tbuckley/cabot-search huggingface dataset:
The clonal origins of leukemic progression of myelodysplasia
Authors: T Kim, M S Tyndel, H J Kim, J-S Ahn, S H Choi, H J Park, Y-k Kim, D-H Yang, J-J Lee, S-H Jung, S Y Kim, Y H Min, J-W Cheong, S K Sohn, J H Moon, M Choi, M Lee, Z Zhang, D Kim
Journal: Leukemia (2017)
Gpx3 Determines Competitiveness of Normal and Leukemic Stem Cells.
Authors: Olivier Herault, Kristin J Hope, Eric Deneault, Matthias Trost, Nadine Mayotte, Jalila Chagraoui, Brian T Wilhelm, Sonia Cellot, Martin Sauvageau, Pierre Thibault, Guy Sauvageau
Journal: Blood (2010)
Selective G-Protein Estrogen Receptor (GPER) Activation Triggers Anti-Multiple Myeloma Activity and Synergizes with MiR-29b-Inducing Drugs
Authors: Nicola Amodio, Marzia Leotta, Eugenio Morelli, Teresa Calimeri, Anna Maria Gullà, Maria Angelica Stamato, Enrica Romeo, Umberto Foresta, Antonino Neri, Maria Teresa Di Martino, Pierosandro Tagliaferri, Pierfrancesco Tassone
Journal: Blood (2014)
Long Term Results of Pulmonary Endarterectomy (PEA) in Patients with Chronic Thromboembolic Pulmonary Hypertension (CTEPH). The Pavia Endarterectomy Program.
Authors: Franco Piovella, Andrea M. D’Armini, Marisa Barone, Vincenzo Emmi, Chiara Beltrametti, Mario Viganò
Journal: Blood (2007)
Two-Pore Channel Function Is Crucial for the Migration of Invasive Cancer Cells
Authors: Ong Nam Phuong Nguyen, Christian Grimm, Lina S. Schneider, Yu-Kai Chao, Carina Atzberger, Karin Bartel, Anna Watermann, Melanie Ulrich, Doris Mayr, Christian Wahl-Schott, Martin Biel, Angelika M. Vollmar
Journal: Cancer Research (2017)

Abstract Metastatic invasion is the major cause of cancer-related deaths. In this study, we introduce two-pore channels (TPC), a recently described class of NAADP- and PI(3,5)P2–sensitive Ca2+-permeable cation channels in the endolysosomal system of cells, as candidate targets for the treatment of invasive cancers. Inhibition of the channel abrogated migration of metastatic cancer cells in vitro. Silencing or pharmacologic inhibition of the two-pore channel TPC2 reduced lung metastasis of mammary mouse cancer cells. Disrupting TPC function halted trafficking of β1-integrin, leading to its accumulation in EEA1-positive early endosomes. As a consequence, invasive cancer cells were no longer able to form leading edges, which are required for adequate migration. Our findings link TPC to cancer cell migration and provide a preclinical proof of concept for their candidacy as targets to treat metastatic cancers. Cancer Res; 77(6); 1427–38. ©2017 AACR.
Lymphdx: A Custom Microarray for Molecular Diagnosis and Prognosis in Non-Hodgkin Lymphoma.
Authors: Sandeep S. Dave, G. Wright, B. Tan, A. Rosenwald, W. C. Chan, T. C. Greiner, D. D. Weisenburger, J. C. Lynch, J. M. Vose, J. O. Armitage, R. I. Fisher, R. M. Braziel, L. M. Rimsza, T. M. Grogan, T. P. Miller, M. LeBlanc, E. B. Smeland, S. Kvaloy, H. Holte, J. Delabie, H. K. Muller-Hermelink, G. Ott, R. D. Gascoyne, J. M. Connors, E. Campo, E. Montserrat, W. H. Wilson, E. S. Jaffe, T. A. Lister, A. J. Davies, A. J. Norton, R. Simon, L. Yang, J. Powell, J. Palma, J. Warrington, H. Zhao, M. Chiorazzi, L. M. Staudt
Journal: Blood (2004)
Rituximab for Graft-Versus-Host-Disease-Prophylaxis after Allogeneic Stem Cell Transplantation Given as Treatment of High Risk Relapse of Aggressive Lymphoma: Results of a Randomized Phase II Study.
Authors: Bertram Glass, Justin Hasenkamp, Anke Görlitz, Peter Dreger, Jörg Schubert, Gerald Wulf, Maike Nickelsen, Lorenz H. Truemper, Norbert Schmitz
Journal: Blood (2008)
Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expression
Authors: Qin-nan Chen, Xin Chen, Zhen-yao Chen, Feng-qi Nie, Chen-chen Wei, Hong-wei Ma, Li Wan, Shuai Yan, Sheng-nan Ren, Zhao-xia Wang
Journal: Molecular Cancer (2017)

Numerous studies have shown that long non-coding RNAs (lncRNAs) behave as a novel class of transcript during multiple cancer processes, such as cell proliferation, apoptosis, migration, and invasion. LINC00152 is located on chromosome 2p11.2, and has a transcript length of 828 nucleotides. The biological role of LINC00152 in LAD(lung adenocarcinoma) remains unknown.Quantitative reverse transcription PCR(qRT-PCR) was used to detect LINC00152 expression in 60 human LAD tissues and paired normal tissues. In vitro and in vivo studies showed the biological function of LINC00152 in tumour progression. RNA transcriptome sequencing technology was performed to identify the downstream suppressor IL24(interleukin 24) which was further examined by qRT-PCR, western bolt and rescue experiments. RNA immunoprecipitation (RIP), RNA pulldown, and Chromatin immunoprecipitation (ChIP) assays were carried out to reveal the interaction between LINC00152, EZH2 and IL24.LINC00152 expression was upregulated in 60 human LAD tissues and paired normal tissues. High levels of LINC00152 expression were correlated with advanced TNM stage, larger tumor size, and lymph node metastasis, as well as shorter survival time. Silencing of LINC00152 suppressed cell growth and induced cell apoptosis. LINC00152 knockdown altered the expression of many downstream genes, including IL24. LINC00152 could interact with EZH2 and inhibit IL24 transcription. Moreover, the ectopic expression of IL24 repressed cell proliferation and partly reversed LINC00152 overexpression-induced promotion of cell growth in LAD.Our study reveals an oncogenic role for LINC00152 in LAD tumorigenesis, suggesting that it could be used as a therapeutic target in LAD treatment.
Inhibition of heat shock protein 90 exerts an antitumour effect in angiosarcoma: involvement of the vascular endothelial growth factor signalling pathway
Authors: S. Yamada-Kanazawa, I. Kajihara, S. Fukushima, M. Jinnin, M. Masuzawa, M. Masuzawa, Y. Amoh, D. Hoshina, R. Abe, H. Ihn
Journal: British Journal of Dermatology (2017)

Angiosarcoma is a rare malignant neoplasm derived from endothelial cells, and because advanced angiosarcoma is resistant to standard chemotherapy its prognosis is poor. Therefore, new therapies are urgently needed. Heat shock protein (HSP)90 has been identified as a molecular chaperone that regulates various cancer-related proteins. Numerous clinical trials are currently testing the effectiveness of HSP90 inhibitors in various types of malignancies.To investigate the role of HSP90 in the pathogenesis of angiosarcoma and whether the inhibition of HSP90 may have antitumour activity.The expression of HSP90 protein in angiosarcoma was examined using immunohistochemistry and immunoblotting. The effects of HSP90 inhibition were proven using proliferation, migration and invasion assay in angiosarcoma cells. The mechanism of antitumour effect by HSP90 inhibition was investigated by the transfection of small interfering RNA (siRNA).The levels of HSP90 protein expression in cultured angiosarcoma cell lines were markedly increased compared with those in normal tissue cell lines. Immunohistochemical analyses revealed that the expression of HSP90 protein was strongly detected in angiosarcoma tissues compared with that in normal dermal vessels or senile angioma tissues. Ganetespib, an HSP90 inhibitor, with or without taxanes, inhibited the proliferation of angiosarcoma cells via apoptosis in a dose-dependent manner. HSP90 siRNA suppressed the proliferation, migration and invasion of angiosarcoma cells. Knock-down of HSP90 did not suppress vascular endothelial growth factor receptor 2 directly, but selectively suppressed several downstream targets of vascular endothelial growth factor signalling in angiosarcoma cells.HSP90 could be a novel therapeutic target for angiosarcoma.
Ph-Negative Chronic Myeloproliferative Neoplasms – Population Analysis, a Single Center 10-years’ Experience
Authors: Vasily Shuvaev, Irina Martynkevich, Alla Abdulkadyrova, Vera Udaleva, Tatyana Zamotina, Mikhail Fominykh, Regina Golovchenko, Irina Zotova, Dzhariyat Shikhbabaeva, Lyubov Polushkina, Kudrat Abdulkadyrov
Journal: Blood (2014)
The Hematopoietic Stem Cell (HSC) Compartment in Tristetraprolin (TTP) Knock-out Mice Is Abnormal Phenotypically but Normal Functionally.
Authors: Ian M Kaplan, Sebastien Morisot, Diane Heiser, Wen-Chih Cheng, Christina LaDana, Curt I. Civin
Journal: Blood (2009)
Circulating Tissue Factor Procoagulant Activity (TF-PCA) Is Elevated in Type 1 Diabetes Mellitus: Differential Regulation of TF-PCA in Type 1 and Type 2 Diabetes
Authors: Anamika Singh, Guenther Boden, Carol Homko, Jay Gunawardana, A. Koneti Rao
Journal: Blood (2011)
Long-Term Follow-up of Chronic Phase Chronic Myeloid Leukemia Patients Who Failed Interferon Alpha and Switched to Imatinib
Authors: Massimo Breccia, Giuseppina Loglisci, Adriano Salaroli, Alessandra Serrao, Irene Zacheo, Roberto Latagliata, Giuliana Alimena
Journal: Blood (2012)
Chronic Kidney Disease Induces a Reduction In Hematopoietic Stem –and Progenitor Cell Frequencies.
Authors: Melissa van Pel, Matthieu Monge, Michiel Siebelt, Marina M. Aleksinskaya, Hetty C. de Boer, Jacques Duijs, Coen van Solingen, Ziad Massy, Ton J. Rabelink, Willem E. Fibbe, Anton-Jan van Zonneveld
Journal: Blood (2010)
Mantle Cell Lymphoma International Prognostic Score Is Valid and Confirmed in Unselected Cohort of Patients Treated in Rituximab Era
Authors: David Salek, Ingrid Vasova, Robert Pytlik, David Belada, Tomas Papajik, Katerina Kubackova, Jan Pirnos, Ludmila Boudova, Roman Kodet, Petra Obrtlikova, Hana Krejcova, Marek Trneny
Journal: Blood (2008)
Proaerolysin Multi Color Flow-Fish Reveals Shortened Telomere Length in GPI− as Compared to GPI+ Granulocytes from Patients with Paroxysmal Nocturnal Hemoglobinuria (PNH).
Authors: Fabian Beier, Stefan Balabanov, Tom Buckley, M. Rojewski, T. Becker, Lothar Kanz, Hubert Schrezenmeier, Tim H. Brummendorf
Journal: Blood (2004)
Phase I Trial of CG53135-05 to Prevent Mucositis in Patients Undergoing High-Dose Chemotherapy (HDCT) and Autologous Peripheral Blood Stem Cell Transplantation (PBSCT).
Authors: Michael W. Schuster, Tsiporah B. Shore, June Greenberg, Bita Jalilizeinali, Scott Possley, Vincent I. Annino, William Hahne
Journal: Blood (2004)
FLT3 and JAK2 Mutations in Acute Myeloid Leukemia Promote Interchromosomal Homologous Recombination and the Potential for Copy Neutral Loss of Heterozygosity
Authors: Terry J. Gaymes, Azim Mohamedali, Anthony L. Eiliazadeh, David Darling, Ghulam J. Mufti
Journal: Cancer Research (2017)

Abstract Acquired copy neutral LOH (CN-LOH) is a frequent occurrence in myeloid malignancies and is often associated with resistance to standard therapeutic modalities and poor survival. Here, we show that constitutive signaling driven by mutated FLT3 and JAK2 confers interchromosomal homologous recombination (iHR), a precedent for CN-LOH. Using a targeted recombination assay, we determined significant iHR activity in internal tandem duplication FLT3 (FLT3-ITD) and JAK2V617F-mutated cells. Sister chromatid exchanges, a surrogate measure of iHR, was significantly elevated in primary FLT3-ITD normal karyotype acute myeloid leukemia (NK-AML) compared with wild-type FLT3 NK-AML. HR was harmonized to S phase of the cell cycle to repair broken chromatids and prevent iHR. Increased HR activity in G0 arrested primary FLT3-ITD NK-AML in contrast to wild-type FLT3 NK-AML. Cells expressing mutated FLT3-ITD demonstrated a relative increase in mutation frequency as detected by thymidine kinase (TK) gene mutation assay. Moreover, resistance was associated with CN-LOH at the TK locus. Treatment of FLT3-ITD– and JAK2V617F-mutant cells with the antioxidant N-acetylcysteine diminished reactive oxygen species (ROS), restoring iHR and HR levels. Our findings show that mutated FLT3-ITD and JAK2 augment ROS production and HR, shifting the cellular milieu toward illegitimate recombination events such as iHR and CN-LOH. Therapeutic reduction of ROS may thus prevent leukemic progression and relapse in myeloid malignancies. Cancer Res; 77(7); 1697–708. ©2017 AACR.
Moving From Discovery to System-Wide Change: The Role of Research in a Learning Health Care System: Experience from Three Decades of Health Systems Research in the Veterans Health Administration
Authors: David Atkins, Amy M. Kilbourne, David Shulkin
Journal: Annual Review of Public Health (2017)

The Veterans Health Administration is unique, functioning as an integrated health care system that provides care to more than six million veterans annually and as a home to an established scientific enterprise that conducts more than $1 billion of research each year. The presence of research, spanning the continuum from basic health services to translational research, has helped the Department of Veterans Affairs (VA) realize the potential of a learning health care system and has contributed to significant improvements in clinical quality over the past two decades. It has also illustrated distinct pathways by which research influences clinical care and policy and has provided lessons on challenges in translating research into practice on a national scale. These lessons are increasingly relevant to other health care systems, as the issues confronting the VA—the need to provide timely access, coordination of care, and consistent high quality across a diverse system—mirror those of the larger US health care system.
VO2/DO2 relationship III
Authors: P. F. Laterre, A. Dougnac, G. Hanique, Th. Dugemier, M. Andresen, J. Roeseler, M. S. Reynaert, J. Solé, F. Baigorri, A. De Monte, R. Fernàndez, L. Blanch, J. Mestre, A. Artigas, C. Simon, F. Salis, A. Roman, J. L. Vincent, P. Van der Linden, A. Deltell, I. Rausin, Y. Bekkrar, N. Caruso, D. De Bels, D. Henin, M. Evenepoel, O. Deckers
Journal: Intensive Care Medicine (1992)
In Vivo Lentiviral Marking Demonstrates Long-Term Myeloid and Lymphoid Lineage Contribution of Individual Hematopoietic Stem Cell Clones to Murine Steady-State Hematopoiesis.
Authors: Oksana Zavidij, Claudia R Ball, Sylvia Fessler, Daniela Belle, Manfred Schmidt, Christof von Kalle, Hanno Glimm
Journal: Blood (2009)
Outcomes of Patients with Haematological Malignancies Admitted to Either High Dependency Unit (HDU) or Intensive Care Unit (ICU) with or without Haemopoeitic Stem Cell Transplantation (HSCT): Analysis of Prognostic Factors for Survival
Authors: Youssef Sorour, Stephen J Webber, Josh G Wright, Nicholas J Morley, John T Reilly, Christopher D Dalley, John A Snowden
Journal: Blood (2008)
Monozygotic Twins with Childhood ALL Demonstrate Prenatal Origin of the Philadelphia Chromosome and Post-Natal Ikaros Deletion.
Authors: Giovanni Cazzaniga, Luca Lo Nigro, Joannah Score, Silvia Bungaro, Fred van Delft, Ilaria Iacobucci, Lilia Corral, Elena Mirabile, Anthony Ford, Giovanni Martinelli, Nicholas C.P. Cross, Mel Greaves, Andrea Biondi
Journal: Blood (2009)
CD30 ligand (CD30L) ln acute myeloid leukemias (AMLs) correlates with the detection of interleukin-4 (IL-4) receptors (RS) on blast cells and is associated with CD30 expression and IL4 production by residual normal T cells.
Authors: [No Value] Gattei, M Degan, FM Rossi, FT Mazzocco, R Di Francia, D Aldinucci, L Tuyt, T Pinto
Journal: Blood (1999)
Laboratory of genetics and physiology 2 (LGP2) plays an essential role in hepatitis C virus infection‐induced interferon responses
Authors: Lei Hei, Jin Zhong
Journal: Hepatology (2017)

Retinoic acid-inducible gene I (RIG-I)-like receptors are cytosolic pattern recognition receptors (PRRs) that detect non-self-RNA and activate downstream interferon (IFN) signaling. One of the RIG-I-like receptors, laboratory of genetics and physiology 2 (LGP2), was originally thought to be a negative feedback regulator in the RIG-I signaling pathway, but growing evidence indicates that LGP2 is one cofactor of melanoma differentiation-associated protein 5 (MDA5) in MDA5-mediated IFN signaling activation. Our previous work showed that MDA5 was the major PRR to sense hepatitis C virus (HCV) infection in hepatocytes, but the role of LGP2 in HCV infection-induced IFN signaling has not been elucidated. In this study, we reported that LGP2 was a positive regulator of HCV infection-induced IFN signaling. Knockout of LGP2 in hepatocytes significantly diminished IFN production in response to HCV infection, but not to HCV 3'untranslated region RNA transfection. Mechanistic studies showed that LGP2 exerted its function at a step upstream of MDA5 in the IFN signaling. HCV infection promoted the molecular interaction between LGP2 and MDA5, which, in turn, enhanced MDA5/HCV RNA association. Finally, we demonstrated that the ATPase activity of LGP2 was critical for assisting MDA5/HCV RNA interaction and activating IFN signaling during HCV infection.Our work demonstrated that LGP2 plays an essential role in activating IFN signaling against HCV infection by promoting MDA5 recognition of HCV pathogen-associated molecular patterns. (Hepatology 2017;65:1478-1491).
Central Nervous System and Intracranial Myeloma: a Retrospective Italian Multicenter Study.
Authors: Alessandro Gozzetti, Stefania Oliva, Fabiana Gentilini, Elena Marchini, Maria Teresa Petrucci, Francesca Patriarca, Alessandro Petrucci, Luisa Giaccone, Elena Zamagni, Mariella Genuardi, Michele Cavo, Antonio Palumbo, Davide Rossi, Massimo Offidani, Alfonso Cerase, Lorenzo De Paoli, Michele Floridia, Giuseppe Mele, Monica Galli, Salvatore Beretta, Francesco Di Raimondo, Roberto Vallone, Francesco Lauria
Journal: Blood (2009)
Treg Depletion with Interleukin-2-Diphteriatoxin (IL-2DT) Is Sufficient to Induce Tumor Clearance in Acute Myeloid Leukemia (AML)
Authors: Christoph Bucher, Johanna Zhou, Heidi Mondale, Meghan Johnson, Luna Liu, Christine Vogtenhuber, Chris Lees, Yoichiro Iwakura, Daniel A Vallera, Brenda Weigel, Bruce R. Blazar
Journal: Blood (2008)
Pivotal Role of Survivin in Leukemogenesis by E2A-HLF Chimeric Transcription Factor.
Authors: Mayuko Okuya, Hidemitsu Kurosawa, Takayuki Matsunaga, Mitsuoki Eguchi, Yusuke Furukawa, Takeshi Inukai, Hirotaka Matsui, A. Thomas Look, Toshiya Inaba
Journal: Blood (2005)
Change in Chronic Low-Grade Nonhematologic Adverse Events (AEs) and Quality of Life (QoL) in Adult Patients (pts) with Philadelphia Chromosome–Positive (Ph+) Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Switched From Imatinib (IM) to Nilotinib (NIL)
Authors: Jorge E. Cortes, Jeffrey H. Lipton, Carole B. Miller, Sikander Ailawadhi, Luke Akard, Javier Pinilla-Ibarz, Felice P. Lin, Solveig G. Ericson, Michael J. Mauro
Journal: Blood (2012)
Type and Number of Secondary Molecular Lesions Improve Outcome Prediction in Acute Myeloid Leukemia (AML) with inv(16) or t(16;16): A Study of the German-Austrian AML Study Group (AMLSG).
Authors: Peter Paschka, Juan Du, Richard F. Schlenk, Verena I. Gaidzik, Lars Bullinger, Andrea Corbacioglu, Manuela Zucknick, Axel Benner, Frank Stegelmann, Daniela Späth, Sabine Kayser, Brigitte Schlegelberger, Jürgen Krauter, Arnold Ganser, Hartmut Döhner, Konstanze Döhner
Journal: Blood (2009)
EPCR promotes breast cancer progression by altering SPOCK1/testican 1-mediated 3D growth
Authors: Naiara Perurena, Carolina Zandueta, Susana Martínez-Canarias, Haritz Moreno, Silvestre Vicent, Ana S. Almeida, Elisabet Guruceaga, Roger R. Gomis, Marta Santisteban, Mikala Egeblad, José Hermida, Fernando Lecanda
Journal: Journal of Hematology & Oncology (2017)

Activated protein C/endothelial protein C receptor (APC/EPCR) axis is physiologically involved in anticoagulant and cytoprotective activities in endothelial cells. Emerging evidence indicates that EPCR also plays a role in breast stemness and human tumorigenesis. Yet, its contribution to breast cancer progression and metastasis has not been elucidated. Transcriptomic status of EPCR was examined in a cohort of 286 breast cancer patients. Cell growth kinetics was evaluated in control and EPCR and SPARC/osteonectin, Cwcv, and kazal-like domains proteoglycan (SPOCK1/testican 1) silenced breast cancer cells in 2D, 3D, and in co-culture conditions. Orthotopic tumor growth and lung and osseous metastases were evaluated in several human and murine xenograft breast cancer models. Tumor-stroma interactions were further studied in vivo by immunohistochemistry and flow cytometry. An EPCR-induced gene signature was identified by microarray analysis. Analysis of a cohort of breast cancer patients revealed an association of high EPCR levels with adverse clinical outcome. Interestingly, EPCR knockdown did not affect cell growth kinetics in 2D but significantly reduced cell growth in 3D cultures. Using several human and murine xenograft breast cancer models, we showed that EPCR silencing reduced primary tumor growth and secondary outgrowths at metastatic sites, including the skeleton and the lungs. Interestingly, these effects were independent of APC ligand stimulation in vitro and in vivo. Transcriptomic analysis of EPCR-silenced tumors unveiled an effect mediated by matricellular secreted proteoglycan SPOCK1/testican 1. Interestingly, SPOCK1 silencing suppressed in vitro 3D growth. Moreover, SPOCK1 ablation severely decreased orthotopic tumor growth and reduced bone metastatic osteolytic tumors. High SPOCK1 levels were also associated with poor clinical outcome in a subset breast cancer patients. Our results suggest that EPCR through SPOCK1 confers a cell growth advantage in 3D promoting breast tumorigenesis and metastasis. EPCR represents a clinically relevant factor associated with poor outcome and a novel vulnerability to develop combination therapies for breast cancer patients.
The Pharmacokinetics, Safety and Lack of Antibody Production from Multiple Doses of Intravenous Pegylated Asparaginase in Adults with Newly Diagnosed Acute Lymphoblastic Leukemia.
Authors: Dan Douer, Kristy Watkins, Niyati Nathwani, Alexandra M. Levine, Prakash N. Tiwari, Vassilos I. Avramis
Journal: Blood (2006)
STAT3/NF-κB-Regulated Lentiviral TK/GCV Suicide Gene Therapy for Cisplatin-Resistant Triple-Negative Breast Cancer
Authors: Wei-Ying Kuo, Luen Hwu, Chun-Yi Wu, Jhih-Shian Lee, Chi-Wei Chang, Ren-Shyan Liu
Journal: Theranostics (2017)

Triple-negative breast cancer (TNBC) represents approximately 20% of all breast cancers and appears resistance to conventional cytotoxic chemotherapy, demonstrating a particularly poor prognosis and a significantly worse clinical outcome than other types of cancer. Suicide gene therapy has been used for the in vivo treatment of various solid tumors in recent clinical trials. In tumor microenvironment, STAT3/NF-κB pathways are constitutively activated in stromal cells as well as in cancer stem cells (CSCs). In this study, we have cloned a novel STAT3/NF-κB-based reporter system to drive the expression of herpes simplex virus thymidine kinase (HSV-TK) against breast cancer. Lentiviral vector expressing HSV-TK under the regulation of STAT3/NF-κB fused response element was developed. In this setting, we exploited the constitutive STAT3/NF-κB activation in tumors to achieve higher transgene expression than that driven by a constitutively active CMV promotor in vivo. An orthotropic MDA-MB-231 triple negative breast cancer mouse model was used for evaluating the feasibility of STAT3-NF-κB-TK/GCV suicide gene therapy system. The basal promoter activity of Lenti-CMV-TK and Lenti-STAT3-NF-κB-TK in MDA-MB-231 cells was compared by 3H-FEAU uptake assay. The Lenti-CMV-TK showed ~5 fold higher 3H-FEAU uptake then Lenti -STAT3-NF-κB-TK. In clonogenic assay, cells expressing Lenti-CMV-TK were 2-fold more sensitive to GCV than Lenti-STAT3-NF-κB-TK transduced cells. In vitro effect of STAT3-NF-κB-induced transgene expression was determined by 10ng/mL TNF-α induction and confirmed by western blot analysis and DsRedm fluorescent microscopy. In vivo evaluation of therapeutic effect by bioluminescence and [18F]FHBG microPET imaging indicated that Lenti-STAT3-NF-κB-TK showed more tumor growth retardation than Lenti-CMV-TK when GCV (20 mg/kg) was administered. The invasiveness and expression of cancer stem cell markers were both decreased after STAT3/NF-κB-regulated HSV-TK/GCV therapy. Moreover, STAT3/NF-κB signaling targeting could further sensitize tumor cells to cisplatin. This study successfully established a theranositic approach to treat triple-negative breast cancer via STAT3-NF-κB responsive element-driven suicide gene therapy. This platform may also be an alternative strategy to handle with drug-resistant cancer cells.