tbuckley/cabot-search huggingface dataset:
Abstract 999: Utilization of catastrophic autophagy in ovarian cancer
Authors: Joe R. Delaney, Chandni Patel, Dwayne G. Stupack
Journal: Cancer Research (2015)

Abstract In ovarian cancer, the dysfunction of apoptotic effectors such as p53 suggests that therapies which act tangential to ‘apoptotic’ pathways may offer alternative avenues to target recalcitrant disease. These pathways include necroptosis, ER stress, and autophagy. Evaluating combinations of agents which impact these pathways, we found that effects of ‘non-toxic’ drugs that induced ER stress and autophagy were potentiated when used with drugs that prevented autophagy resolution. At the cellular level, LC3-II levels were elevated in response to these agents, and predicted efficacy. GRP78 and SQSTM1/p62 were similarly elevated, indicating induction of the ER stress pathway impaired autophagic flux, respectively. The resulting death, via ‘catastrophic autophagy,’ may be an effective way to target traditional-chemotherapy-resistant ovarian cancer. Citation Format: Joe R. Delaney, Chandni Patel, Dwayne G. Stupack. Utilization of catastrophic autophagy in ovarian cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 999. doi:10.1158/1538-7445.AM2015-999
Abstract 1427: Embigin is overexpressed in pancreatic ductal adenocarcinoma and regulates cell motility through epithelial to mesenchymal transition via the TGF-β pathway
Authors: Dawoon E. Jung, Jeong Mi Kim, Chanyang Kim, Si Young Song
Journal: Cancer Research (2015)

Abstract Embigin is a member of the immunoglobulin superfamily and encodes a transmembrane glycoprotein. Strong expression of Embigin has been observed in the mouse endoderm during early postimplantation embryogenesis and in the gut and visceral endoderm at the somite stage. There have been reports of Embigin involvement in neuromuscular junction formation and plasticity; however, the molecular functions of Embigin in other organs are unknown. Pancreatic cancer is an extremely aggressive malignancy, and it is necessary to understand the biology of pancreatic cancer to better detect and treat this disease. Our aim was to investigate the possible role of Embigin in pancreatic cancer. In pancreatic ductal adenocarcinoma tissues, Embigin expression was higher than that in normal pancreatic tissues. Immunohistochemical analysis revealed expression of Embigin in pancreatic cancer cells, as well as expression of monocarboxylate transporter 2 (MCT2) in cancer tissues. To gain further insight, we transfected BxPC-3 and HPAC pancreatic cancer cells with siRNA or shRNA targeting Embigin and observed reductions in cell proliferation, migration, invasion, wound healing, and reduced levels of matrix metalloproteinases-2 and -9. Silencing of Embigin increased intracellular L-lactate concentration by 1.5-fold and decreased MCT2 levels at the plasma membrane. Furthermore, Embigin silencing led to a reduced expression of PI3K, GSK3-β, and Snail/Slug. Upon treating BxPC-3 cells with transforming growth factor-β (TGF-β), we observed elevated expression of Snail/Slug, Embigin, and Vimentin; meanwhile, when treating cells with SB-216763, a GSK3-β inhibitor, we noted decreases in GSK3-β, Snail/Slug, and Embigin expression, suggesting that the TGF-β signaling cascade, comprising PI3K, GSK3-β, Snail/Slug, and Embigin signals, mediates epithelial to mesenchymal transition (EMT) in pancreatic cancer cells. These findings indicate the involvement of Embigin in EMT in pancreatic cancer progression and suggest Embigin as a putative target for the detection and/or treatment of pancreatic cancer. Citation Format: Dawoon E. Jung, Jeong Mi Kim, Chanyang Kim, Si Young Song. Embigin is overexpressed in pancreatic ductal adenocarcinoma and regulates cell motility through epithelial to mesenchymal transition via the TGF-β pathway. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1427. doi:10.1158/1538-7445.AM2015-1427
Safety and efficacy of modified schedula of anti-EGFR monoclonal antibodies plus chemotherapy as first line treatment in metastatic colorectal cancer patients
Authors: S. Mancarella, O. Poti, D. De Giorgi, M.L. Schirinzi, G. De Maria, A. Rizzo, A. De Benedittis, M.M. Galante
Journal: Annals of Oncology (2015)
Strong Therapeutic Effect Of Anti-IL1RAP Immunotherapy In a Xenograft Model Of Acute Myeloid Leukemia
Authors: Helena Agerstam, Maria Askmyr, Nils Hansen, Marianne Rissler, Gunnar Juliusson, Johan Richter, Mark Wunderlich, Marcus Järås, James C. Mulloy, Thoas Fioretos
Journal: Blood (2013)
Analysis of Zoledronic ACID Therapy for Patients with Multiple Myeloma with Asymptomatic Biochemical Relaps.
Authors: Ramón García-Sanz, Albert Oriol, Javier De La Rubia, Luis Palomera, Paz Ribas, Miguel Teodoro Hernández, Maria José Moreno, Joan Bargay, Angel Ramírez, Ana Isabel Teruel, María Jesús Blanchard, Mercedes Gironella, Miquel Granell, Eugenia Abella, J.F. San Miguel
Journal: Blood (2012)
Unrelated Cord Blood Versus Non-T Cell Depleted Haploidentical Stem Cell Transplantation: Comparable Results in Adults with Acute Leukemia, a Eurocord and ALWP-EBMT Study
Authors: Annalisa Ruggeri, Myriam Labopin, Guillermo F. Sanz, Simona Piemontese, William Arcese, Andrea Bacigalupo, Didier Blaise, Alberto Bosi, He Huang, Dimitrios Karakasis, Yener Koc, Mauricette Michallet, Alessandra Picardi, Jaime Sanz, Stella Santarone, Henrik Sengelov, Jorge Sierra, Laure Vincent, Fernanda Volt, Arnon Nagler, Eliane Gluckman, Fabio Ciceri, Vanderson Rocha, Mohamad Mohty
Journal: Blood (2014)
The Optimal Body Mass Index Range for Patients With Colorectal Cancer
Authors: Hyun-seok Kim, Adaugo Ike, Sushil K. Ahlawat
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
Cytokine Environement Analysis During Allogeneic Hematopoietic Stem Cell Transplantation for Inherited Diseases
Authors: Fabien Touzot, Bryan Fiema, Sophie Paczesny, Isabelle Andre-Schmutz, Dominique Helley, Despina Moshous, Corinne De Chappedelaine, Stephane Blanche, Alain Fischer, Marina Cavazzana-Calvo
Journal: Blood (2012)
4-1BBL-Expressing aAPCs Attenuate IL-15-Induced NK Cell Expansion and Cytokine Production In Vitro but Induce NK Cell-Mediated Gvhd In Vivo
Authors: Christian M. Capitini, Joanna L. Meadors, Monica M. Cho, Rimas J. Orentas, Crystal L. Mackall, Terry J. Fry
Journal: Blood (2010)
Detectable Minimal Residual Disease before Haematopoietic Stem Cell Transplantation Predicts Extremely Poor Prognosis in Children with Acute Lymphoblastic Leukaemia.
Authors: Katerina Muzikova, Eva Fronkova, Lucie Sramkova, Leona Reznickova, Renata Formankova, Petr Sedlacek, Jan Stary, Jan Trka
Journal: Blood (2005)
Abstract SY27-02: Tumour heterogeneity and therapy resistance in melanoma
Authors: Claudia Wellbrock
Journal: Cancer Research (2015)

Abstract Solid tumors are structurally very complex; they consist of heterogeneous cancer cell populations, other non-cancerous cell types and a distinct extracellular matrix. Interactions of cancer cells with non-cancerous cells is well investigated, and our recent work in melanoma has demonstrated that the cellular environment that surrounds cancer cells has a major impact on the way a patient responds to MAP-kinase pathway targeting therapy. We have shown that intra-tumor signaling within a heterogeneous tumor can have a major impact on the efficacy of BRAF and MEK inhibitors. With the increasing evidence of genetic and phenotypic heterogeneity within tumors, intra-tumor signaling between individual cancer-cell subpopulations is therefore a crucial factor that needs to be considered in future therapy approaches. Our work has identified the ‘melanocyte-lineage survival oncogene’ MITF as an important player in phenotypic heterogeneity (MITFhigh and MITFlow cells) in melanoma, and MITF expression levels are crucial for the response to MAP-kinase pathway targeted therapy. We found that ‘MITF heterogeneity’ can be caused by cell-autonomous mechanisms or by the microenvironment, including the immune-microenvironment. We have identified various mechanisms underlying MITF action in resistance to BRAF and MEK inhibitors in melanoma. In MITFhigh expressing cells, MITF confers cell-autonomous resistance to MAP-kinase pathway targeted therapy. Moreover, it appears that in melanomas heterogeneous for MITF expression (MITFhigh and MITFlow cells), individual subpopulations of resistant and sensitive cells communicate and MITF can contribute to overall tumor-resistance through intra-tumor signaling. Finally, we have identified a novel approach of interfering with MITF action, which profoundly sensitizes melanoma to MAP-kinase pathway targeted therapy. Citation Format: Claudia Wellbrock. Tumour heterogeneity and therapy resistance in melanoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr SY27-02. doi:10.1158/1538-7445.AM2015-SY27-02
109. Replicating Oncolytic Chimeric Adenovirus Expressing shRNA Improves Inhibition of Human Colorectal Carcinoma (CRC) Growth
Authors: John M. Jessup, Abid R. Mattoo, Nikolay Korokhov
Journal: Molecular Therapy (2015)

RNAi combined with oncolytic viral vector therapy may provide a new approach to control malignant disease since allele specific shRNA to a retrogene that modulates stemness will inhibit growth of human CRC in vivo. Our original delivery vector was nonreplicating Lentiviral vectors (LV) but now oncolytic adenovirus is the vector. We have created a conditionally replicating chimeric oncolytic adenovirus (CRAd) expressing a shRNA to inhibit growth of established tumors in preclinical models. shRNA is directed to NANOGP8, a retrogene that differs from parental NANOG primarily in a single nucleotide variant: c.759G>C, p.Gln253His. Oncolytic adenoviruses were generated with a 5/3 fiber with either a control (Ad5/3-wtE1a-shNEG (Ad5/3shNEG)) or an anti-NANOGP8 shRNA (Ad5/3-wtE1a-shNp8 (Ad5/3shNp8)). LV shNEG or LV shNp8 were added 24 hr after creation of 3-D organoid cultures of human CRC cells (Clone A, CX-1 or LS174T) in serum-free medium. LV transduced 45 – 90% of cells in culture and shNp8 inhibited organoids by ~50% compared to either shNEG or untreated CRC organoids. In addition, LV injected into 7 -9 mm diameter CX-1 tumors in NOD/SCID mice reduced tumor growth in vivo by 40% for 11 days, but then tumors grew at an accelerated rate. NMF cluster analysis reveals that LVshNp8 affects a gene expression profile that is distinct from that of either LVshNEG or untreated controls. In contrast, Ad5/3shNp8 inhibited organoid growth by more than 70% and controlled growth of CX-1 and LS174T in vivo. Infection of cells in vitro was over 90%. Thus, shNp8 alters gene expression and replicating oncolytic virus with shNp8 has a more persistent inhibitory effect than that achieved with non-replicating LV-delivered shRNA.
Direct Reprogramming of Human Dermal Fibroblasts Into Endothelial Cells Using ER71/ETV2
Authors: Sangho Lee, Changwon Park, Ji Woong Han, Ju Young Kim, Kyuwon Cho, Eun Jae Kim, Sangsung Kim, Shin-Jeong Lee, Se Yeong Oh, Yoshiaki Tanaka, In-Hyun Park, Hyo Jae An, Claire Min Shin, Shraya Sharma, Young-sup Yoon
Journal: Circulation Research (2016)

Direct conversion or reprogramming of human postnatal cells into endothelial cells (ECs), bypassing stem or progenitor cell status, is crucial for regenerative medicine, cell therapy, and pathophysiological investigation but has remained largely unexplored.We sought to directly reprogram human postnatal dermal fibroblasts to ECs with vasculogenic and endothelial transcription factors and determine their vascularizing and therapeutic potential.We utilized various combinations of 7 EC transcription factors to transduce human postnatal dermal fibroblasts and found that ER71/ETV2 (ETS variant 2) alone best induced endothelial features. KDR+ (kinase insert domain receptor) cells sorted at day 7 from ER71/ETV2-transduced human postnatal dermal fibroblasts showed less mature but enriched endothelial characteristics and thus were referred to as early reprogrammed ECs (rECs), and did not undergo maturation by further culture. After a period of several weeks' transgene-free culture followed by transient reinduction of ER71/ETV2, early rECs matured during 3 months of culture and showed reduced ETV2 expression, reaching a mature phenotype similar to postnatal human ECs. These were termed late rECs. While early rECs exhibited an immature phenotype, their implantation into ischemic hindlimbs induced enhanced recovery from ischemia. These 2 rECs showed clear capacity for contributing to new vessel formation through direct vascular incorporation in vivo. Paracrine or proangiogenic effects of implanted early rECs played a significant role in repairing hindlimb ischemia.This study for the first time demonstrates that ER71/ETV2 alone can directly reprogram human postnatal cells to functional, mature ECs after an intervening transgene-free period. These rECs could be valuable for cell therapy, personalized disease investigation, and exploration of the reprogramming process.
Expression of Activation Marker, CMRF-44, on Blood CD11c+ Dendritic Cells Is Closely Associated with the Severity of Acute GVHD after Allogeneic Haematopoietic Stem Cell Transplant.
Authors: Jenny Lau, Mary Sartor, Slavica Vuckovic, David Munster, Derek N. Hart, Kenneth F. Bradstock
Journal: Blood (2005)
Abstract 2056: SIRT1 silencing suppresses prostate cancer growth and metastasis in an orthotopic prostate cancer mouse model
Authors: Yan Dai, Lijia Zhu, Elizabeth Cho, Audrey Hagiwara, Douglas Faller, Sun-Jin Kim, Isaiah J. Fidler, Marina Amaro
Journal: Cancer Research (2015)

Abstract Tumor environment is critical for tumor growth and progression, and orthotopic mouse model allows accurately study tumor development in an appropriate tumor environment. SIRT1, a class III histone deacetylase, has been shown overexpressed in prostate cancer and is a biomarker for prostate cancer recurrence. Although these data have suggested the importance of the role SIRT1 plays in prostate cancer progression, the role of SIRT1 in tumor growth and progression within, specifically, a prostate tumor environment has not been established. In this study, we established an advanced prostate cancer PC3MM2 orthotopic mouse model to study the effects of SIRT1 silencing on prostate cancer growth and progression. Our data has shown that SIRT1 knockdown greatly suppresses tumor formation within a prostate tumor environment, along with an inhibition of metastasis to bone and liver. To further study the mechanism by which SIRT1 controls tumor growth and progression, we demonstrated that SIRT1 silencing reduces prostate cancer cell adhesion to cell matrix, and that this silencing also suppresses cancer cell growth and colony formation in a cell matrix dependent manner. Moreover, our data showed that SIRT1 regulates integrin expression and focal adhesion complex formation. Furthermore, we shows that SIRT1 silencing from prostate cancer cell significantly inhibited human umbilical vein endothelial cell (HUVEC) tube formation, suggests an important role of SIRT1 in prostate cancer angiogenesis. Thus, we have reported for the first time that SIRT1 plays a critical role in prostate cancer growth and progression using orthotopic mouse model, and demonstrated for the first time that SIRT1 regulates integrin expression, focal adhesion formation, tumor cell and matrix interaction, and angiogenesis. These results suggest SIRT1 regulates prostate cancer growth and progression through multiple mechanisms and that SIRT1 is a potential target in prostate cancer treatment. Citation Format: Yan Dai, Lijia Zhu, Elizabeth Cho, Audrey Hagiwara, Douglas Faller, Sun-Jin Kim, Isaiah J. Fidler, Marina Amaro. SIRT1 silencing suppresses prostate cancer growth and metastasis in an orthotopic prostate cancer mouse model. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2056. doi:10.1158/1538-7445.AM2015-2056
Risk Factor Analysis of Outcomes after Unrelated Cord Blood Transplantation for Children with Hurler’s Syndrome. An Eurocord-Duke University Collaborative Study.
Authors: Jaap Jan Boelens, Vanderson Rocha, Mieke Aldenhoven, Robert Wynn, Anne O’Meara, Marina Cavazzana-Calvo, Irina Ionescu, Suhag Parikh, Vinod Prasad, Maria Escolar, Eliane Gluckman, Joanne Kurtzberg
Journal: Blood (2007)
Adoptive Infusion of Allogeneic KIR Ligand Mismatched NK Cells Reduce GVHD in an MHC Matched Allogeneic Stem Cell Transplantation Model.
Authors: Andreas Lundqvist, Leigh Samsel, Michael Eckhaus, Ramaprasad Srinivasan, Yoshiyuki Takahashi, Maarten Snoeijs, Philip J. McCoy, Maria Berg, Richard Childs
Journal: Blood (2005)
Subanalysis of the StiL NHL 1–2003 Study: Achievement of Complete Response with Bendamustine-Rituximab (B-R) and CHOP-R in the First-Line Treatment of Indolent and Mantle Cell Lymphomas Results in Superior Survival Compared to Partial Response.
Authors: Mathias J. Rummel, Norbert Niederle, Georg Maschmeyer, G.-Andre Banat, Ulrich von Grünhagen, Chrisoph Losem, Dorothea Kofahl-Krause, Gerhard Heil, Manfred Welslau, Christina Balser, Ulrich Kaiser, Eckhart Weidmann, Heinz A. Duerk, Harald Ballo, Martina Beate Stauch, Fritz Roller, Juergen Barth, Axel Hinke, Alexander C. Burchardt, Wolfram Brugger
Journal: Blood (2012)
ROS-Induced DNA Damage Causing Genomic Instability in CML Stem and/or Progenitor Cells and in Quiescent and/or Proliferating Cells: Role of Mitochondrial Respiratory Chain Complex III.
Authors: Margaret Nieborowska-Skorska, Mateusz Koptyra, Elisabeth Bolton, Regina Ray, Danielle Ngaba, Grazyna Hoser, Tomasz Stoklosa, Artur Slupianek, Piotr Kopinski, Tomasz Skorski
Journal: Blood (2009)
Clinical presentations and outcomes of bile duct loss caused by drugs and herbal and dietary supplements
Authors: Herbert L. Bonkovsky, David E. Kleiner, Jiezhun Gu, Joseph A. Odin, Mark W. Russo, Victor M. Navarro, Robert J. Fontana, Marwan S. Ghabril, Huiman Barnhart, Jay H. Hoofnagle
Journal: Hepatology (2016)

Bile duct loss during the course of drug-induced liver injury is uncommon, but can be an indication of vanishing bile duct syndrome (VBDS). In this work, we assess the frequency, causes, clinical features, and outcomes of cases of drug-induced liver injury with histologically proven bile duct loss. All cases of drug-induced liver injury enrolled into a prospective database over a 10-year period that had undergone liver biopsies (n = 363) were scored for the presence of bile duct loss and assessed for clinical and laboratory features, causes, and outcomes. Twenty-six of the 363 patients (7%) with drug-, herbal-, or dietary-supplement-associated liver injury had bile duct loss on liver biopsy, which was moderate to severe (<50% of portal areas with bile ducts) in 14 and mild (50%-75%) in 12. The presenting clinical features of the 26 cases varied, but the most common clinical pattern was a severe cholestatic hepatitis. The implicated agents included amoxicillin/clavulanate (n = 3), temozolomide (n = 3), various herbal products (n = 3), azithromycin (n = 2), and 15 other medications or dietary supplements. Compared to those without, those with bile duct loss were more likely to develop chronic liver injury (94% vs. 47%), which was usually cholestatic and sometimes severe. Five patients died and 2 others underwent liver transplantation for progressive cholestasis despite treatment with corticosteroids and ursodiol. The most predictive factor of poor outcome was the degree of bile duct loss on liver biopsy.Bile duct loss during acute cholestatic hepatitis is an ominous early indicator of possible VBDS, for which at present there are no known means of prevention or therapy. (Hepatology 2017;65:1267-1277).
75. MicroRNA-Based Multi-Tissue Detargeted Mengovirus Therapy for Multiple Myeloma
Authors: Autumn J. Ruiz, Elizabeth M. Hadac, Rebecca A. Nace, Stephen J. Russell
Journal: Molecular Therapy (2015)

Multiple myeloma is a plasma cell malignancy for which no cure is currently available. It is a disseminated cancer that is highly vascular, expresses minimal extracellular matrix, and is metabolically active making it an ideal candidate for oncolytic virotherapy. Oncolytic picornaviruses for cancer therapy have shown great promise in human clinical trials. Mengovirus is a novel picornavirus with potent oncolytic activity in a broad range of cancer cells, however it causes encephalitis and myocarditis. The pathogenesis of this virus can be attenuated by shortening a polycytidine tract in the 5' untranslated region (UTR), but the toxicity profile of this virus (MC24) in mice bearing multiple myeloma tumors is still suboptimal. In this study we enhanced the safety profile of MC24 by incorporating sequences complementary to miR-124 (enriched in nervous tissue), miR-133 and miR-208 (both enriched in cardiac tissue) in the 5' and 3' UTRs of the viral genome. All microRNA target sequences were tolerated by MC24 and the viral replication kinetics in HeLa cells was unaltered. miR-124 targets in the 5' UTR suppressed replication in the central nervous system. Insertions in the 3' UTR led to nonspecific suppression of viral pathogenicity. The combination of miR-133 and miR-208 targets in the 3' UTR resulted in suppressed viral replication in cardiac tissue. Finally, a dual-targeted virus, MC24-NC, eliminated the toxicity of the virus while maintaining oncolytic efficacy similar to unmodified MC24. 5 out of 10 immune competent BALB/c mice bearing subcutaneous murine multiple myeloma MPC-11 tumors developed hind-limb paralysis in the first five days following intratumoral treatment with MC24. In contrast no mice treated with MC24-NC developed hind-limb paralysis in the first five days. 2 out of 10 mice in both groups developed hind-limb paralysis between days 24 and 29 following treatment, however no infectious virus could be recovered from the nervous or cardiac tissues of these animals and all had developed metastatic tumor nodules. MC24-NC resulted in complete tumor regression in 4 out of 10 mice and significantly prolonged survival compared to saline treated mice. This study showed that dual-tropic microRNA-targeting of MC24 significantly improves the safety profile of the virus without altering the oncolytic activity.