal subjects. A positive correlation was found between onco-miR-125b and high Gleason score (r = 0.763, p&amp;lt;0.01). Conclusion: Our findings underline the role of exosomes-associated onco-miRs in health disparity of PCa. The differential expression of onco-miRs and their tumor suppressor genes in AA men projects their potential role as prognostic markers and/or future therapeutic targets in the context of racial disparity. Citation Format: Ahmed A. Moustafa, Andrew B. Sholl, Koji Tsumagari, Mohamed Hassan, Emad Kandil, Asim B. Abdel-Mageed, Zakaria Y. Abd Elmageed. Differential expression of exosomes-associated onco-microRNAs in African Americans with prostate 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 1775.
Occurrence of death and stroke in patients in 47 countries 1 year after presenting with atrial fibrillation: a cohort study
Authors: Jeff S Healey, Jonas Oldgren, Michael Ezekowitz, Jun Zhu, Prem Pais, Jia Wang, Patrick Commerford, Petr Jansky, Alvaro Avezum, Alben Sigamani, Albertino Damasceno, Paul Reilly, Alex Grinvalds, Juliet Nakamya, Akinyemi Aje, Wael Almahmeed, Andrew Moriarty, Lars Wallentin, Salim Yusuf, Stuart J Connolly
Journal: The Lancet (2016)
Ethanol-induced DNA damage and the expression of repair-related molecules in human gastric carcinoma AGS cells with use of an acid pump antagonist and proton pump inhibitor.
Authors: H. Cho, H. Chun, B. Keum, Y. Kim, Y. Jeen, Y. Seo, H. Lee, S. Um, C. Kim, H. Ryu
Journal: Journal of Clinical Oncology (2011)

30 Background: Proton pump inhibitor (PPI) inhibits gastric acid secretion by strongly suppressing H + / K +- ATPase of parietal cells and is a major drug for peptic ulcers and gastroesophageal reflux. Recently it was reported that PPI has antioxidant and anti- inflammatory effects as well as a powerful acid inhibitory effect. To analyze the DNA repair capacity from the antioxidant effect of acid pump antagonist (Revanex-RN) and proton pump inhibitor (Omeprazole-OP), this study examined ethanol-induced DNA damage and the expression of repair related molecules in human gastric cancer AGS cells pretreated with an acid pump antagonist and a proton pump inhibitor. Methods: AGS, a human gastric cancer cell line was obtained from ATCC, was treated with ethanol (0, 2, 4, 6, 8, 10%) during 1hr. MTT and Comet assay were performed to evaluate ethanol-induced DNA damage. The optimum concentration of ethanol which caused DNA damage was established. And AGS cells were cultured in proper concentration of RN or OP overnight. Then, these cells were treated with 5% ethanol during 1hr. DNA damage and recovery were represented the value of Olive tail moment in comet assay. Western blot was also performed to detect expression of DNA polymerase beta, APE/ref-1, PCNA, and GADD45. Results: The DNA damage of AGS cell depended upon ethanol concentration distinctly. Damaged cells showed up recovered tendency in the group treated with low dose RN or OP. In addition, DNA repair enzymes including DNA polymerase beta and APE/ref-1 which were associated with mechanism of base excision repair (BER) were increased. A relevant protein such as GADD45 was also increased significantly. Conclusions: PPI has capacity to recover damaged DNA, which is associated with increased expression of GADD45 directly. Therefore, PPI offers cancer prevention by reducing the level of DNA damage in the gastric mucosa. GADD45 is also likely to suggest that it could be used a major factor on the injury mechanism and an indicator of mucosal damage in stomach. Moreover, RN, an acid pump antagonist is expected to have the higher safety compared to the existing PPIs and considered to be equal to PPIs in terms of anti-cancer effect. No significant financial relationships to disclose.