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8. 41P A window-of-opportunity study with atezolizumab and the oncolityc virus pelareorep in early breast cancer (REO-027, AWARE-1)

Author

Manso, L., primary, Villagrasa, P., additional, Chic, N., additional, Cejalvo, J.M., additional, Izarzugaza, Y., additional, Cantos, B., additional, Blanch, S., additional, Juan, M., additional, González-Farré, B., additional, Laeufle, R., additional, Nuovo, G., additional, Wilkinson, G., additional, Coffey, M., additional, González, A., additional, Martínez, D., additional, Paré, L., additional, Salvador, F., additional, González-Farré, X., additional, Prat, A., additional, and Gavila Gregori, J., additional

Published
2020
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11. The differing pathophysiologies that underlie COVID‐19‐associated perniosis and thrombotic retiform purpura: a case series.

Author

Magro, C.M., Mulvey, J.J., Laurence, J., Sanders, S., Crowson, A.N., Grossman, M., Harp, J., and Nuovo, G.

Subjects
TYPE I interferons, VIRAL proteins, COVID-19, SCHOENLEIN-Henoch purpura, CUTANEOUS manifestations of general diseases, SARS-CoV-2, COMPLEMENT activation
Abstract

Background: There are two distinctive acral manifestations of COVID‐19 embodying disparate clinical phenotypes. One is perniosis occurring in mildly symptomatic patients, typically children and young adults; the second is the thrombotic retiform purpura of critically ill adults with COVID‐19. Objectives: To compare the clinical and pathological profiles of these two different cutaneous manifestations of COVID‐19. Methods: We compared the light microscopic, phenotypic, cytokine and SARS‐CoV‐2 protein and RNA profiles of COVID‐19‐associated perniosis with that of thrombotic retiform purpura in critical patients with COVID‐19. Results: Biopsies of COVID‐19‐associated perniosis exhibited vasocentric and eccrinotropic T‐cell‐ and monocyte‐derived CD11c+, CD14+ and CD123+ dendritic cell infiltrates. Both COVID‐associated and idiopathic perniosis showed striking expression of the type I interferon‐inducible myxovirus resistance protein A (MXA), an established marker for type I interferon signalling in tissue. SARS‐CoV‐2 RNA, interleukin‐6 and caspase 3 were minimally expressed and confined to mononuclear inflammatory cells. The biopsies from livedo/retiform purpura showed pauci‐inflammatory vascular thrombosis without any MXA decoration. Blood vessels exhibited extensive complement deposition with endothelial cell localization of SARS‐CoV‐2 protein, interleukin‐6 and caspase 3; SARS‐CoV‐2 RNA was not seen. Conclusions: COVID‐19‐associated perniosis represents a virally triggered exaggerated immune reaction with significant type I interferon signaling. This is important to SARS‐CoV‐2 eradication and has implications in regards to a more generalized highly inflammatory response. We hypothesize that in the thrombotic retiform purpura of critically ill patients with COVID‐19, the vascular thrombosis in the skin and other organ systems is associated with a minimal interferon response. This allows excessive viral replication with release of viral proteins that localize to extrapulmonary endothelium and trigger extensive complement activation. What is already known about this topic? Acral perniotic‐like lesions are seen in mildly symptomatic patients with COVID‐19 – typically children – while acral retiform purpura associated with pauci‐inflammatory thrombosis is a manifestation of patients who are critically ill with COVID‐19. What does this study add? This study emphasizes that the disparate clinical and pathological manifestations of two distinct forms of acral disease in the setting of COVID‐19 are reflective of differences in interferon signalling.In the mild perniotic presentation, interferon signalling is robust, inflammation is striking and viral load in tissue samples is expectedly minimal.In contrast, in retiform purpura of severe COVID‐19, interferon signalling is absent, viral protein localization to endothelium is extensive and complement deposition with vascular thrombosis is impressive. Linked Comment:Bessis. Br J Dermatol 2021; 184:11–12. [ABSTRACT FROM AUTHOR]

Published
2021
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12. EGFR and MET receptor tyrosine kinase-altered microRNA expression induces tumorigenesis and gefitinib resistance in lung cancers

Author

Garofalo, M., Romano, G., Leva, G. D., Nuovo, G., Jeon, Y., Ngankeu, A., Sun, J., Lovat, F., Alder, H., Condorelli, G., Engelman, J. A., Ono, M., Rho, J. K., Cascione, L., Volinia, Stefano, Nephew, K. P., Croce, Carlo Maria, Garofalo, Michela, Romano, G., Di Leva, G., Nuovo, G., Jeon, Y. J., Ngankeu, A., Sun, J., Lovat, F., Alder, H., Condorelli, Gerolama, Engelman, J. A., Ono, M., Rho, J. K., Cascione, L., Volinia, S., Nephew, K. P., and Croce, C. M.

Subjects
neoplasms, Article, respiratory tract diseases
Abstract

The involvement of the MET oncogene in de novo and acquired resistance of non-small cell lung cancers (NSCLCs) to tyrosine kinase inhibitors (TKIs) has previously been reported, but the precise mechanism by which MET overexpression contributes to TKI-resistant NSCLC remains unclear. MicroRNAs (miRNAs) negatively regulate gene expression, and their dysregulation has been implicated in tumorigenesis. To understand their role in TKI-resistant NSCLCs, we examined changes in miRNA that are mediated by tyrosine kinase receptors. Here we report that miR-30b, miR-30c, miR-221 and miR-222 are modulated by both epidermal growth factor (EGF) and MET receptors, whereas miR-103 and miR-203 are controlled only by MET. We showed that these miRNAs have important roles in gefitinib-induced apoptosis and epithelial-mesenchymal transition of NSCLC cells in vitro and in vivo by inhibiting the expression of the genes encoding BCL2-like 11 (BIM), apoptotic peptidase activating factor 1 (APAF-1), protein kinase C ɛ (PKC-ɛ) and sarcoma viral oncogene homolog (SRC). These findings suggest that modulation of specific miRNAs may provide a therapeutic approach for the treatment of NSCLCs.

Published
2011

15. EGFR and MET induce tumorigenesis and gefitinib resistance in lung cancers by controlling microRNA expression

Author

Garofalo M1, Romano G, Di Leva G, Nuovo G, Jeon YJ, Ngankeu A, Sun J, Lovat F, Alder H, Condorelli G, Engelman JA, Ono M, Rho JK, Cascione L, Volinia S, Nephew KP, and Croce CM.

Subjects
EGFR, MET, tumorigenesis, cancers, microRNA, respiratory tract diseases
Abstract

The involvement of the MET oncogene in de novo and acquired resistance of non-small cell lung cancers (NSCLCs) to tyrosine kinase inhibitors (TKIs) has previously been reported, but the precise mechanism by which MET overexpression contributes to TKI-resistant NSCLC remains unclear. MicroRNAs (miRNAs) negatively regulate gene expression, and their dysregulation has been implicated in tumorigenesis. To understand their role in TKI-resistant NSCLCs, we examined changes in miRNA that are mediated by tyrosine kinase receptors. Here we report that miR-30b, miR-30c, miR-221 and miR-222 are modulated by both epidermal growth factor (EGF) and MET receptors, whereas miR-103 and miR-203 are controlled only by MET. We showed that these miRNAs have important roles in gefitinib-induced apoptosis and epithelial-mesenchymal transition of NSCLC cells in vitro and in vivo by inhibiting the expression of the genes encoding BCL2-like 11 (BIM), apoptotic peptidase activating factor 1 (APAF-1), protein kinase C ? (PKC-?) and sarcoma viral oncogene homolog (SRC). These findings suggest that modulation of specific miRNAs may provide a therapeutic approach for the treatment of NSCLCs.

Published
2011

16. OP25INTRAVENOUS DELIVERY OF ONCOLYTIC REOLYSIN®TO PRIMARY AND SECONDARY BRAIN TUMOURS

Author

Jebar, A., primary, West, E., additional, Scott, K., additional, Nuovo, G., additional, Fuller, M., additional, Thomson, S., additional, Corns, R., additional, Mathew, R., additional, SivaKumar, G., additional, Cockle, J., additional, Van Hille, P., additional, Errington, F., additional, Appleton, E., additional, Migneco, G., additional, Taggart, D., additional, Coffey, M., additional, Rose, A., additional, Griffin, S., additional, and Anth, Ralph C., additional

Published
2015
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19. P12 * A PHASE I TRIAL OF INTRAVENOUS ONCOLYTIC REOLYSIN(R) IN PATIENTS WITH BRAIN TUMOURS

Author

Jebar, A., primary, West, E., additional, Scott, K., additional, Thomson, S., additional, Corns, R., additional, Mathew, R., additional, SivaKumar, G., additional, Coffey, M., additional, Nuovo, G., additional, Rose, A., additional, Ralph, C., additional, Twelves, C., additional, Anthoney, A., additional, Griffin, S., additional, Short, S., additional, and Melcher, A., additional

Published
2014
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21. Parvoviral infection of endothelial cells and stromal fibroblasts: a possible pathogenetic role in scleroderma

Author

Magro, M. C., Nuovo, G., Ferri, Clodoveo, Crowson, A. N., Giuggioli, D., and Sebastiani, Marco

Subjects
Adult, Male, parvovirus B19, systemic sclerosis, Reverse Transcriptase Polymerase Chain Reaction, Tumor Necrosis Factor-alpha, Endothelial Cells, Complement Membrane Attack Complex, Fibroblasts, Middle Aged, Parvoviridae Infections, Fluorescent Antibody Technique, Direct, Scleroderma, Limited, DNA, Viral, Scleroderma, Diffuse, Parvovirus B19, Human, Humans, RNA, Viral, Capsid Proteins, Female, RNA, Messenger, Stromal Cells, Aged
Abstract

Systemic sclerosis (SSc) is a connective tissue disease (CTD) which differs from other CTDs by progressive irreversible fibrosis in lung, kidney, skin, and heart. It has a worse prognosis compared to several other CTDs. The pathogenesis may reflect a humorally mediated microangiopathy in concert with the overproduction of collagen triggered by immune-mediated cytokine production. Having previously demonstrated parvovirus B19 (B19) DNA in bone marrow and skin biopsies of SSc patients in the absence of B19 viremia, we sought to further elucidate a role for B19 in the pathogenesis of SSc.Twelve patients who fulfilled American College of Rheumatology criteria for a diagnosis of SSc were encountered. Ten were serologically screened for B19 infection. Solution phase polymerase chain reaction (PCR) for B19 DNA was performed on skin tissue from six patients, and in all biopsies, reverse transcriptase in situ PCR (RT in situ PCR) for B19 and tumor necrosis factor (TNF)-alpha mRNA was performed. B19 viral protein (VP2) expression was sought by immunohistochemistry and correlated to PCR findings and to light microscopy of hematoxylin and eosin-stained sections. Frozen tissue was also available on five of the patients. Two control groups were assessed for B19 and TNF expression comprising one with irrelevant primers and the other representing 18 cases of inflammatory skin lesions where the etiology was known and unrelated to B19 infection. In addition, frozen and paraffin-embedded tissues procured from skin lesions unrelated to B19 infection were assessed for B19 genome. In all cases, pretreatment with RNase was also performed to verify that any positive signal was indeed RNA based.Diffuse SSc was seen in seven patients, and limited disease in five. All patients had an antinuclear antibody--specifically, an antinucleolar, anticentromere, and/or anti-Scl 70 antibody. Eleven of the 12 had lung involvement, whereas eight patients had myocardial disease. Of 12 patients tested serologically, nine had B19-specific antibodies, which included immunoglobulin M (IgM)-specific antibodies in two cases. Solution phase PCR showed B19 DNA in the skin in three cases and in the bone marrow in three cases, including two in whom skin-based B19 DNA was observed. In all cases, RT in situ PCR demonstrated B19 and TNF-alpha mRNA in endothelia, fibroblasts, mast cells, and perivascular inflammatory cells. Immunohistochemistry to assess VP2 was either negative or equivocal. Immunofluorescent studies revealed prominent deposition of C5b-9 within the cutaneous vasculature from biopsies of all patients tested. The control samples were negative for B19 and TNF RNA and DNA.Parasitism of endothelia and fibroblasts by B19 with resultant enhanced TNF-alpha expression may be of pathogenetic importance in SSc even in the absence of demonstrable viremia. The vascular deposition of C5b-9 suggests a role for humoral immunity possibly induced by a state of endothelial neoantigenicity evoked by virally mediated cell injury. Treatment strategies include anti-viral therapy, including in the context of intravenous gamma-globulin and anti-TNF therapy.

Published
2003

22. Reprogramming of the tumour microenvironment by stromal PTEN-regulated miR-320

Author

Bronisz, A, Godlewski, J, Wallace, JA, Merchant, AS, Nowicki, MO, Mathsyaraja, H, Srinivasan, R, Trimboli, AJ, Martin, CK, Li, F, Yu, L, Fernandez, SA, Pecot, T, Rosol, TJ, Cory, S, Hallett, M, Park, M, Piper, MG, Marsh, CB, Yee, LD, Jimenez, RE, Nuovo, G, Lawler, SE, Chiocca, EA, Leone, G, Ostrowski, MC, Bronisz, A, Godlewski, J, Wallace, JA, Merchant, AS, Nowicki, MO, Mathsyaraja, H, Srinivasan, R, Trimboli, AJ, Martin, CK, Li, F, Yu, L, Fernandez, SA, Pecot, T, Rosol, TJ, Cory, S, Hallett, M, Park, M, Piper, MG, Marsh, CB, Yee, LD, Jimenez, RE, Nuovo, G, Lawler, SE, Chiocca, EA, Leone, G, and Ostrowski, MC

Abstract

PTEN (Phosphatase and tensin homolog deleted on chromosome 10) expression in stromal fibroblasts suppresses epithelial mammary tumours, but the underlying molecular mechanisms remain unknown. Using proteomic and expression profiling, we show that Pten loss from mammary stromal fibroblasts activates an oncogenic secretome that orchestrates the transcriptional reprogramming of other cell types in the microenvironment. Downregulation of miR-320 and upregulation of one of its direct targets, ETS2 (v-ets erythroblastosis virus E26 oncogene homolog 2) are critical events in Pten-deleted stromal fibroblasts responsible for inducing this oncogenic secretome, which in turn promotes tumour angiogenesis and tumour-cell invasion. Expression of the Pten-miR-320-Ets2-regulated secretome distinguished human normal breast stroma from tumour stroma and robustly correlated with recurrence in breast cancer patients. This work reveals miR-320 as a critical component of the Pten tumour-suppressor axis that acts in stromal fibroblasts to reprogramme the tumour microenvironment and curtail tumour progression.

Published
2012

23. The efficacy of in situ PCR, CARD and nanogold systems for gene detection

Author

Nuovo, G. J.

Subjects
Silver Staining, Letter, Carcinoma, Papillomavirus Infections, Gene Amplification, Silver Compounds, Uterine Cervical Neoplasms, Acetates, Catalysis, Gold Compounds, Tumor Virus Infections, Bacterial Proteins, Genes, Reporter, Tumor Cells, Cultured, Humans, Female, Streptavidin, DNA Probes, Papillomaviridae, In Situ Hybridization
Abstract

The usefulness of standard in situ hybridization for viral nucleic acid detection is occasionally limited by its sensitivity limit of 10 to 50 copies per cell. A modified version of the recently described signal amplification method, catalyzed reporter deposition (CARD), and its application to formalin-fixed cells and tissue sections is presented. Deposition of the reporter is facilitated by using horseradish peroxidase catalyzing the deposition of biotinylated tyramide on the location of the probe target. The biotin accumulation created is usually detected with streptavidin-labeled enzymes or fluorochromes. In the present investigation, this step was replaced by streptavidin-Nanogold and combined with silver acetate autometallography. This resulted in deep-black precipitation at positive in situ hybridized reaction sites. The sensitivity of this new approach was tested with a biotinylated, genomic probe specific for human papillomavirus (HPV)-16/18. SiHa cells, a cervical carcinoma-derived cell line with one to two HPV16 copies per cell, and 10 histologically confirmed cervical carcinomas were used for the study. All samples were previously HPV16 positive with solution polymerase chain reaction, but only two of the cervical carcinomas were positive with standard in situ hybridization with barely visible signals. When employing CARD-Nanogold, SiHa cells and 9 of 10 biopsies proved positive with marked signals. It is concluded that this nonisotopic method can detect single viral copies in situ in routinely fixed material and may have the potential to replace in situ polymerase chain reaction in many applications.

Published
1997

24. AIDS dementia is associated with massive, activated HIV-1 infection and concomitant expression of several cytokines

Author

Nuovo, G. J. and Alfieri, M. L.

Subjects
Acquired Immunodeficiency Syndrome, AIDS Dementia Complex, Transcription, Genetic, Tumor Necrosis Factor-alpha, Brain, Gene Expression, Macrophage Inflammatory Proteins, Polymerase Chain Reaction, Spinal Cord, DNA, Viral, HIV-1, Cytokines, Humans, RNA, Viral, RNA, Messenger, Nitric Oxide Synthase, Chemokine CCL4, In Situ Hybridization, Research Article
Abstract

BACKGROUND: We recently showed that acquired immunodeficiency syndrome (AIDS) dementia is associated with activated infection of microglia, neurons, and astrocytes by HIV-1. However, it is doubtful whether infection per se is responsible for the dramatic symptoms associated with AIDS dementia. The purpose of this study was to determine the histologic distribution of messenger RNAs (mRNAs) of several cytokines that have been implicated in AIDS pathogenesis and to correlate this expression pattern with the in situ localization of polymerase chain reaction (PCR)-amplified HIV-1 nucleic acids in the central nervous system (CNS). MATERIALS AND METHODS: HIV-1 DNA was detected by PCR in situ hybridization. HIV-1 RNA and cytokine expression, including tumor necrosis factor alpha (TNF), inducible nitric oxide synthetase (iNOS), and macrophage inflammatory protein alpha (MIP-1 alpha) and MIP-1 beta mRNA were detected by reverse transcriptase (RT) in situ PCR. RESULTS: Amplified viral DNA was detected in each of the seven HIV-1-positive cases and in none of the five negative controls. In people with AIDS dementia, many HIV-1 DNA-positive cells were detected in regions of the CNS that corresponded to clinical symptomatology. In AIDS patients with minimal CNS involvement, rare HIV-1-infected microglial cells were noted. Viral RNA was detected primarily in cases of AIDS dementia. TNF, iNOS, MIP-1 alpha and MIP-1 beta expression localized to tissues from AIDS dementia cases where HIV-1 infected cells were plentiful. Colocalization experiments showed that these cytokines were transcribed mostly by viral-negative cells. CONCLUSIONS: These results suggest that two key elements in AIDS dementia are massive productive viral infection, involving microglia, neurons, and astrocytes, and concomitant stimulation of cytokine transcription in the neighboring uninfected cells.

Published
1996

25. Analysis of fatal pulmonary hantaviral infection in New York by reverse transcriptase in situ polymerase chain reaction

Author

Nuovo, G. J., Simsir, A., Steigbigel, R. T., and Kuschner, M.

Subjects
Lung Diseases, Male, DNA, Complementary, Base Sequence, Hantavirus Infections, Molecular Sequence Data, RNA-Directed DNA Polymerase, Middle Aged, Polymerase Chain Reaction, Fatal Outcome, Child, Preschool, DNA, Viral, Humans, Female, Tissue Distribution, Oligonucleotide Probes, Lung, Research Article, Aged
Abstract

The purpose of this study was to analyze the histological distribution of polymerase chain reaction (PCR)-amplified hantaviral cDNA in three cases of fatal hantaviral infection that occurred 2 years ago in Long Island, NY. The three otherwise healthy patients had a rapid death characterized by fever and pulmonary failure and were identified from the autopsy files at University Hospital, Stony Brook. Six autopsy controls with either no pulmonary disease (three) or fatal pneumonitis of known etiology (three) were also studied. PCR-amplified hantaviral cDNA was detected in the lung tissue of the three cases and none of the six controls using the reverse transcriptase in situ PCR technique. In the positive cases, viral RNA was detected in approximately 20% of pneumocytes and alveolar endothelial cells as determined with a consensus and Four Corners-specific primer pair. Infected endothelial cells were identified in a wide variety of other sites, but at rates much lower than in the lungs. The selective localization of the viral RNA in many pneumocytes and pulmonary endothelial cells using a highly sensitive PCR-based test demonstrates a correlation between direct viral infection in the lung and the disease process.

Published
1996

26. LAB-CELL BIOLOGY AND SIGNALING

Author

Kijima, N., primary, Hosen, N., additional, Kagawa, N., additional, Hashimoto, N., additional, Chiba, Y., additional, Kinoshita, M., additional, Sugiyama, H., additional, Yoshimine, T., additional, Kim, Y. Z., additional, Kim, K. H., additional, Lee, E. H., additional, Hu, B., additional, Sim, H., additional, Mohan, N., additional, Agudelo-Garcia, P., additional, Nuovo, G., additional, Cole, S., additional, Viapiano, M. S., additional, McFarland, B. C., additional, Hong, S. W., additional, Rajbhandari, R., additional, Twitty, G. B., additional, Kenneth Gray, G., additional, Yu, H., additional, Langford, C. P., additional, Yancey Gillespie, G., additional, Benveniste, E. N., additional, Nozell, S. E., additional, Nitta, R., additional, Mitra, S., additional, Bui, T., additional, Li, G., additional, Munoz, J. L., additional, Rodriguez-Cruz, V., additional, Rameshwar, P., additional, See, W. L., additional, Mukherjee, J., additional, Shannon, K. M., additional, Pieper, R. O., additional, Floyd, D. H., additional, Xiao, A., additional, Purow, B. W., additional, Lavon, I., additional, Zrihan, D., additional, Refael, M., additional, Bier, A., additional, Canello, T., additional, Siegal, T., additional, Granit, A., additional, Xie, Q., additional, Wang, X., additional, Gong, Y., additional, Mao, Y., additional, Chen, X., additional, Zhou, L., additional, Lee, S. X., additional, Tunkyi, A., additional, Wong, E. T., additional, Swanson, K. D., additional, Zhang, K., additional, Chen, L., additional, Zhang, J., additional, Shi, Z., additional, Han, L., additional, Pu, P., additional, Kang, C., additional, Cho, W. H., additional, Ogawa, D., additional, Godlewski, J., additional, Bronisz, A., additional, Antonio Chiocca, E., additional, Mustafa, D. A. M., additional, Sieuwerts, A. M., additional, Smid, M., additional, de Weerd, V., additional, Martens, J. W., additional, Foekens, J. A., additional, Kros, J. M., additional, McCulloch, C., additional, Graff, J., additional, Sui, Y., additional, Dinn, S., additional, Huang, Y., additional, Li, Q., additional, Fiona, G., additional, Nakashima, H., additional, Leiss, L., additional, Manini, I., additional, Enger, P. O., additional, Yang, C., additional, Iyer, R., additional, Yu, A. C. H., additional, Li, S., additional, Ikejiri, B. L., additional, Zhuang, Z., additional, Lonser, R., additional, Massoud, T. F., additional, Paulmurugan, R., additional, Gambhir, S. S., additional, Merrill, M. J., additional, Sun, M., additional, Chen, M., additional, Edwards, N. A., additional, Shively, S. B., additional, Lonser, R. R., additional, Baia, G. S., additional, Caballero, O. L., additional, Orr, B. A., additional, Lal, A., additional, Ho, J. S., additional, Cowdrey, C., additional, Tihan, T., additional, Mawrin, C., additional, Riggins, G. J., additional, Lu, D., additional, Leo, C., additional, Wheeler, H., additional, McDonald, K., additional, Schulte, A., additional, Zapf, S., additional, Stoupiec, M., additional, Kolbe, K., additional, Riethdorf, S., additional, Westphal, M., additional, Lamszus, K., additional, Timmer, M., additional, Rohn, G., additional, Koch, A., additional, Goldbrunner, R., additional, Ruggieri, R., additional, Vanan, I., additional, Dong, Z., additional, Sarkaria, J. N., additional, Tran, N. L., additional, Berens, M. E., additional, Symons, M., additional, Rowther, F. B., additional, Dawson, T., additional, Ashton, K., additional, Darling, J., additional, Warr, T., additional, Okamoto, M., additional, Palanichamy, K., additional, Gordon, N., additional, Patel, D., additional, Walston, S., additional, Krishanan, T., additional, Chakravarti, A., additional, Kalinina, J., additional, Carroll, A., additional, Wang, L., additional, Yu, Q., additional, Mancheno, D. E., additional, Wu, S., additional, Liu, F., additional, Ahn, J., additional, He, M., additional, Mao, H., additional, Van Meir, E. G., additional, Debinski, W., additional, Gonzales, O., additional, Beauchamp, A., additional, Gibo, D. M., additional, Seals, D. F., additional, Speranza, M. C., additional, Frattini, V., additional, Kapetis, D., additional, Pisati, F., additional, Eoli, M., additional, Pellegatta, S., additional, Finocchiaro, G., additional, Maherally, Z., additional, Smith, J. R., additional, Pilkington, G. J., additional, Zhu, W., additional, Wang, Q., additional, Clark, P. A., additional, Yang, S.-S., additional, Lin, S.-H., additional, Kahle, K. T., additional, Kuo, J. S., additional, Sun, D., additional, Hossain, M. B., additional, Cortes-Santiago, N., additional, Gururaj, A., additional, Thomas, J., additional, Gabrusiewicz, K., additional, Gumin, J., additional, Xipell, E., additional, Lang, F., additional, Fueyo, J., additional, Yung, W. K. A., additional, Gomez-Manzano, C., additional, Cook, N. J., additional, Lawrence, J. E., additional, Rovin, R. A., additional, Belton, R. J., additional, Winn, R. J., additional, Ferluga, S., additional, Lee, S.-H., additional, Khwaja, F. W., additional, Zerrouqi, A., additional, Devi, N. S., additional, Drucker, K. L., additional, Lee, H. K., additional, Finniss, S., additional, Cazacu, S., additional, Poisson, L., additional, Xiang, C., additional, Rempel, S. A., additional, Mikkelsen, T., additional, Brodie, C., additional, Shen, J., additional, Kenchappa, R. S., additional, Valadez, J. G., additional, Cooper, M. K., additional, Carter, B. D., additional, Forsyth, P. A., additional, Lee, J. S., additional, Erdreich-Epstein, A., additional, Song, H.-R., additional, Lawn, S., additional, Kenchappa, R., additional, Forsyth, P., additional, Lim, K. J., additional, Bar, E. E., additional, Eberhart, C. G., additional, Blough, M., additional, Alnajjar, M., additional, Chesnelong, C., additional, Weiss, S., additional, Chan, J., additional, Cairncross, G., additional, Wykosky, J., additional, Cavenee, W., additional, Furnari, F., additional, Brown, K. E., additional, Keir, S. T., additional, Sampson, J. H., additional, Bigner, D. D., additional, Kwatra, M. M., additional, Kotipatruni, R. P., additional, Thotala, D. K., additional, Jaboin, J., additional, Taylor, T. E., additional, Schinzel, A. C., additional, Hahn, W. C., additional, Cavenee, W. K., additional, Furnari, F. B., additional, Kapoor, G. S., additional, Macyszyn, L., additional, Bi, Y., additional, Fetting, H., additional, Poptani, H., additional, Ittyerah, R., additional, Davuluri, R. V., additional, O'Rourke, D., additional, Pitter, K. L., additional, Hosni-Ahmed, A., additional, Colevas, K., additional, Holland, E. C., additional, Jones, T. S., additional, Malhotra, A., additional, Potts, C., additional, Fernandez-Lopez, A., additional, Kenney, A. M., additional, Cheng, S., additional, Feng, H., additional, Jarzynka, M. J., additional, Li, Y., additional, Keezer, S., additional, Johns, T. G., additional, Hamilton, R. L., additional, Vuori, K., additional, Nishikawa, R., additional, Fenton, T., additional, Cheng, T., additional, Mikheev, A. M., additional, Mikheeva, S. A., additional, Silber, J. R., additional, Horner, P. J., additional, Rostomily, R., additional, Henson, E. S., additional, Brown, M., additional, Eisenstat, D. D., additional, Gibson, S. B., additional, Price, R. L., additional, Song, J., additional, Bingmer, K., additional, Oglesbee, M., additional, Cook, C., additional, Kwon, C.-H., additional, Nguyen, T. T., additional, Chiocca, E. A., additional, Lukiw, W. J., additional, Culicchia, F., additional, Jones, B. M., additional, Zhao, Y., additional, and Bhattacharjee, S., additional

Published
2012
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27. Synergistic cytotoxicity of oncolytic reovirus in combination with cisplatin–paclitaxel doublet chemotherapy

Author

Roulstone, V, primary, Twigger, K, additional, Zaidi, S, additional, Pencavel, T, additional, Kyula, J N, additional, White, C, additional, McLaughlin, M, additional, Seth, R, additional, Karapanagiotou, E M, additional, Mansfield, D, additional, Coffey, M, additional, Nuovo, G, additional, Vile, R G, additional, Pandha, H S, additional, Melcher, A A, additional, and Harrington, K J, additional

Published
2012
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28. Reprogramming of the tumour microenvironment by stromal PTEN-regulated miR-320

Author

Bronisz, A., primary, Godlewski, J., additional, Wallace, J. A., additional, Merchant, A.S., additional, Nowicki, M.O., additional, Mathsyaraja, H., additional, Srinivasan, R., additional, Trimboli, A. J., additional, Martin, C. K., additional, Li, F., additional, Yu, L., additional, Fernandez, S. A., additional, Pécot, T., additional, Rosol, T. J., additional, Cory, S., additional, Hallett, M., additional, Park, M., additional, Piper, M. G., additional, Marsh, C. B., additional, Yee, L. D., additional, Jimenez, R. E., additional, Nuovo, G., additional, Lawler, S. E., additional, Chiocca, E. A., additional, Leone, G., additional, and Ostrowski, M. C., additional

Published
2011
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30. CELL BIOLOGY AND SIGNALING

Author

Furnari, F., primary, Fenton, T., additional, Nathanson, D., additional, de Alberquerque, C. P., additional, Kuga, D., additional, Wanami, A., additional, Dang, J., additional, Yang, H., additional, Tanaka, K., additional, Gao, L., additional, Oba-Shinjo, S., additional, Uno, M., additional, Inda, M.-d.-M., additional, Bachoo, R., additional, James, C. D., additional, DePinho, R., additional, Vandenberg, S., additional, Zhou, H., additional, Marie, S., additional, Mischel, P., additional, Cavenee, W., additional, Szerlip, N., additional, Pedraza, A., additional, Huse, J., additional, Mikkelsen, T., additional, Brennan, C., additional, Castellani, R. J., additional, Ivanova, S., additional, Gerzanich, V. V., additional, Simard, J. M., additional, Ito, M., additional, See, W., additional, Mukherjee, J., additional, Ohba, S., additional, Tan, I.-L., additional, Pieper, R. O., additional, Lukiw, W. J., additional, Culicchia, F., additional, Pogue, A., additional, Bhattacharjee, S., additional, Zhao, Y., additional, Proescholdt, M. A., additional, Merrill, M., additional, Storr, E. M., additional, Lohmeier, A., additional, Brawanski, A., additional, Abraham, S., additional, Jensen, R., additional, Khatua, S., additional, Gopal, U., additional, Du, J., additional, He, F., additional, Golub, T., additional, Isaacs, J. S., additional, Dietrich, J., additional, Kalogirou-Valtis, Y., additional, Ly, I., additional, Scadden, D., additional, Proschel, C., additional, Mayer-Proschel, M., additional, Rempel, S. A., additional, Schultz, C. R., additional, Golembieski, W., additional, Brodie, C., additional, Mathew, L. K., additional, Skuli, N., additional, Mucaj, V., additional, Imtiyaz, H. Z., additional, Venneti, S., additional, Lal, P., additional, Zhang, Z., additional, Davuluri, R. V., additional, Koch, C., additional, Evans, S., additional, Simon, M. C., additional, Ranganathan, P., additional, Clark, P., additional, Salamat, S., additional, Kuo, J. S., additional, Kalejta, R. F., additional, Bhattacharjee, B., additional, Renzette, N., additional, Moser, R. P., additional, Kowalik, T. F., additional, McFarland, B. C., additional, Ma, J.-Y., additional, Langford, C. P., additional, Gillespie, G. Y., additional, Yu, H., additional, Zheng, Y., additional, Nozell, S. E., additional, Huszar, D., additional, Benveniste, E. N., additional, Lawrence, J. E., additional, Cook, N. J., additional, Rovin, R. A., additional, Winn, R. J., additional, Godlewski, J. A., additional, Ogawa, D., additional, Bronisz, A., additional, Lawler, S., additional, Chiocca, E. A., additional, Lee, S. X., additional, Wong, E. T., additional, Swanson, K. D., additional, Liu, K.-w., additional, Feng, H., additional, Kazlauskas, A., additional, Smith, E. M., additional, Symes, K., additional, Hamilton, R. L., additional, Nagane, M., additional, Nishikawa, R., additional, Hu, B., additional, Cheng, S.-Y., additional, Silber, J., additional, Jacobsen, A., additional, Ozawa, T., additional, Harinath, G., additional, Brennan, C. W., additional, Holland, E. C., additional, Sander, C., additional, Huse, J. T., additional, Sengupta, R., additional, Dubuc, A., additional, Ward, S., additional, Yang, L., additional, Northcott, P., additional, Kroll, K., additional, Taylor, M., additional, Wechsler-Reya, R., additional, Rubin, J., additional, Chu, W.-T., additional, Lee, H.-T., additional, Huang, F.-J., additional, Aldape, K., additional, Yao, J., additional, Steeg, P. S., additional, Lu, Z., additional, Xie, K., additional, Huang, S., additional, Sim, H., additional, Agudelo-Garcia, P. A., additional, Viapiano, M. S., additional, Saldivar, J., additional, Dolan, C., additional, Mora, M., additional, Nuovo, G., additional, Cole, S., additional, Stegh, A. H., additional, Ryu, M.-J., additional, Liu, Y., additional, Zhong, X., additional, Marwaha, S., additional, Li, H., additional, Wang, J., additional, Chang, Q., additional, Zhang, J., additional, Ng, H.-K., additional, Poon, W. S., additional, Zhou, L., additional, Pang, J. C., additional, Chan, A., additional, Didier, S., additional, Kwiatkowska, A., additional, Ennis, M., additional, Fortin, S., additional, Rushing, E., additional, Eschbacher, J., additional, Tran, N., additional, Symons, M., additional, Roldan, G., additional, McIntyre, J. B., additional, Easaw, J., additional, Magliocco, A., additional, Wykosky, J., additional, Furnari, F., additional, Lu, D., additional, Mreich, E., additional, Chung, S., additional, Teo, C., additional, Wheeler, H., additional, McDonald, K. L., additional, Lawn, S., additional, Forsyth, P., additional, Sonabend, A. M., additional, Lei, L., additional, Kennedy, B., additional, Soderquist, C., additional, Guarnieri, P., additional, Leung, R., additional, Yun, J., additional, Sisti, J., additional, Castelli, M., additional, Bruce, S., additional, Bruce, R., additional, Ludwig, T., additional, Rosenfeld, S., additional, Bruce, J. N., additional, Canoll, P., additional, Lamszus, K., additional, Schulte, A., additional, Gunther, H. S., additional, Riethdorf, S., additional, Phillips, H. S., additional, Westphal, M., additional, Siegal, T., additional, Zrihan, D., additional, Granit, A., additional, Lavon, I., additional, Singh, M., additional, Chandra, J., additional, Nakashima, H., additional, Godlewski, J., additional, Chiocca, A. E., additional, Kapoor, G. S., additional, Poptani, H., additional, Ittyerah, R., additional, O'Rourke, D. M., additional, Sadraei, N. H., additional, Burgett, M., additional, Ahluwalia, M., additional, Tipps, R., additional, Khosla, D., additional, Weil, R., additional, Nowacki, A., additional, Prayson, R., additional, Shi, T., additional, Gladson, C., additional, Moeckel, S., additional, Meyer, K., additional, Bosserhoff, A., additional, Spang, R., additional, Leukel, P., additional, Vollmann, A., additional, Jachnick, B., additional, Stangl, C., additional, Proescholdt, M., additional, Bogdahn, U., additional, Hau, P., additional, Kaur, G., additional, Sun, M., additional, Kaur, R., additional, Bloch, O., additional, Jian, B., additional, Parsa, A. T., additional, Hossain, A., additional, Shinojima, N., additional, Gumin, J., additional, Feng, G., additional, Lang, F. F., additional, Li, L., additional, Yang, C.-R., additional, Chakraborty, S., additional, Hatanpaa, K., additional, Chauncey, S., additional, Jiwani, A., additional, Habib, A., additional, Nguyen, T., additional, Munson, J., additional, Machaidze, R., additional, Kaluzova, M., additional, Bellamkonda, R., additional, Hadjipanayis, C. G., additional, Zhang, Y., additional, McFarland, B., additional, Bredel, M., additional, Lee, S.-H., additional, Zerrouqi, A., additional, Khwaja, F., additional, Devi, N. S., additional, Van Meir, E. G., additional, Haseley, A., additional, Boone, S., additional, Wojton, J., additional, Yu, L., additional, Kaur, B., additional, Wojton, J. A., additional, Naduparambil, J., additional, Denton, N., additional, Chakravarti, A., additional, Conrad, C. A., additional, Wang, X., additional, Sheng, X., additional, Nilsson, C., additional, Marshall, A. G., additional, Emmett, M. R., additional, Hu, Y., additional, Mark, L., additional, Zhou, Y.-H. Z., additional, Dhruv, H., additional, McDonough, W., additional, Armstrong, B., additional, Tuncali, S., additional, Kislin, K., additional, Berens, M., additional, Plas, D., additional, Gallo, C., additional, Stringer, K., additional, Kendler, A., additional, McPherson, C., additional, Castelli, M. A., additional, Ellis, J. A., additional, Assanah, M., additional, Ogden, A., additional, Liang, J., additional, Piao, Y., additional, deGroot, J. F., additional, Gordon, N., additional, Patel, D., additional, Palanichamy, K., additional, Hervey-Jumper, S., additional, Wang, A., additional, He, X., additional, Zhu, T., additional, Heth, J., additional, Muraszko, K., additional, Fan, X., additional, Liu, W. M., additional, Huang, P., additional, Rani, S., additional, Stettner, M. R., additional, Jerry, S., additional, Dai, Q., additional, Kappes, J., additional, Gladson, C. L., additional, Chakravarty, D., additional, Koul, D., additional, Alfred Yung, W. K., additional, Jensen, S. A., additional, Luciano, J., additional, Calvert, A., additional, Nagpal, V., additional, Stegh, A., additional, Kang, S.-H., additional, Yu, M. O., additional, Lee, M.-G., additional, Chi, S.-G., additional, Chung, Y.-G., additional, Cooper, M. K., additional, Valadez, J. G., additional, Grover, V. K., additional, Kouri, F. M., additional, Chin, L., additional, Ahluwalia, M. S., additional, Weil, R. J., additional, McGraw, M., additional, Barnett, G. H., additional, Kang, C., additional, Zou, J., additional, Lan, F., additional, Yue, X., additional, Shi, Z., additional, Zhang, K., additional, Han, L., additional, Pu, P., additional, Seaman, B. F., additional, Tran, N. D., additional, Battiste, J. D., additional, Sirasanagandla, S., additional, Maher, E. A., additional, Sugiarto, S., additional, Persson, A., additional, Munoz, E. G., additional, Waldhuber, M., additional, Stallcup, W., additional, Philips, J., additional, Berger, M. S., additional, Bergers, G., additional, Weiss, W. A., additional, and Petritsch, C., additional

Published
2011
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31. miR-21 and miR-155 are associated with mitotic activity and lesion depth of borderline melanocytic lesions

Author

Grignol, V, primary, Fairchild, E T, additional, Zimmerer, J M, additional, Lesinski, G B, additional, Walker, M J, additional, Magro, C M, additional, Kacher, J E, additional, Karpa, V I, additional, Clark, J, additional, Nuovo, G, additional, Lehman, A, additional, Volinia, S, additional, Agnese, D M, additional, Croce, C M, additional, and Carson, W E, additional

Published
2011
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35. Questioning in situ PCR. In situ cDNA polymerase chain reaction: A novel technique for detecting mRNA expression

Author

Nuovo, G. J.

Subjects
Pore Forming Cytotoxic Proteins, Letter, DNA, Complementary, Membrane Glycoproteins, Perforin, Biopsy, T-Lymphocytes, Molecular Sequence Data, Serine Endopeptidases, Gene Amplification, Kidney, Immunohistochemistry, Kidney Transplantation, Polymerase Chain Reaction, Granzymes, Blotting, Southern, Endopeptidases, Humans, RNA, Messenger, Cells, Cultured, In Situ Hybridization, T-Lymphocytes, Cytotoxic
Abstract

We report a novel method for detecting intracellular messenger RNA by combining the techniques of in situ hybridization and polymerase chain reaction (PCR) (in situ cDNA PCR). The technique could detect low abundancy signals and distinguish different levels of gene expression. We examined the expression of the functional markers of activated cytotoxic T lymphocytes, granzyme A, and perforin in human lymphocytes from in vitro cultures. The amplification products were found in the cells and the supernatants, with the distribution critically affected by the protease digestion conditions. The specificity of amplification was confirmed by electrophoretic analysis and Southern blotting. We conclude that the in situ cDNA PCR technique offers a sensitive method of measuring the frequency of signal-expressing cells and has significant research and clinical applications.

Published
1994

36. In situ detection of polymerase chain reaction-amplified HIV-1 nucleic acids and tumor necrosis factor-alpha RNA in the central nervous system

Author

Nuovo, G. J., Gallery, F., MacConnell, P., and Braun, A.

Subjects
Adult, Aged, 80 and over, Male, Acquired Immunodeficiency Syndrome, Brain Diseases, Tumor Necrosis Factor-alpha, Antibodies, Monoclonal, Brain, Infant, HIV Infections, Middle Aged, Immunohistochemistry, Polymerase Chain Reaction, Child, Preschool, DNA, Viral, HIV-1, Humans, RNA, Viral, Female, RNA, Messenger, In Situ Hybridization, Research Article, Aged, Interleukin-1
Abstract

This study determined the distribution of in situ polymerase chain reaction (PCR)-amplified HIV-1 nucleic acids in the central nervous system (CNS). Amplified viral DNA was detected in each of the seven HIV-1-positive cases and in none of the seven negative controls. HIV-1 DNA was rarely detected with standard in situ hybridization, consistent with low levels of proviral DNA. In patients with minimal clinical and pathological CNS involvement, only rare HIV-1 DNA-positive perivascular microglial cells were noted. In patients with dementia, many infected neurons and astrocytes as well as microglial cells were detected. Severe disease was also characterized by the detection of tumor necrosis factor-alpha (TNF-alpha) mRNA and viral RNA by reverse transcription (RT) in situ PCR. These results suggest that HIV-1 commonly exists in the CNS in the asymptomatic patient and that progression is marked by a dramatic increase of the number of cells with HIV-1 DNA, including neurons and astrocytes, and a concomitant upregulation of both viral and TNF-alpha transcription.

Published
1994

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