tbuckley/cabot-search huggingface dataset:
Comparison of a Standard Regimen (CHOP) with Three Intensive Chemotherapy Regimens for Advanced Non-Hodgkin's Lymphoma
Authors: Richard I. Fisher, Ellen R. Gaynor, Steve Dahlberg, Martin M. Oken, Thomas M. Grogan, Evonne M. Mize, John H. Glick, Charles A. Coltman, Thomas P. Miller
Journal: New England Journal of Medicine (1993)

CHOP is a first-generation, combination-chemotherapy regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone that has cured approximately 30 percent of patients with advanced stages of intermediate-grade or high-grade non-Hodgkin's lymphoma in national cooperative-group trials. However, studies at single institutions have suggested that 55 to 65 percent of such patients might be cured by third-generation regimens such as ones consisting of low-dose methotrexate with leucovorin rescue, bleomycin, doxorubicin, cyclophosphamide, vincristine, and dexamethasone (m-BACOD); prednisone, doxorubicin, cyclophosphamide, and etoposide, followed by cytarabine, bleomycin, vincristine, and methotrexate with leucovorin rescue (ProMACE-CytaBOM); and methotrexate with leucovorin rescue, doxorubicin, cyclophosphamide, vincristine, prednisone, and bleomycin (MACOP-B).
Abstract 5686: Linoleic acid supplementation upregulates phosphatidylinositol-3-kinase signaling by increasing the association between Gab1 and EGFR
Authors: Keith D. Kikawa, Eric D. Johnson, Kristen M. McKinnon, Kristina R. Rogers, Ronald S. Pardini
Journal: Cancer Research (2010)

Abstract The omega-6 polyunsaturated fatty acid, linoleic acid (LA), is prevalent in Western diets and is known to enhance the tumorigenesis of mammary cancer models; with previous work demonstrating an upregulation of phosphatidylinositol-3-kinase (PI3K) signaling may play a key role. The Grb2-associated binding protein 1 (Gab1) is a scaffolding protein that can complex with the epidermal growth factor receptor (EGFR) to activate PI3K signaling. Recent studies in our laboratory reveal LA supplementation of the breast cancer cell lines MDA-MB-231 and BT-474 greatly increases the association between Gab1 and EGFR, while at the same time dramatically decreasing Gab1 protein levels. These changes are concomitant with increases in activated Akt (pAkt), a downstream signaling component in the PI3K signaling pathway. Moreover, inhibitors of EGFR and Gab1-specific siRNAs are capable of reversing LA-induced upregulation of pAkt, as well as observed increases in cell proliferation for these models. Finally, we were able to confirm these findings in the A549 lung cancer cell line, validating the potential relevance to tissues other than breast cancer cell lines. These data establish Gab1 as major target in LA-induced enhancement of tumorigenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5686.
AB0574 A Prospective Follow-Up of Young, Male Patients with Behcet's Disease without Major Organ Involvement
Authors: F. Alibaz-Oner, E. Karatay, I.N. Akpınar, T. Ergun, H. Direskeneli
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Objectives</h3> Vascular involvement, especially in young males, is one of the main causes of mortality and morbidity in Behcet9s Disease (BD). However, the prognosis and predictors of vascular involvement is unsufficiently studied in the literature. In this study, we aimed to follow-up male BD patients without major organ involvement, prospectively. Subclinical vascular involvement and markers of endothelial dysfunction (ADMA, E-selectin and VWF levels) in these patients is also investigated. <h3>Methods</h3> Thirty-six male patients with BD, 35 males with ankylosing spondylitis and 36 healthy males were included into the study. Bilateral upper and lower extremity venous doppler ultrasonography (US) and brachial and carotid arterial US were performed in baseline visit for all study groups and in the first year follow-up visit for BD patients. Serum samples were also taken to analyse ADMA, E-selectin and VWF levels. The same protocol was also applied to all patients coming with an emergency visit for acute vascular events. <h3>Results</h3> The rate of venous insufficiency was significantly higher in male BD patients without vascular events, compared to healthy controls. Immunsuppresive (IS) therapy was required in 22% (n=8) of patients with BD in the follow-up period (mean 20.6 months). The cause of IS therapy was major organ involvement in 4 (11%, 3 vascular and 1 ocular involvement) patients and refractory mucocutaneous symptoms in other 4 (11%) patients. Markers of endothelial dysfunction (FMD and NID) were similar between BD patients and healthy controls, however CIMT (Carotid intima media thickness) was significantly higher in BD. In first year follow-up visit, endothelial functions and CIMT were observed to be significantly improved compared to baseline. Serum VWF levels were also significantly higher in BD, whereas ADMA and E-selectin levels were similar between BD patients and healthy controls. <h3>Conclusions</h3> Preliminary results of our study (which will be a long-term cohort) demonstrated a lower incidence of major vascular events in male BD patients during prospective follow-up, compared to historic controls in the literature. Although we could not show an impaired endothelial function in BD patients without vascular events, the decreased rate of baseline FMD in patients with later IS requirement, suggest that FMD can be a predictor for major organ involvement in BD. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3375
Abstract 782: Characterization of genetic changes in oligodendroglial tumors including glioblastomas with oligodendroglial component
Authors: Barbara Klink, Dietmar Krex, Eva-Maria Gerlach, Ben Schlingelhof, Karl Hackmann, Stephan Patt, Evelin Schrock
Journal: Cancer Research (2010)

Abstract In contrast to astrocytic tumors including glioblastomas (GBM), oligodendrogliomas (O) show a better prognosis and increased responsiveness to chemotherapy. Interestingly, a small subgroup of glioblastomas contains areas with histological features of oligodendroglial differentiation. In the current WHO classification (2007) these tumors are now included as a variant of glioblastomas and are called glioblastomas with oligodendroglial component (GBMO). However, definitive diagnostic criteria still do not exist. In this study we used a genome wide approach (chromosomal comparative genomic hybridization (CGH) and molecular karyotyping) in combination with interphase fluoreszence in situ hybridization (FISH) (regions 1p, 1q, 7q, 10q, 17p, 19q, cen18, 21q) to genetically characterize GBMO and “classical” O. We analyzed the oligodendroglial and the astrocytic glioblastoma parts of 13 GBMO separately by chromosomal CGH of microdissected paraffin embedded tumor tissue and interphase FISH on paraffin sections. Furthermore, freshly frozen material of six oligodendrogliomas (4 WHO grade II, 6 WHO-grade III) was examined genome wide by using the standard Agilent 244A chip. We identified four distinct genetic subtypes in GBMO: an “astrocytic” subtype (9/13) characterized by +7/-10; an “oligodendroglial” subtype with −1p/-19q (1/13); an “intermediate” subtype showing +7/-1p (1/13), and an “other” subtype having none of the former aberrations typical for gliomas (2/13). In contrast, most “classical” O (5/6) showed combined 1p/19q deletion, corresponding genetically to the “oligodendroglial” subtype. Four of the O with 1p/19q codeletion showed additional aberrations (e. g. −4, −14, −9, −18). The different histological tumor parts of GBMO revealed common genetic changes in all tumors and showed additional aberrations specific for their oligodendroglial and astrocytic parts. These findings demonstrate the monoclonal origin of the tumor followed by the formation of the astrocytic and oligodendroglial components. We are currently evaluating the array CGH results of six oligodendrogliomas, which will also be presented. The diagnostic determination of these genetic signatures may allow for a better prognostication of the patients. Our results underline the importance of molecular cytogenetic analyses to supplement the histological diagnosis of gliomas. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 782.
Improving Prostate Cancer Screening and Diagnosis
Authors: Hiten D. Patel, Heather J. Chalfin, H. Ballentine Carter
Journal: JAMA Oncology (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Oncology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Oncology journal
p53 Loss in MYC-Driven Neuroblastoma Leads to Metabolic Adaptations Supporting Radioresistance
Authors: Orli Yogev, Karen Barker, Arti Sikka, Gilberto S. Almeida, Albert Hallsworth, Laura M. Smith, Yann Jamin, Ruth Ruddle, Alexander Koers, Hannah T. Webber, Florence I. Raynaud, Sergey Popov, Chris Jones, Kevin Petrie, Simon P. Robinson, Hector C. Keun, Louis Chesler
Journal: Cancer Research (2016)

Neuroblastoma is the most common childhood extracranial solid tumor. In high-risk cases, many of which are characterized by amplification of MYCN, outcome remains poor. Mutations in the p53 (TP53) tumor suppressor are rare at diagnosis, but evidence suggests that p53 function is often impaired in relapsed, treatment-resistant disease. To address the role of p53 loss of function in the development and pathogenesis of high-risk neuroblastoma, we generated a MYCN-driven genetically engineered mouse model in which the tamoxifen-inducible p53ER(TAM) fusion protein was expressed from a knock-in allele (Th-MYCN/Trp53(KI)). We observed no significant differences in tumor-free survival between Th-MYCN mice heterozygous for Trp53(KI) (n = 188) and Th-MYCN mice with wild-type p53 (n = 101). Conversely, the survival of Th-MYCN/Trp53(KI/KI) mice lacking functional p53 (n = 60) was greatly reduced. We found that Th-MYCN/Trp53(KI/KI) tumors were resistant to ionizing radiation (IR), as expected. However, restoration of functional p53ER(TAM) reinstated sensitivity to IR in only 50% of Th-MYCN/Trp53(KI/KI) tumors, indicating the acquisition of additional resistance mechanisms. Gene expression and metabolic analyses indicated that the principal acquired mechanism of resistance to IR in the absence of functional p53 was metabolic adaptation in response to chronic oxidative stress. Tumors exhibited increased antioxidant metabolites and upregulation of glutathione S-transferase pathway genes, including Gstp1 and Gstz1, which are associated with poor outcome in human neuroblastoma. Accordingly, glutathione depletion by buthionine sulfoximine together with restoration of p53 activity resensitized tumors to IR. Our findings highlight the complex pathways operating in relapsed neuroblastomas and the need for combination therapies that target the diverse resistance mechanisms at play. Cancer Res; 76(10); 3025-35. ©2016 AACR.
An Immunologic Survey of Forty-Eight Patients with Myasthenia Gravis
Authors: Marvin M. Adner, Joseph D. Sherman, Caroline Isé, Robert S. Schwab, William Dameshek, Suzanne Wilson
Journal: New England Journal of Medicine (1964)

FOR many years it has been recognized that myasthenia gravis is associated, in a high percentage of cases, with structural abnormalities of the thymus.1 Many patients, especially the younger ones, have shown marked clinical improvement after thymectomy or thymic irradiation or both.2 3 4 Yet the exact role of the thymus in myasthenia gravis is not known. Because thymectomy in the young animal is followed by lymphocytopenia, together with some impairment of humoral-antibody production and expression of the reaction of delayed (cellular) hypersensitivit-,5 6 7 8 9 we wondered whether similar changes occurred in thymectomized patients with myasthenia gravis. In addition, recent studies of myasthenic patients . . .
Sex After Chemo: A Neglected Issue
Authors: E. Blume
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Sex After Chemo: A Neglected Issue Get access Elaine Blume Elaine Blume Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 10, 19 May 1993, Pages 768–770, https://doi.org/10.1093/jnci/85.10.768 Published: 19 May 1993
Abstract LB-162: Blockade of PD-L1 signaling, but not depletion of regulatory T cells, delays tumor growth in a murine pancreatic tumor model
Authors: Nasreen A. Vohra, Amod Sarnaik, Amy Mackay, Tomar Ghansah, Shari Pilon-Thomas
Journal: Cancer Research (2011)

Abstract Pancreatic cancer is an aggressive disease with poor prognosis. Immunotherapy may be less effective in treating pancreatic tumors due to tumor-mediated suppression. Several mechanisms may contribute to immune suppression seen in mice bearing Panc02 pancreatic adenocarcinomas. We measured an increase in the percentage of CD4+CD25+foxp3+ regulatory T cells (Tregs) in the tumor and spleens of mice bearing Panc02 tumors (p&amp;lt;0.001 compared to non-tumor bearing mice). These Tregs were capable of suppressing antigen-specific T cell proliferation in a dose-dependent manner. Treatment of mice bearing Panc02 tumors using combination therapy with dendritic cells (DC) and anti-CD25 antibody (PC-61) did not demonstrate a delay in tumor growth or survival. As depletion of Tregs had little effect on Panc02 tumor growth, we examined another mechanism of immune suppression. We measured the expression of programmed death ligand-1 (PD-L1) on the surface of Panc02. PD-L1 plays a crucial role in inhibiting T cell responses and maintaining peripheral tolerance. PD-L1 expression has been measured on most pancreatic adenocarcinomas and may lead to down-regulation of antigen-specific T cell responses. To examine PD-L1 signaling blockade, mice bearing Panc02 tumors were treated with anti-PD-L1 antibody at 3 day intervals. After 3 weeks, mice receiving anti-PD-L1 antibody displayed smaller tumors than mice receiving control antibody (134 mm2 vs 221mm2 respectively, p&amp;lt;0.05). Splenocytes from PD-L1 treated mice secreted IFN-gamma in response to restimulation with Panc02 (p&amp;lt;0.01 compared to control treated mice). Furthermore, treatment with anti-PD-L1 antibody in Panc02-bearing athymic nude mice had no effect on tumor growth, indicating that treatment is T cell dependent. Survival benefit was measured in tumor-bearing mice when anti-PD-L1 antibody treatment was combined with DC immunizations (35% survival on day 75 compared to 0% in all control groups, p&amp;lt;0.05). To enhance this treatment, we examined combination therapy with DC, anti-PD-L1 and PC-61 antibodies. Depletion of Tregs did not enhance therapy with DC and anti-PD-L1 antibody. Together, these studies show that blockade of PD-L1 signaling inhibited tumor growth in mice with pancreatic cancer. Depletion of Tregs alone or in combination with PD-L1 blockade demonstrated no benefit in this model. Studies to optimize combination therapy using anti-PD-L1 antibody and DC-based vaccines are ongoing. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-162. doi:10.1158/1538-7445.AM2011-LB-162
Abstract 4149: Pathway-based serum microRNA profiling and late-stage non-small cell lung cancer survival
Authors: Yan Wang, Scott M. Lippman, John D. Minna, Jack A. Roth, Xifeng Wu
Journal: Cancer Research (2012)

Abstract Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer mortality in the world. Nearly half of NSCLC patients are diagnosed with late-stage (stage III or stage IV) disease with an overall 5-year survival rate of less than 15%. Deregulation of microRNAs (miRNAs) is involved in cancer development, progression, and prognosis. Circulating miRNAs have been suggested as promising biomarkers for early detection, diagnosis, and prognosis of cancer. This ongoing study is to utilize a pathway-based approach to screen and validate serum miRNA profiles as predictors of survival using a large patient cohort of 348 late-stage NSCLC patients. In the testing set, pre-treatment serum miRNA profiles of four good- (survival time &amp;gt; 24 months) and four poor-survival (survival time &amp;lt; 6 months) patients were compared by Taqman miRNA microarray. 145 highly expressed serum miRNAs were identified from initial screening and 37 of them were mapped onto the 3′UTRs of a panel of 23 genes in TGF-β signaling pathway using computer-assisted miRNA target prediction program. All 37 miRNA candidates were subject to large-scale single-probe quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). The expression level of serum miR-30d, which targets TGFBR2 and was a previously reported serum marker for early-stage lung cancer survival, was significantly higher in the poor-survival group than the good-survival group (P = 0.0208) in our study population of late-stage lung cancer. The level of serum miR-93-3p that targets SMAD7 was significantly higher in the poor-survival group than the good-survival group (P = 9x10−6). The 2-year overall survival rate in patients with high serum miR-93-3p expression was significantly lower than that in those with low expression with an adjusted HR of 1.59 (95% CI, 1.24 - 2.03) (P = 2x10−4). In contrast, serum level of let-7g, that targets SMAD2, TGFBR1 and the activin A receptor family was significantly lower in the poor-survival group than in the good-survival group (P = 7x10−4), and patients with high serum let-7g expression was associated with a significantly better two-year survival (HR=0.48, 95% CI, 0.37 - 0.62, P = 1x10−8). Our results suggest that serum miR-30d, miR-93-3p and let-7g may become valuable biomarkers for survival in late-stage NSCLC patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4149. doi:1538-7445.AM2012-4149
Abstract 1603: The VEGF, PDGF and STAT3 pathways are the potential therapeutic targets to treat endometrial cancer
Authors: Victoria P. Korovkina
Journal: Cancer Research (2010)

Abstract Progesterone inhibits growth of endometrial cancer through its receptors A (PRA) and B (PRB) although the molecular mechanisms of inhibition have yet to be fully characterized. A global analysis of gene regulation in human endometrial cancer cells that express heterologous progesterone receptors was performed to identify the candidate genes that mediate inhibitory effects of progesterone in endometrium. Data indicate that progesterone down-regulates the expression of vascular endothelial growth factor A (VEGFA), platelet derived growth factor A (PDGFA) and signal transducer and activator of transcription 3 (STAT3). Down-regulation of VGFA is mediated by the PRA whereas both PRA and PRB are required to attenuate expression of PDGFA and STAT3 genes. These results suggest that progesterone exerts the growth-limiting effects in endometrium via inhibition of angiogenesis and proliferation. VGFA, PDGFA and STAT3 pathways may be central to the inhibitory effects of progesterone in endometrial cancer and may constitute the important targets for therapeutic interventions. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1603.
SP0024 Microparticles in haemostasis and thrombosis
Authors: N. Mackman
Journal: Annals of the Rheumatic Diseases (2013)

Microparticles (MPs) (also known as microvesicles) are small membrane vesicles that are released from activated and apoptotic cells. They are defined as 0.1-1 μm in diameter and are therefore larger than exosomes. Formation of MPs requires activation of an ATP-dependent lipid transporter called scramblase that translocated phosphatidylserine (PS) from the inner to outer leaflet. Subsequent membrane blebbing is followed by release of a MP. MPs are procoagulant because the exposed PS provides a docking site for the assembly of different coagulation protease complexes. In addition, the presence of the transmembrane glycoprotein called tissue factor (TF) increases their procoagulant activity. Levels of TF-positive MPs are increased in a variety of diseases, including acute coronary syndromes, sepsis, diabetes, sickle cell disease and cancer. Hyperlipidemia induces TF expression in circulating monocytes and these cells subsequently release TF-positive MPs that may contribute to arterial thrombosis after rupture of atherosclerotic plaques. In cancer, tumors release high levels of TF-positive MPs into the circulation and they may trigger venous thrombosis. These studies suggest that levels of TF-positive MPs can be used clinically to assess thrombotic risk in different diseases. <h3>Disclosure of Interest</h3> N. Mackman Consultant for: Merck
819 HEPATITIS C VIRUS INDUCES THE CLEAVAGE OF POLY ADP-RIBOSE POLYMERASE THROUGH FOCAL ADHESION KINASE AND DRIVES HEPATIC STELLATE CELLS TO GAIN PRO-FIBROGENIC ACTIVITY
Authors: A. Alisi, M. Arciello, S. Petrini, B. Conti, C. Balsano
Journal: Journal of Hepatology (2012)
A rare case of extramedullary hematopoiesis in the mediastinum diagnosed by endoscopic ultrasound
Authors: Marco Camunha, Augusto Carbonari, Julia Araujo, Ivan Rondelli, Mauro Saieg, Lucio Rossini
Journal: Endoscopy (2015)

A 48-year-old woman with chest pain for the preceding 2 months and a previous history of hereditary spherocytosis was referred for endoscopic ultrasound (EUS) to evaluate mediastinal lymphadenopathy and a heterogeneous mediastinal mass diagnosed by computed tomography (CT). EUS (Fujinon, Saitama City, Japan) showed a hyperechogenic and heterogeneous peri-esophageal, supra-diaphragmatic lesion ([Fig. 1]) and a peri-aortic/vertebral lesion ([Fig. 2]). EUS also demonstrated multiple lymph nodes in the para-esophageal, subcarinal, and right high paratracheal regions, suggesting a reactive process. The patient underwent EUS-guided fine-needle aspiration (EUS-FNA) of the right supra-diaphragmatic lesion, performed with a 19-gauge needle (Cook Medical, Limerick, Ireland) ([Fig. 3]). Analysis of the histologic sections confirmed the diagnosis of extramedullary hematopoiesis in the mediastinum ([Fig. 4]).