tbuckley/cabot-search huggingface dataset:
Blood Cells Dynamic and Thrombo-Haemorragic Events in Low Risk Essential Thrombocytosis Patients. A North Italian and Austrian Study.
Authors: Andrea Piccin, Michael Steurer, Manfred Mitterer, Elisabeth Blöchl, Luigi Marcheselli, Irene Pusceddu, Alessandra Marabese, Irene Bertozzi, Maria Luigia Randi, Elena Elli, Enrico Maria Pogliani, Dino Veneri, Omar Perbellini, Enrica Pacquola, Michele Gottardi, Mario Tiribelli, Anna Guella, Barbara Inella, Paolo Vivaldi, Ercole De Biasi, Rosaria Sancetta, Renato Bassan, Filippo Gherlinzoni, Giovanni Pizzolo, Gunther Gastl, Sergio Cortelazzo
Journal: Blood (2012)
PACIENTES CON CRITERIOS ESTANDAR DE CANCER GASTRICO PRECOZ: UTILIDAD DIAGNOSTICOTERAPEUTICA DE LA MUCOSECTOMIA ENDOSCOPICA CON BANDAS
Authors: J Espinel Diez, E Pinedo, N Fernandez
Journal: Endoscopy (2015)

Introducción: El cáncer gástrico precoz (CGP) es aquel limitado a la mucosa o submucosa, independientemente de la existencia de metástasis ganglionares. La Resección Endoscópica (RE) permite un tratamiento mínimamente invasivo y es su principal método de estadificación. La Mucosectomía está indicada en pacientes que cumplen criterios estándar.
Lenalidomide Targets Myeloma Cells Preferentially During Prolonged Early G1 Arrest but Not Synchronization Into S Phase by Selective and Reversible Inhibition of CDK4/CDK6 through Loss of IRF-4
Authors: Xiangao Huang, Maurizio Di Liberto, David Jayabalan, Mohamad Hussein, Sophia Randolph, Ruben Niesvizky, Selina Chen-Kiang
Journal: Blood (2010)
A Novel Mouse Model to Study Image-Guided, Radiation-Induced Intestinal Injury and Preclinical Screening of Radioprotectors
Authors: Ioannis I. Verginadis, Rahul Kanade, Brett Bell, Sravya Koduri, Edgar Ben-Josef, Constantinos Koumenis
Journal: Cancer Research (2016)

Abstract Radiation is an important treatment modality for gastrointestinal tumors, but intestinal injury is a common side effect. Here we describe a physiologically relevant model for studying the molecular determinants of radiation-induced intestinal damage and testing novel radioprotectors. The model employs a radiopaque marker implanted into the surface of the mouse jejunum, serving as a fiducial marker for precise radiation targeting. Mice were imaged with Cone-Beam CT (CBCT) and irradiated (IR) to the marked area using the Small Animal Radiation Research Platform (SARRP). IR-induced damage was acute but reversible and largely restricted to the area of the marker, leaving the surrounding tissues intact. Although whole gut irradiation with these doses caused lethal GI syndrome, focal (5 mm) radiation of the intestine did not cause any weight loss or lethality. However, fibrosis and collagen deposition 4 months post-IR indicated chronic intestinal damage. A separate cohort of mice was treated daily with curcumin, a clinically tested radioprotector, prior to and post-IR. Curcumin-treated mice showed significant decreases in both local and systemic inflammatory cytokine levels and in fibrosis, suggesting it is an effective radioprotector of the intestine. Our results indicate that this model, which emulates clinically relevant intestinal radiation-induced injury, can be used to assess radioprotectors prior to testing in the clinic. Cancer Res; 77(4); 908–17. ©2016 AACR.
Expression and Role of hERG1 Channels in Pediatric Acute Lymphoblastic Leukemias: Shortcoming of Drug Resistance by hERG1 Channel Inhibitors in Stoma-Supported Leukaemia Cell Cultures In Vitro.
Authors: Serena Pillozzi, Benedetta Accordi, Marinella Veltroni, Marika Masselli, Elisa Pancrazzi, Giuseppe Gaipa, Alma Lippi, Gabriella Bernini, Giuseppe Basso, Annarosa Arcangeli
Journal: Blood (2007)
CXCL13 and tertiary lymphoid structures formation in the anti-breast cancer immune response
Authors: E. Migliori, C. Gu-Trantien, S. Garaud, L. Buisseret, H. Duvillier, J.-N. Lodewyckx, L. Van Schoonwinkel, A. Boisson, K. Willard-Gallo
Journal: Annals of Oncology (2015)
Abstract 1008: Cytoplasmic p53 protects against MG132-induced apoptosis in a cell state-dependent manner
Authors: Ho Wa (Jacky) Cheng, Aster Legesse-Miller
Journal: Cancer Research (2015)

Abstract Since the approval of proteasome inhibitor, Bortezomib, for use in multiple myeloma in 2003, pharmacological proteasome inhibitors has been shown to be an important strategy for treating many types of cancer. While proteasome inhibitors induce apoptosis in certain rapidly proliferating cancer cells, some cells enters quiescence and survives. The mechanism by which quiescent cells become resistant to proteasome inhibitors is largely unknown. The tumor suppressor protein p53 plays an essential role in establishing and maintain quiescence in human cells. It also regulates several cell survival mechanisms, including cell cycle arrest, autophagy, and activation of reactive oxygen detoxifying enzymes. Here, we investigated the role of p53 in establishing resistance against proteasome inhibitors in quiescent cells. We found that MG132 (a know proteasome inhibitor) treatment induces the accumulation of p53 and its downstream target p21 more in quiescent cells than in proliferating primary human fibroblasts. shRNA mediated down-regulation of p53 sensitizes both proliferating and quiescent fibroblasts to MG132-mediated apoptosis and cell death, suggesting that p53 plays a protective role in all cell states. Additional experiments demonstrated that proliferating fibroblasts are susceptible to inhibition of cytoplasmic p53 activity, whereas quiescent fibroblasts are sensitive to inhibition of nuclear p53 activity. These findings suggest that p53 induces different protective mechanisms against MG132-mediated cell death, depending of the proliferative state of the cells. Autophagy, an alternative degradation pathway regulated by p53, is also induced in both cell states upon MG132 treatment. Identification of p53-mediated regulatory mechanisms that are activated in quiescent cells in response to proteasome inhibition may help to suggest strategies for improving the effectiveness of proteasome inhibitors in treating cancer. This work was supported by NCI K01 CA128887 to Aster Legesse-Miller. Citation Format: Ho Wa (Jacky) Cheng, Aster Legesse-Miller. Cytoplasmic p53 protects against MG132-induced apoptosis in a cell state-dependent manner. [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 1008. doi:10.1158/1538-7445.AM2015-1008
Abstract 4496: Genomics-based resistome analysis revealed endogenous adenosine kinase levels as a chief determinant of specificity for a novel nucleoside analog lymphoma inhibitor
Authors: Utthara Nayar, Jonathan Reichel, Jouliana Sadek, Denise Hernandez-Hopkins, Gunkut Akar, Hufeng Zhou, Michelle A. Sahai, Peter Barelli, Ilaria Guasparri, Jennifer Totonchy, Duane Hassane, Shizuko Sei, Robert H. Shoemaker, J. David Warren, Olivier Elemento, Kenneth M. Kaye, Ethel Cesarman
Journal: Cancer Research (2015)

Abstract We used KSHV-infected primary effusion lymphoma (PEL) cells as a model to search for novel drugs through a combination of screening and genomic approaches. We discovered 6-ethylthioinosine (6-ETI), a nucleoside analog, as a highly effective and selective inhibitor of PEL. This compound induces necrosis accompanied by S-phase arrest without affecting known oncogenic viral proteins. To understand the selectivity towards PEL, we performed unbiased genomic analysis of 6-ETI-resistant subclones using RNASeq, which revealed that 6-ETI is activated through phosphorylation by cellular adenosine kinase (ADK). PEL cell lines have higher basal levels of ADK than resistant lymphoma cell lines, and resistant lymphoma cell lines could be sensitized by cell crowding-induced ADK upregulation. Finally, 6-ETI was shown to be highly efficacious against incipient and established tumors in a mouse model of PEL, with no apparent toxicity. Thus, we have successfully used RNASeq-based “resistome” analysis to identify the mechanism of specificity for a new and preclinically effective nucleoside analog. Citation Format: Utthara Nayar, Jonathan Reichel, Jouliana Sadek, Denise Hernandez-Hopkins, Gunkut Akar, Hufeng Zhou, Michelle A. Sahai, Peter Barelli, Ilaria Guasparri, Jennifer Totonchy, Duane Hassane, Shizuko Sei, Robert H. Shoemaker, J. David Warren, Olivier Elemento, Kenneth M. Kaye, Ethel Cesarman. Genomics-based resistome analysis revealed endogenous adenosine kinase levels as a chief determinant of specificity for a novel nucleoside analog lymphoma inhibitor. [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 4496. doi:10.1158/1538-7445.AM2015-4496
Detection of T-Cell Clonality in Bone Marrow in Peripheral T-Cell Lymphoma, Not Otherwise Specified
Authors: Natalia G. Chernova, Yulia V. Sidorova, Natalia V. Ryzhikova, Svetlana Yu. Smirnova, Hunan L. Julhakyan, Andrey B. Sudarikov, Yulia E. Vinogradova, Alla M. Kovrigina, Eugene E. Zvonkov, Elena N. Parovichnikova, Valeri G. Savchenko
Journal: Blood (2015)
A Report of Transplantation of 224 Patients with Beta Thalassemia Major in Tehran, 1991– 2004.
Authors: Ardeshir Ghavamzadeh, Mohamad Jahani, Kamran Alimoghaddam, Masoud Iravani, Babak Bahar, Asadolah Mousavi, Simin Gholibeikian, Shervin Pejhan, Zahra Orouji, Nima Babhadiashar, Asieh Ashouri
Journal: Blood (2004)
Abstract 2070: Stxbp4 suppresses APC/C mediated turnover of p63 and increases tumorigenicity and malignancy
Authors: Yukihiro Otaka, Susumu Rokudai, Kyoichi Kaira, Kimihiro Shimizu, Masashi Ito, Ami Ichihara, Reika Kawabata, Shinji Yoshiyama, Arito Yamane, Takayuki Asao, Carol Prives, Masahiko Nishiyama
Journal: Cancer Research (2015)

Abstract p63 plays a pivotal role in epithelial development and maintenance of epithelial proliferative potential. The delN isoforms of p63 are thought to be involved in both basal-epidermal gene expression and maintenance of epithelial progenitor proliferative potential. It is also thought that delN versions of p63 and p73 can serve to inhibit the abilities of their TA isoform counterparts to induce cell cycle arrest and apoptosis. Consistent with this, after DNA damage or during terminal differentiation, delNp63 proteins are quickly down regulated. Although p53 is frequently mutated in human cancers, p63 mutation is rare and it overexpresses especially in squamous carcinomas, such as lung, bladder, breast, and head and neck squamous cell carcinoma. Indeed several report concluded that immuno histochemistry with delNp63 is a powerful ancillary method for classifying lung adenocarcinoma and squamous carcinoma, a distinction with important therapeutic implications. We previously reported that APC/C plays a role in ubiquitin-mediated turnover of delNp63 and that Stxbp4 suppresses the degradation of delNp63 by the APC/C and Rack1-VHL. Importantly, both Stxbp4 and APC/C degradation-resistant delNp63 suppress the terminal differentiation process in 3D organotypic culture model as well as in vitro culture. To investigate the effect and the mechanism of delNp63 for tumorigenicity and malignancy in Lung squamous carcinoma, we examined a transcriptome analysis (RNA-seq) of delNp63 and Stxbp4 with NGS (Next Generation Sequencer) and generated xenograft mice model. Thus, our study provides insight into a novel mechanism for delNp63 in regulating tumorigenicity and malignancy in squamous cell carcinoma as well as epitherial development. Citation Format: Yukihiro Otaka, Susumu Rokudai, Kyoichi Kaira, Kimihiro Shimizu, Masashi Ito, Ami Ichihara, Reika Kawabata, Shinji Yoshiyama, Arito Yamane, Takayuki Asao, Carol Prives, Masahiko Nishiyama. Stxbp4 suppresses APC/C mediated turnover of p63 and increases tumorigenicity and malignancy. [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 2070. doi:10.1158/1538-7445.AM2015-2070
Final survival results of the randomized phase III study of trabectedin with pegylated liposomal doxorubicin (PLD) versus PLD in recurrent ovarian cancer.
Authors: B. J. Monk, T. J. Herzog, S. B. Kaye, C. N. Krasner, J. B. Vermorken, F. Muggia, E. Pujade-Lourraine, P. Zintl, T. V. Parekh, A. Poveda
Journal: Journal of Clinical Oncology (2011)

5046 Background: Trabectedin (T) in combination with pegylated liposomal doxorubicin (PLD) was demonstrated to improve progression-free survival (PFS) and overall response rate (ORR) in comparison to PLD alone as a second-line treatment of recurrent ovarian cancer (J Clin Oncol 28:3107-14, 2010). We report the protocol defined final analysis of overall survival (OS). Methods: Women ≥18 years, stratified by performance status (0-1 vs 2) and platinum-free interval (PFI) <6 vs > 6 months(m), were randomly assigned to receive an IV infusion of PLD 30 mg/m2 followed by a 3-hour infusion of T 1.1 mg/m2 every 3 weeks or PLD 50 mg/m2 every 4 weeks. The primary endpoint was PFS by independent radiology assessment and secondary endpoints included OS and ORR. Results: The final OS analysis was performed on 12 Nov 2010. The median follow-up was 47.4m. Among the 672 randomized subjects, 522 (77.7%) deaths were observed (258 in the T+PLD arm and 264 in the PLD arm). The median OS for T+PLD and PLD arms was 22.2 and 18.9m, respectively (HR= 0.86; 95%CI: 0.72, 1.02; p=0.0835 [unstratified log-rank test]). There was an unanticipated imbalance in the PFI between the two arms favoring the PLD arm (mean PFI: PLD=13.3m, T+D=10.6m. To provide a better estimate of the true treatment effect of adding T to PLD, a multivariate analysis adjusted for key prognostic factors (including PFI) was performed which demonstrated a significant improvement in OS in subjects treated with the combination (HR=0.82; 95%CI: 0.69,0.98; p=0.0285). Consistent improvement in OS was seen across all PFI subgroups, which was more pronounced in 6-12PFI subgroup (Table). Conclusions: T+PLD combination showed an improvement in OS in recurrent ovarian cancer compared with PLD alone. Randomized trials of T+PLD versus platinum combinations are indicated. Subgroup analysis by PFI. Subgroup by PFI (m) Median PLD (m) Median T+PLD (m) HR (95%CI) 0-6 12.3 14.2 0.94 (0.71, 1.25) 6-12 16.4 22.4 0.64 (0.47, 0.86) >12 31.7 36.5 0.83 (0.59, 1.16)
Interaction of Human Mesenchymal Stem Cells with Alloantigen-Induced T Lymphocyte Activation Favors the Differentiation of CD4+ T Cell Subsets Expressing CD25 and/or CTLA4 Molecules.
Authors: Rita Maccario, Marina Podestà, Antonia Moretta, Angela Cometa, Patrizia Comoli, Daniela Montagna, Adalberto Ibatici, Giovanna Piaggio, Sarah Pozzi, Francesco Frassoni, Franco Locatelli
Journal: Blood (2004)
The Use of Erythropoietic-Stimulating Agents (ESAs) with Ruxolitinib in Patients with Primary Myelofibrosis (PMF), Post-Polycythemia Vera Myelofibrosis (PPV-MF), and Post-Essential Thrombocythemia Myelofibrosis (PET-MF).
Authors: Mary Frances McMullin, Claire N Harrison, Dietger Niederwieser, Hilde Demuynck, Nadja Jakel, Andres Sirulnik, Mari McQuity, Viktoriya Stalbovskaya, Christian Recher, Koen Theunissen, Heinz Gisslinger, Jean-Jacques Kiladjian, Haifa-Kathrin Al- Ali
Journal: Blood (2012)
Peripolesis of Fibroblasts around Megakaryocytes: A New Pathological Cellular Interaction Leading to Megakaryocyte Para-Apoptosis in Gata1low Mice.
Authors: Maria Zingariello, Domenico Bosco, Barbara Ghinassi, Rosa Alba Rana, Francesco Antonio Manzoli, Anna Rita Migliaccio
Journal: Blood (2006)
A novel concept of adoptive immunotherapy using interleukin-2-stimulated liver natural killer cells for treatment of liver transplantation with hepatocellular carcinoma.
Authors: M. Ohira, S. Nishida, P. Tryphonopoulos, A. Tekin, G. Selvaggi, J. Moon, D. Levi, L. G. Feun, P. Ruiz, C. Ricordi, K. Ishiyama, H. Ohdan, A. Tzakis
Journal: Journal of Clinical Oncology (2011)

e13006 Background: Tumor recurrence is the main limitation of liver transplantation (LT) in patients with hepatocellular carcinoma (HCC) and can be promoted by immunosuppressants. However, there is no prevention or treatment for HCC recurrence after LT. Here, we describe a novel concept of adoptive immunotherapeutic approach that uses natural killer (NK) cells derived from deceased donor liver graft perfusate to prevent tumor recurrence after LT. Methods: To determine whether NK cells extracted from deceased donor liver graft perfusate acquire anti-tumor effect, we demonstrated the phenotypical and functional properties of activated liver NK cells under current Good Manufacturing Practice (cGMP) conditions. Results: Liver mononuclear cells (LMNC) that were extracted from deceased donor liver graft perfusate contained a large percentage of NK cells (45.0 ± 4.0 %) compared with peripheral blood mononuclear cells (PBMC) (21.8 ± 5.2 %) from the same donor. The CD69 activation marker and the natural cytotoxicity receptors, NKp44 and NKp46, were expressed at high levels in freshly isolated liver NK cells. Furthermore, interleukin (IL)-2-stimulated NK cells showed greater upregulation of activation markers and the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which is critical for NK cell-mediated anti-tumor cell death and increased production of interferon. Moreover, IL-2 stimulation induced LMNC to exhibit a stronger cytotoxicity against NK-susceptible K562 target cells compared with PBMC (p < 0.01). Finally, we also showed that the final product contained a very low T-cell contamination (0.02 × 106 cells×kg-1), which could be acceptable in allogeneic cell transplantation. Conclusions: It was strongly suggested that the adoptive transfer of IL-2 stimulated NK cells from deceased donor liver graft perfusate could be safe and effective in LT patients with HCC.
Stable MAGEC1/CT7 Inhibition by Short Hairpin RNA (shRNA) Does Not Affect Tumor Cell Proliferation and Invasive Potential in Sko-007 Multiple Myeloma Cell Line.
Authors: Fabricio de Carvalho, Anamaria A. Camargo, Érico T. Costa, Cibele Masotti, Valéria C.C. Andrade, Bryan E. Strauss, Otávia L. Caballero, Gisele W.B. Colleoni
Journal: Blood (2009)
Abstract 2699: Targeting GSK-3: a novel approach to enhance glioblastoma chemosensitivity
Authors: Andrey Ugolkov, Oleksii Dubrovskyi, Irina Gaisina, Alex Yemelyanov, Gennadiy Bondarenko, Charles James, James Chandler, Thomas O'Halloran, Alan Kozikowski, Jeffry Raizer, Andrew Mazar
Journal: Cancer Research (2015)

Abstract Glioblastoma (GBM) is, in essence, an incurable cancer, with most patients surviving 12-15 months following initial diagnosis. Previously published studies identified Glycogen Synthase Kinase-3 (GSK-3) as a new therapeutic target in GBM. Because GSK-3beta is a positive regulator of NF-kappaB-mediated survival and chemoresistance in cancer cells, we hypothesize that the inhibition of GSK-3 may overcome NF-kappaB-mediated chemoresistance to conventional drugs in human GBM. Using IVIS imaging of live mice, we found that: 1) NF-kappaB is constitutively active in orthotopic GBM patient-derived xenograft (PDX) tumors expressing an NF-kappa luciferase reporter; and 2) a single intravenous injection of our novel GSK-3 inhibitor 9-ING-41 (25 mg/kg) significantly reduced NF-kappaB transcriptional activity in orthotopic GBM PDX. Using 3 different orthotopic GBM PDX- tumor models, enabled for bioluminescence imaging through luciferase modification, we evaluated antitumor effects of 9-ING-41, alone as well as in combination with irinotecan, CCNU and temozolomide. Our in vivo results revealed that treatment with a combination of 9-ING-41 and irinotecan delays GBM PDX tumor growth, relative to either agent as a monotherapy, and, even more promising, 9-ING-41+CCNU leads to a complete tumor regression. Histological evaluation of mouse brain confirmed the absence of cancer cells and a formation of cyst at the location of intracranial tumor in mice treated with 9-ING-41+CCNU. Our results provide a rationale to advance 9-ING-41 for clinical evaluation in treating GBM, especially when combined with CCNU cytotoxic therapy. Citation Format: Andrey Ugolkov, Oleksii Dubrovskyi, Irina Gaisina, Alex Yemelyanov, Gennadiy Bondarenko, Charles James, James Chandler, Thomas O'Halloran, Alan Kozikowski, Jeffry Raizer, Andrew Mazar. Targeting GSK-3: a novel approach to enhance glioblastoma chemosensitivity. [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 2699. doi:10.1158/1538-7445.AM2015-2699
662. An Oncolytic Adenovirus Gene Therapy Targeting Both Tumor Cell Survival and Desmoplasia in Pancreatic Cancer
Authors: Ioanna Milenova, Emma Eriksson, Rafael Moreno, Ramon Alemany, Angelica Loskog
Journal: Molecular Therapy (2016)

The tumor microenvironment (TEM) supports the growth of tumor cells. In pancreatic cancer, the tumor lesions consist mostly of stellate cells, immune cells and extracellular matrix, a condition referred to as desmoplasia. The tumor cells can be less than twenty percent of the lesion. IL6 is overexpressed in pancreatic cancer and drives STAT3 activation leading to transforming growth factor (TGF) beta production and, hence, production of collagen type 1. TGF beta in the TEM also promotes immunosuppression by direct inhibition of T cells and expansion of T regulatory cells (Tregs). Hence, IL6 is one of the regulators of desmoplasia and is associated to poor prognosis of pancreatic cancer. To address the IL6 pathway as a target as well as the ongoing immunosuppression in pancreatic cancer, we developed a novel oncolytic adenovirus gene therapy expressing both an anti-IL6 receptor antibody single chain fragment (aIL6R scFv) and a trimerized membrane-bound CD40 ligand (TMZ-CD40L). LOAd713 is an Ad5/35 virus containing E2F binding sites that control the expression of an E1a gene deleted at the pRB-binding domain to achieve replication conditional on a dysfunctional, hyperphosphorylated retinoblastoma pathway. The genome was further altered by removing E3-6.7K and gp19K, changing the serotype 5 fiber to a serotype 35 fiber to target CD46 expressed by most tumors, as well as by adding a CMV-driven transgene cassette with the transgenes for TMZ-CD40L and anti-IL6R scFv. The activity of LOAd713 was compared to the activity of an empty LOAd(-) virus, a virus containing only TMZ-CD40L or uninfected cells. LOAd viruses including LOAd713 had oncolytic capacity in a panel of pancreatic cancer cell lines as shown by performing a standard MTS viability assay. Human pancreatic stellate cells were infected with LOAd viruses and analyzed by ProSeek proteomics. LOAd713 significantly decreased the expression of hepatocyte growth factor (HGF), TGF beta, fibroblast growth factor-5 (FGF-5) and collagen type I, all connected to stellate cell function and desmoplasia as well as to a poor prognosis. However, the LOAd713-infected stellate cells increased their expression of the cytokines IL1 alpha, IL6 and IL8 as well as the chemokines CXCL10 and CCL20. Infection of immature human dendritic cells (DCa) showed an increased level of maturation markers such as CD83 and IL12 as shown by flow cytometry and MesoScale, and such DCs could expand antigen-specific T cells. In conclusion, LOAd713 is an oncolytic virus that also targets the IL6/ IL6R pathway resulting in reduction of factors that drive desmoplasia. Further, via TMZ-CD40L, LOAd713 can activate DCs to produce IL12, which in turn can activate T cell responses.