tbuckley/cabot-search huggingface dataset:
Abstract 4327: Mitochondrial reprogramming in triple negative breast cancer progression
Authors: Junhyoung Park, Kavisha Arora, Sajna A. Vithayathil, Taraka R. Donti, Chad Creighton, Michael T. Lewis, Arun Sreekumar, Lee-Jun Wong, Benny A. Kaipparettu
Journal: Cancer Research (2014)

Abstract Unlike other subgroups of patients with breast cancer (BCa), for triple negative (TN) BCa, there is a current lack of understanding of driver pathways and hence are often managed using more generic therapies. Thus, it is important to identify the underlying mechanisms of triple negative breast cancer progression and its racial disparity. Mitochondria-nuclear crosstalk is a bidirectional pathway of communication between mitochondria and nucleus that influences many cellular and organismal activities. This crosstalk can regulate several oncogenic pathways that regulate cellular tumor characteristics. With the advent of transmitochondrial cybrid (cybrid) technology, it is now possible to examine the specific contribution of tumor-associated mitochondria in neoplastic growth and development under a defined common nuclear background. We used this model system to identify mitochondria regulated pathways in TN BCa. Among different oncogenic pathways, Src pathway is frequently over-expressed in TN BCa and Src inhibitors are proposed as one of their current treatments of choice. However, single drug therapy with Src inhibitors failed to control metastatic TN BCa in recent Phase-II trials. These highlight an important question on the mechanism behind the regulation of Src oncogenic signature in TN BCa. Using cybrid technology, we have discovered critical role of cancer mitochondria in the post-translational modification of Src oncogenic pathway. Interestingly we discovered that the Src autophosphorylation, which activate Src-mediated oncogenic pathway, depends on mitochondrial tumor characteristics. Specifically, our strong preliminary data suggest that mitochondrial reprogramming is a critical step in the autophosphorylation and activation of Src pathway in metastatic TN BCa cells. Our findings suggest mitochondria targeted drugs as promising combination therapy for the management of Src positive TN BCa. Citation Format: Junhyoung Park, Kavisha Arora, Sajna A. Vithayathil, Taraka R. Donti, Chad Creighton, Michael T. Lewis, Arun Sreekumar, Lee-Jun Wong, Benny A. Kaipparettu. Mitochondrial reprogramming in triple negative breast cancer progression. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4327. doi:10.1158/1538-7445.AM2014-4327
Advancing survivorship care through the National Cancer Survivorship Resource Center
Authors: Rebecca Cowens‐Alvarado, Katherine Sharpe, Mandi Pratt‐Chapman, Anne Willis, Ted Gansler, Patricia A. Ganz, Stephen B. Edge, Mary S. McCabe, Kevin Stein
Journal: CA A Cancer Journal for Clinicians (2013)

Abstract The National Cancer Survivorship Resource Center (The Survivorship Center) began in 2010 as a collaboration between the American Cancer Society and the George Washington University Cancer Institute and was funded by the Centers for Disease Control and Prevention. The Survivorship Center aims to improve the overall health and quality of life of posttreatment cancer survivors. One key to addressing the needs of this ever‐growing population is to develop clinical follow‐up care guidelines that emphasize not only the importance of surveillance for cancer recurrence, but also address the assessment and management of the physical and psychosocial long‐term and late effects that may result from having cancer and undergoing cancer treatment as well as highlight the importance of healthy behaviors that can reduce the risk of cancer recurrence, second primary cancers, and other chronic diseases. Currently, The Survivorship Center is coordinating the work of experts in oncology, primary care, and other health care professions to develop follow‐up care guidelines for 10 priority cancer sites. CA Cancer J Clin 2013. © 2013 American Cancer Society.
Bactericidal activity response of blood neutrophils from critically ill patients to in vitro granulocyte colony-stimulating factor stimulation
Authors: Kun Yang, Élie Azoulay, Lynda Attalah, Jean-Ralph Zahar, Andry Van de Louw, Charles Cerf, Claude-James Soussy, Philippe Duvaldestin, Laurent Brochard, Christian Brun-Buisson, Alain Harf, Christophe Delclaux
Journal: Intensive Care Medicine (2003)
Annual Meeting of the American Association for Cancer Research, Inc.
Authors: Hugh J. Creech
Journal: JNCI Journal of the National Cancer Institute (1974)

The scientific sessions of the 52d Annual Meeting of the American Association for Cancer Research, Inc., will be held at Haddon Hall, Atlantic City, New Jersey, on April 7–9, 1961.  The following revised regulations concerning abstracts and presentation of papers have been approved by the Board of Directors. All abstracts of papers that are submitted in conformity with the regulations and are considered of acceptable quality by the Program Committee will be published in the  Proceedings of the American Association for Cancer Research . No abstract of a paper accepted by the Program Committee can be withdrawn from publication or altered in composition by the author. Authors must accept sole responsibility for their statements and should exercise great care in the editorial preparation of their abstracts. Reprints of abstracts will not be available from the publisher. Those papers that are selected for oral presentation at the meeting will have their titles and authors printed in the Program; no “read by title” listings will be made.
The Roswell Park Cancer Institute experience with extramammary Paget’s disease
Authors: J.D. Zollo, N.C. Zeitouni
Journal: British Journal of Dermatology (2000)

Extramammary Paget's disease (EMPD) is a rare intraepithelial neoplasm. Common sites of occurrence include the vulva, perianal region, perineum and scrotum. Despite frequent recurrences, surgery is the standard treatment. This study examines the recurrence rate for EMPD treated by conventional surgical management. Alternative and multimodal therapeutic approaches are reviewed. This retrospective analysis included all 30 patients treated for EMPD at Roswell Park Cancer Institute (RPCI) between 1970 and 1998. Following conventional surgical treatment, 44% of our patients developed recurrence. Vulvectomy provided the lowest recurrence rate, but involved extensive tissue loss and functional debility. Multimodal treatment using Mohs' micrographic surgery and photodynamic therapy has been used at RPCI to manage EMPD with minimal tissue loss and no functional impairment. Surgical treatment offers a moderate chance of EMPD cure. Long-term multimodal approaches require close follow-up, but may conserve both tissue and function.
Abstract 16801: Improved Transplant-Free Survival of Children With Dilated Cardiomyopathy: Analysis of Two Decades From the Pediatric Cardiomyopathy Registry
Authors: Rakesh K Singh, Charles Canter, Ling Shi, Steven D Colan, Debra A Dodd, Melanie D Everitt, John L Jefferies, Paul F Kantor, Minmin Lu, Elfriede Pahl, Joseph Rossano, Jeffrey A Towbin, James D Wilkinson, Steven E Lipshultz
Journal: Circulation (2014)

Background: Previous studies of pediatric patients with dilated cardiomyopathy (DCM) have suggested improvement in survival has been due to utilization of heart transplantation. We sought to characterize the changing clinical characteristics and outcomes of pediatric patients with DCM phenotype over the past two decades. Methods: Longitudinal data from 1953 children diagnosed with DCM in the NHLBI Pediatric Cardiomyopathy Registry (PCMR) from 1990-2009 were divided into two cohorts based upon year of diagnosis: “Era 1” (1990-1999, n=1199) and “Era 2” (2000-2009, n=754). Clinical information at diagnosis and incidence of transplant and death without transplant were analyzed by DCM etiology and era. Competing risks methodology was used to estimate the cumulative incidence of death or transplant by era. Results: The majority of patients in both groups had idiopathic DCM (71 vs. 71%, p=0.96). Median age (1.6 vs. 1.7 yrs, p=0.45), left ventricular end diastolic Z scores (+4.2 vs. +4.2, p=0.84) and fractional shortening (16 vs. 17%, p=0.28) at diagnosis were similar. Era 2 patients were more likely to be treated with ACE inhibitors (71 vs. 62%, p=0.004), beta-blockers (24 vs. 6%, p&lt;0.001), and diuretics (89 vs. 84%, p=0.002). A total of 291 patients (15%) died without transplantation, with a median time from diagnosis to death of 0.4 years. Cox regression modeling demonstrated Era 1 was associated with a higher rate of death (HR=1.5, 95% CI=1.2-2.0, p=0.002) but not transplant (0.9, 95% CI=0.7-1.1, p=0.25) when controlling for etiology group. Competing risks estimate (Figure) showed that Era 1 was associated with a higher death rate (p&lt;0.001), while heart transplant rate was not significantly different by era (p=0.068). Conclusions: Children with DCM phenotype have improved survival in the more recent era. This appears to be associated with factors other than the availability of transplantation, which was equally prevalent in both eras.
Abstract 12169: Mast Cells Regulate Cardiomyocyte Contractility and Myofilament Ca2+ Sensitization Following Myocardial Infarction
Authors: Anta Ngkelo, Jonathan Kirk, Adele Richart, Jose Vilar, Pauline Marck, Christophe Heymes, Hans-Reimer Rodewald, David Kass, Jean-Sebastien Silvestre
Journal: Circulation (2014)

Inflammatory cells orchestrate post-ischemic cardiac remodeling after myocardial infarction (MI). Studies in Kit mutant mice suggest key roles for mast cells in post-ischemic tissue remodeling. However, Kit mutations affect multiple cell types of both immune and non-immune origin. The aim of this study was to address the impact of mast cells on cardiac function following MI, using selectively mast cell-deficient mice (Cpa3Cre/+ mice).

The number of mast cell progenitors (Lin-CD45+CD34+FcγRII/III+β7+) increased on day 3 post MI in the bone marrow and the white adipose tissue and on day 5 in the heart. Mature mast cells (Cd117+FceRI+Sca1+) peaked at day 7 in the cardiac tissue accompanied with a peak of mMCP4 and tryptase beta2 mRNA expression. To assess the functional effect of mast cell infiltration, the cardiac function 14 days post MI was assessed in WT, kitW/Wv and Cpa3Cre/+ mice. There was a significant decrease of the left ventricular shortening fraction in both the Cpa3Cre/+ and the kitW/Wv mice compared to WT mice (p<0.01, n=8-10). Although the reduction of heart function in the kitW/Wv mice correlated with increased cardiomyocyte apoptosis, there was no effect on cardiac remodeling (fibrosis, cardiomyocyte apoptosis or infarct size) observed in the Cpa3Cre/+ originated hearts. By contrast, in the Cpa3Cre/+ mice we observed a significant reduction in cardiomyocyte contractility (at 1, 2 & 4 Hz, 4ms pulse, 10volts amplitude) compared to WT. Cell shortening and maximal contracting/relaxing velocity were significantly decreased (p<0.01) with no effect on Ca2+ transient peak or sarcoplasmic reticulum load. Myofilament force-calcium relationships were measured in post-MI skinned myocytes. Compared to WT, calcium sensitivity declined significantly in Cpa3Cre/+ -derived myocytes (p<0.01) with no effect on maximal calcium-activated force.

This work re-evaluates existing mast-cell deficient models on their effect on cardiac remodeling and identifies a novel function for mast cells on modulation of cardiomyocyte contractility and Ca2+ sensitization. Identification of the mast cell-dependent molecular regulators that target myofilament proteins will provide a new platform of regulators with potential cardioprotective properties.
Abstract 3559: Long non-coding RNA subtype classification of clear-cell renal cell carcinoma
Authors: Gabriel G. Malouf, Jianping Zhang, Nizar Tannir, Erika J. Thompson, David Khayat, Jean-Philippe Spano, Xiaoping Su
Journal: Cancer Research (2014)

Abstract Background: Long non-coding RNAs (lncRNA) play a key role in regulating cell physiology through different mechanisms including regulation of transcription and splicing, and recruitment of histone-modifying enzymes. The portrait of lncRNA in kidney cancers remains fully unknown. Material and Methods: we performed a genomic analysis of GENCODE lncRNAs in clear-cell renal cell carcinoma (ccRCC), using The Cancer Genome Atlas (TCGA) molecular RNAseq profiles of 475 primary tumors. Furthermore, we described global correlations between lncRNA and expression of cis- and trans-acting genes, and established lncRNA expression subtypes based on distinct signatures. In addition, lncRNA expression was correlated with miRNA, copy-number alterations and the chromatin landscape of human kidney. Results: Using stringent criteria (RPKM ≥1 in at least 10% of ccRCC), we identified 1,934 lncRNAs and predicted those that are potential drivers of cancer progression through integrative analysis. The expression of 1,057 (54.6%) lncRNAs showed a positive correlation with the mRNA expression of their neighboring genes, while only 13 (0.7%) lncRNAs showed a negative correlation. Overall, 844 (43.6%) lncRNAs were pre-marked by H3K4me3 in normal kidney, suggesting that those lncRNA might arise from promoter-associated elements. Conversely, only 81 (4.2%) and 182 (9.4%) lncRNAs were pre-marked by H3K36me3 and H3K27me3, respectively. Unsupervised clustering of lncRNA expression revealed four robust subtypes, which differ from the ccRCC transcriptomic subgroups. Interestingly, patients belonging to cluster II (n=111) displayed poor overall survival as compared to patients of other clusters (p=2.6x10-6). Intriguingly, there were 37 (7.8%) ccRCC belonging to cluster IV, and those were enriched for TFE3/TFEB RCC. Furthermore, tumors within cluster IV were devoid from 3p loss and 5q gain which represent the most frequent genomic aberrations in ccRCC. Finally, GREAT analysis reveals that overexpressed lncRNA in cluster IV were exclusively enriched for genes belonging to collecting duct (p=1.6x10-13) highly suggesting that their cell of origin might be different. Conclusion: This study describes the first portrait of lncRNA in ccRCC and proposes a robust lncRNA subtype classification of ccRCC, which may serve in predicting patient outcome. Furthermore, we identified a small ccRCC subgroup with distinct lncRNA and karyotypic phenotype. Citation Format: Gabriel G. Malouf, Jianping Zhang, Nizar Tannir, Erika J. Thompson, David Khayat, Jean-Philippe Spano, Xiaoping Su. Long non-coding RNA subtype classification of clear-cell renal cell carcinoma. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3559. doi:10.1158/1538-7445.AM2014-3559
Immunotherapy of tumors with xenogeneic endothelial cells as a vaccine
Authors: Yu-quan Wei, Qing-ru Wang, Xia Zhao, Li Yang, Ling Tian, You Lu, Bin Kang, Chong-jiu Lu, Mei-juan Huang, Yan-yan Lou, Fei Xiao, Qiu-ming He, Jing-mei Shu, Xing-jiang Xie, Yun-qiu Mao, Shong Lei, Feng Luo, Li-qun Zhou, Chong-en Liu, Hao Zhou, Yu Jiang, Feng Peng, Liang-ping Yuan, Qiu Li, Yang Wu, Ji-yan Liu
Journal: Nature Medicine (2000)
Pathology of Sickle Cell Disease.
Authors: Joseph Song
Journal: Annals of Internal Medicine (1971)

by Ya\l=s;\argil).There is a section on congenital cysts of the brain by Robinson, and the last chap¬ ter by Brenner and Kraus is on craniosynostosis. All the articles are in English, which means that a number of Amer¬ ican doctors can now have access to the work of their European colleagues: six of the articles are by authors from Germany, Switzerland, Austria, Italy, France, while the others are shared by North Americans from the United States and Canada, and by an Aus¬ tralian. This volume, like the others in this series, aims to present material which includes an extensive literature search, follow-up of clinical material, and critical distillation of what is valuable for theory and practice. Al¬ though these goals are not always at¬ tained, the articles do offer a good re¬ view and presentation of the authors'
Abstract 3705: Overcoming drug resistance in BRaf mutated melanoma cells
Authors: Ramin Samadani, Jun Zhang, Alexander Mackerell, Steven Fletcher, Paul Shapiro
Journal: Cancer Research (2014)

Abstract Targeted inhibition of the ERK1/2 signaling pathway has received much attention after the transient success of the BRaf inhibitor, vemurafenib, in metastatic melanoma patients with the BRafV600E mutation. Approximately 50% of melanomas have an activating mutation to BRaf which drives cancer cell proliferation and survival through the ERK pathway. Therapies targeting BRaf or its downstream kinase MEK1/2 have demonstrated very promising initial clinical results. However, these treatments invariably lead to drug resistance through the activation of alternate pathways or mutations that circumvent the blockade and reactivate ERK1/2. Current efforts are centered on the use of combination therapies as well as the direct inhibition of ERK1/2 itself. The purpose of this study is to examine the effects of putative substrate-selective ERK inhibitors in various clinically relevant models of drug resistance. Specifically melanoma cell lines resistant to BRaf and MEK inhibitors, PLX-4032 and AZD-6244 respectively, were generated to test the efficacy of these novel compounds in cell viability assays. Furthermore, the potency of these molecules was evaluated in the context of activating mutations to MEK1 and drug resistant cell lines that overexpress MAP3K8 (the gene encoding COT/Tpl2). The data shows that these putative substrate-selective ERK inhibitors preferentially inhibit proliferation of cell lines with activated ERK1/2 signaling. In addition, these novel molecularly targeted therapies are equipotent in drug resistant versus non-resistant melanoma cells. Given these compounds' selectivity for BRaf mutated melanoma cells and their efficacy in drug resistance models, we submit these novel chemical entities as potential lead candidates for new salvage therapies in patients who have become resistant to currently available treatments. Moreover, these ATP-independent inhibitors target only select ERK1/2 functions and may be inherently less susceptible to developing their own drug resistance as compared to complete ablation of all ERK1/2 signaling as seen with ATP-competitive inhibitors. Citation Format: Ramin Samadani, Jun Zhang, Alexander Mackerell, Steven Fletcher, Paul Shapiro. Overcoming drug resistance in BRaf mutated melanoma cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3705. doi:10.1158/1538-7445.AM2014-3705
Pain after Haemorrhoidectomy
Authors: F L RAFFUCCI
Journal: BMJ (1965)

Sir George God- ber, Chief Medical Officer, Ministry of Health, reviews the pattern of medical care in Britain, identifies distinctive aspects worth preserving, and discusses the necessary reorganization of medical work (p. 665).Arthritis and Ulcerative Colitis: Dr. V. Wright and Dr. G. Watkinson describe a specific " colitic arthritis " occurring in 11.5% of patients with ulcerative colitis and character- ized by a recurrent, acute, usually monoarticu- lar, synovitis (p. 670).They also report an 18% incidence of radiographical sacro-iliitis in ulcerative colitis and discuss this association (p.675).Leader at p. 663.Breathing Exercises: Dr. K. B. Saunders and Dr. J. E. White describe a controlled trial of breathing exercises in chronic bronchitis and/or emphysema.No improvement in lung function resulted (p.680).Glycodiazine in Diabetes: Dr. R. D. H. Stewart and Dr
A first case report of a patient with paraneoplastic dermatomyositis developing diffuse alveolar haemorrhage
Authors: G. Do-Pham, C. Pagès, C. Picard, L. Galicier, M. Lémann, L. Dubertret, M. Viguier
Journal: British Journal of Dermatology (2010)

Journal Article A first case report of a patient with paraneoplastic dermatomyositis developing diffuse alveolar haemorrhage Get access G. Do‐Pham, G. Do‐Pham Departments of Dermatology Search for other works by this author on: Oxford Academic Google Scholar C. Pagès, C. Pagès Departments of Dermatology Search for other works by this author on: Oxford Academic Google Scholar C. Picard, C. Picard Respiratory Medicine Search for other works by this author on: Oxford Academic Google Scholar L. Galicier, L. Galicier Clinical Immunology Search for other works by this author on: Oxford Academic Google Scholar M. Lémann, M. Lémann Gastroenterology, Saint‐Louis Hospital, Assistance Publique–Hôpitaux de Paris, Paris VII University, 1 avenue Claude‐Vellefaux, 75475 Paris Cedex 10, France Search for other works by this author on: Oxford Academic Google Scholar L. Dubertret, L. Dubertret Departments of Dermatology Search for other works by this author on: Oxford Academic Google Scholar M. Viguier M. Viguier Departments of Dermatology Manuelle Viguier E‐mail: manuelle.viguier@sls.aphp.fr Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 163, Issue 1, 1 July 2010, Pages 227–228, https://doi.org/10.1111/j.1365-2133.2010.09800.x Published: 01 July 2010