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1. Publisher Correction: TGF-β blockade drives a transitional effector phenotype in T cells reversing SIV latency and decreasing SIV reservoirs in vivo

Author

Kim, Jinhee, Bose, Deepanwita, Araínga, Mariluz, Haque, Muhammad R., Fennessey, Christine M., Caddell, Rachel A., Thomas, Yanique, Ferrell, Douglas E., Ali, Syed, Grody, Emanuelle, Goyal, Yogesh, Cicala, Claudia, Arthos, James, Keele, Brandon F., Vaccari, Monica, Lorenzo-Redondo, Ramon, Hope, Thomas J., Villinger, Francois, and Martinelli, Elena

Published
2024
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2. TGF-β blockade drives a transitional effector phenotype in T cells reversing SIV latency and decreasing SIV reservoirs in vivo

Author

Kim, Jinhee, Bose, Deepanwita, Araínga, Mariluz, Haque, Muhammad R., Fennessey, Christine M., Caddell, Rachel A., Thomas, Yanique, Ferrell, Douglas E., Ali, Syed, Grody, Emanuelle, Goyal, Yogesh, Cicala, Claudia, Arthos, James, Keele, Brandon F., Vaccari, Monica, Lorenzo-Redondo, Ramon, Hope, Thomas J., Villinger, Francois, and Martinelli, Elena

Published
2024
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3. HIV vaccine candidate efficacy in female macaques mediated by cAMP-dependent efferocytosis and V2-specific ADCC

Author

Bissa, Massimiliano, Kim, Sohyoung, Galli, Veronica, Fourati, Slim, Sarkis, Sarkis, Arakelyan, Anush, de Castro, Isabela Silva, Rahman, Mohammad Arif, Fujiwara, Saori, Vaccari, Monica, Tomalka, Jeffrey A., Stamos, James D., Schifanella, Luca, Gorini, Giacomo, Moles, Ramona, Gutowska, Anna, Ferrari, Guido, Lobanov, Alexei, Montefiori, David C., Nelson, George W., Cam, Margaret C., Chakhtoura, Marita, Haddad, Elias K., Doster, Melvin N., McKinnon, Katherine, Brown, Sophia, Venzon, David J., Choo-Wosoba, Hyoyoung, Breed, Matthew W., Killoran, Kristin E., Kramer, Joshua, Margolis, Leonid, Sekaly, Rafick P., Hager, Gordon L., and Franchini, Genoveffa

Published
2023
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4. Expression of CD40L by the ALVAC-Simian Immunodeficiency Virus Vector Abrogates T Cell Responses in Macaques.

Author

Silva de Castro, Isabela, Gordon, Shari N, Liu, Jun, Bissa, Massimiliano, McKinnon, Katherine, Trinh, Hung V, Doster, Melvin N, Schifanella, Luca, Liyanage, Namal P, Cao, JinChao, Cheng, Olivia, Foulds, Kathryn, Roederer, Mario, Koup, Richard A, Shen, Xiaoying, Tomaras, Georgia D, Venzon, David J, Forthal, Donald N, Fouts, Timothy, Montefiori, David C, Tartaglia, Jim, Rao, Mangala, Ostrowski, Mario, Franchini, Genoveffa, and Vaccari, Monica

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Biotechnology, Vaccine Related, Immunization, HIV/AIDS, Vaccine Related (AIDS), Infectious Diseases, Prevention, Prevention of disease and conditions, and promotion of well-being, 3.4 Vaccines, Infection, Good Health and Well Being, AIDS Vaccines, Animals, CD40 Ligand, Gene Expression, Genetic Vectors, HEK293 Cells, HIV Envelope Protein gp120, Humans, Immunogenicity, Vaccine, Macaca mulatta, Simian Immunodeficiency Virus, Viral Vaccines, CD4, CD40L, HIV, MDSC, NHP, SIV, vaccine, macaques, Simian immunodeficiency virus, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Agricultural, veterinary and food sciences, Biological sciences, Biomedical and clinical sciences
Abstract

Immunization with recombinant ALVAC/gp120 alum vaccine provided modest protection from human immunodeficiency virus type 1 (HIV-1) and simian immunodeficiency virus (SIV) acquisition in humans and macaques. Vaccine-mediated protection was associated with the elicitation of IgG against the envelope V2 loop and of envelope-specific CD4+ T cell responses. We hypothesized that the simultaneous expression of the costimulatory molecule CD40L (CD154) by the ALVAC-HIV vector could increase both protective humoral and cellular responses. We engineered an ALVAC-SIV coexpressing CD40L with SIVmac251 (ALVAC-SIV/CD40L) gag, pol, and env genes. We compared its immunogenicity in macaques with that of a canonical ALVAC-SIV, with both given as a vector-prime/gp120 in alum boost strategy. The ALVAC-SIV/CD40L was superior to the ALVAC-SIV regimen in inducing binding and tier 1 neutralizing antibodies against the gp120. The increase in humoral responses was associated with the expression of the membrane-bound form of the CD40L by CD4+ T cells in lymph nodes. Unexpectedly, the ALVAC-SIV/CD40L vector had a blunting effect on CD4+ Th1 helper responses and instead favored the induction of myeloid-derived suppressor cells, the immune-suppressive interleukin-10 (IL-10) cytokine, and the down-modulatory tryptophan catabolism. Ultimately, this strategy failed to protect macaques from SIV acquisition. Taken together, these results underlie the importance of balanced vaccine-induced activating versus suppressive immune responses in affording protection from HIV.IMPORTANCE CD40-CD40 ligand (CD40L) interaction is crucial for inducing effective cytotoxic and humoral responses against pathogens. Because of its immunomodulatory function, CD40L has been used to enhance immune responses to vaccines, including candidate vaccines for HIV. The only successful vaccine ever tested in humans utilized a strategy combining canarypox virus-based vector (ALVAC) together with an envelope protein (gp120) adjuvanted in alum. This strategy showed limited efficacy in preventing HIV-1/SIV acquisition in humans and macaques. In both species, protection was associated with vaccine-induced antibodies against the HIV envelope and CD4+ T cell responses, including type 1 antiviral responses. In this study, we tested whether augmenting CD40L expression by coexpressing it with the ALVAC vector could increase the protective immune responses. Although coexpression of CD40L did increase humoral responses, it blunted type 1 CD4+ T cell responses against the SIV envelope protein and failed to protect macaques from viral infection.

Published
2020

5. HIV vaccine candidate activation of hypoxia and the inflammasome in CD14+ monocytes is associated with a decreased risk of SIVmac251 acquisition

Author

Vaccari, Monica, Fourati, Slim, Gordon, Shari N, Brown, Dallas R, Bissa, Massimilano, Schifanella, Luca, Silva de Castro, Isabela, Doster, Melvin N, Galli, Veronica, Omsland, Maria, Fujikawa, Dai, Gorini, Giacomo, Liyanage, Namal PM, Trinh, Hung V, McKinnon, Katherine M, Foulds, Kathryn E, Keele, Brandon F, Roederer, Mario, Koup, Richard A, Shen, Xiaoying, Tomaras, Georgia D, Wong, Marcus P, Munoz, Karissa J, Gach, Johannes S, Forthal, Donald N, Montefiori, David C, Venzon, David J, Felber, Barbara K, Rosati, Margherita, Pavlakis, George N, Rao, Mangala, Sekaly, Rafick-Pierre, and Franchini, Genoveffa

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Vaccine Related (AIDS), Genetics, Vaccine Related, Immunization, Prevention, HIV/AIDS, Good Health and Well Being, AIDS Vaccines, Animals, Antibody Formation, Biomarkers, CD4-Positive T-Lymphocytes, Hypoxia, Inflammasomes, Inflammation, Killer Cells, Natural, Lipopolysaccharide Receptors, Macaca mulatta, Monocytes, Receptors, CCR5, Risk Factors, Simian Immunodeficiency Virus, T-Lymphocytes, Helper-Inducer, Vaccines, DNA, Simian immunodeficiency virus, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract

Qualitative differences in the innate and adaptive responses elicited by different HIV vaccine candidates have not been thoroughly investigated. We tested the ability of the Aventis Pasteur live recombinant canarypox vector (ALVAC)-SIV, DNA-SIV and Ad26-SIV vaccine prime modalities together with two ALVAC-SIV + gp120 protein boosts to reduce the risk of SIVmac251 acquisition in rhesus macaques. We found that the DNA and ALVAC prime regimens were effective, but the Ad26 prime was not. The activation of hypoxia and the inflammasome in CD14+CD16- monocytes, gut-homing CCR5-negative CD4+ T helper 2 (TH2) cells and antibodies to variable region 2 correlated with a decreased risk of SIVmac251 acquisition. By contrast, signal transducer and activator of transcription 3 activation in CD16+ monocytes was associated with an increased risk of virus acquisition. The Ad26 prime regimen induced the accumulation of CX3CR1+CD163+ macrophages in lymph nodes and of long-lasting CD4+ TH17 cells in the gut and lungs. Our data indicate that the selective engagement of monocyte subsets following a vaccine prime influences long-term immunity, uncovering an unexpected association of CD14+ innate monocytes with a reduced risk of SIVmac251 acquisition.

Published
2018

6. Anti-V2 antibodies virus vulnerability revealed by envelope V1 deletion in HIV vaccine candidates

Author

Silva de Castro, Isabela, Gorini, Giacomo, Mason, Rosemarie, Gorman, Jason, Bissa, Massimiliano, Rahman, Mohammad A., Arakelyan, Anush, Kalisz, Irene, Whitney, Stephen, Becerra-Flores, Manuel, Ni, Eric, Peachman, Kristina, Trinh, Hung V., Read, Michael, Liu, Mei-Hue, Van Ryk, Donald, Paquin-Proulx, Dominic, Shubin, Zhanna, Tuyishime, Marina, Peele, Jennifer, Ahmadi, Mohammed S., Verardi, Raffaello, Hill, Juliane, Beddall, Margaret, Nguyen, Richard, Stamos, James D., Fujikawa, Dai, Min, Susie, Schifanella, Luca, Vaccari, Monica, Galli, Veronica, Doster, Melvin N., Liyanage, Namal P.M., Sarkis, Sarkis, Caccuri, Francesca, LaBranche, Celia, Montefiori, David C., Tomaras, Georgia D., Shen, Xiaoying, Rosati, Margherita, Felber, Barbara K., Pavlakis, George N., Venzon, David J., Magnanelli, William, Breed, Matthew, Kramer, Josh, Keele, Brandon F., Eller, Michael A., Cicala, Claudia, Arthos, James, Ferrari, Guido, Margolis, Leonid, Robert-Guroff, Marjorie, Kwong, Peter D., Roederer, Mario, Rao, Mangala, Cardozo, Timothy J., and Franchini, Genoveffa

Published
2021
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7. Acute Respiratory Distress in Aged, SARS-CoV-2–Infected African Green Monkeys but Not Rhesus Macaques

Author

Blair, Robert V., Vaccari, Monica, Doyle-Meyers, Lara A., Roy, Chad J., Russell-Lodrigue, Kasi, Fahlberg, Marissa, Monjure, Chris J., Beddingfield, Brandon, Plante, Kenneth S., Plante, Jessica A., Weaver, Scott C., Qin, Xuebin, Midkiff, Cecily C., Lehmicke, Gabrielle, Golden, Nadia, Threeton, Breanna, Penney, Toni, Allers, Carolina, Barnes, Mary B., Pattison, Melissa, Datta, Prasun K., Maness, Nicholas J., Birnbaum, Angela, Fischer, Tracy, Bohm, Rudolf P., and Rappaport, Jay

Published
2021
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8. An insight into carcinogenic activity and molecular mechanisms of Bis(2-ethylhexyl) phthalate.

Author

Pillo, Gelsomina, Aldrovandi, Federico, Mescoli, Ada, Maffei, Giangabriele, Mascolo, Maria Grazia, Vaccari, Monica, and Colacci, Annamaria

Subjects
CELL transformation, HEALTH risk assessment, REACTIVE oxygen species, TOXICITY testing, ANIMAL experimentation
Abstract

Di(ethylhexyl) phthalate (DEHP) is a ubiquitous environmental contaminant to which humans are exposed via multiple routes. Human health risk assessments for this substance have recently been updated, focusing on reproductive toxicity, including DEHP, in the list of chemicals classified as carcinogenic, mutagenic, or toxic to reproduction (CMR). Moreover, DEHP has also been defined as probably and possibly carcinogenic to humans based on its carcinogenicity in rodents. However, the mechanism of action of DEHP and its relevance in humans remain unclear. Rodent data suggests that DEHP induces cancer through non-genotoxic mechanisms related to multiple molecular signals, including PPARa activation, perturbation of fatty acid metabolism, induction of cell proliferation, decreased apoptosis, production of reactive oxygen species, and oxidative stress. According to the DEHP toxicological dataset, several in vitro cell transformation assays have been performed using different protocols and cellular models to produce different results. This study aimed to evaluate the carcinogenic potential of DEHP by using the A31-1-1 BALB/c-3T3 cell line in a standard cell transformation assay. Additionally, transcriptomic analysis was performed to explore the molecular responses and identify the affected toxicological pathways. Although DEHP treatment did not induce transformation in BALB/c-3T3 cells, the transcriptomic results revealed significant modulation of several pathways associated with DEHP metabolism, tissue-specific functions related to systemic metabolism, and basal cellular signaling with pleiotropic outcomes. Among these signaling pathways, modulation of cell-regulating signaling pathways, such as Notch, Wnt, and TGF-ß, can be highlighted. More specific modulation of such genes and pathways with double functions in metabolism and neurophysiology underlies the well-known crosstalk that may be crucial for the mechanism of action of DEHP. Our findings offer evidence to support the notion that these models are effective in minimizing the use of animal testing for toxicity assessment. [ABSTRACT FROM AUTHOR]

Published
2024
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9. In Vitro Evaluation of the Carcinogenic Potential of Perfluorinated Chemicals.

Author

Vaccari, Monica, Serra, Stefania, Ranzi, Andrea, Aldrovandi, Federico, Maffei, Giangabriele, Mascolo, Maria Grazia, Mescoli, Ada, Montanari, Elisa, Pillo, Gelsomina, Rotondo, Francesca, Scaroni, Ivan, Vaccari, Lorenzo, Zanzi, Cristina, Fletcher, Tony, Paparella, Martin, and Colacci, Annamaria

Abstract

Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are the major components of long-chain per- and polyfluorinated alkyl substances (PFAS), known for their chemical stability and environmental persistence. Even if PFOA and PFOS have been phased out or are limited in use, they still represent a concern for human and environmental health. Several studies have been performed to highlight the toxicological behavior of these chemicals and their mode of action (MoA). Data have suggested a causal association between PFOA or PFOS exposure and carcinogenicity in humans, but the outcomes of epidemiological studies showed some inconsistency. Moreover, the hypothesized MoA based on animal studies is considered not relevant for human cancer. To improve the knowledge on PFAS toxicology and contribute to the weight of evidence for the regulatory classification of PFAS, we used the BALB/c 3T3 cell transformation assay (CTA), an in vitro model under consideration to be included in an integrated approach to testing and assessment for non-genotoxic carcinogens (NGTxCs). PFOS and PFOA were tested at several concentrations using a validated experimental protocol. Our results demonstrate that PFOA does not induce cell transformation, whereas PFOS exposure induced a concentration-related increase of type III foci. Malignant foci formation was triggered at PFOS concentrations equal to or higher than 50 ppm and was not directly associated with cytotoxicity or proliferation induction. The divergent CTA outcomes suggest that different molecular events could be responsible for the toxicological profiles of PFOS and PFOA, which were not fully captured in our study. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Relationship between Vaccine-Induced Antibody Capture of Infectious Virus and Infection Outcomes following Repeated Low-Dose Rectal Challenges with Simian Immunodeficiency Virus SIVmac251

Author

Gach, Johannes S, Venzon, David, Vaccari, Monica, Keele, Brandon F, Franchini, Genoveffa, and Forthal, Donald N

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Immunization, Vaccine Related, Infectious Diseases, HIV/AIDS, Vaccine Related (AIDS), Biotechnology, Prevention, 3.4 Vaccines, Aetiology, Prevention of disease and conditions, and promotion of well-being, 2.1 Biological and endogenous factors, Infection, Good Health and Well Being, Animals, Antibodies, Blocking, Antibodies, Neutralizing, Antibodies, Viral, Macaca mulatta, SAIDS Vaccines, Simian Acquired Immunodeficiency Syndrome, Simian Immunodeficiency Virus, Treatment Outcome, Simian immunodeficiency virus, Biological Sciences, Agricultural and Veterinary Sciences, Medical and Health Sciences, Virology, Agricultural, veterinary and food sciences, Biological sciences, Biomedical and clinical sciences
Abstract

UnlabelledAntibodies are known to enhance in vitro infection by human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV). We measured the ability of antibodies induced by ALVAC-SIV/gp120 vaccination, given with alum or MF59 adjuvant, to capture infectious SIVmac251 and determined the association between capture and infection outcomes following low-dose, repeated rectal challenge of rhesus macaques. We found that capture correlated with the number of transmitted/founder (T/F) variants that established infection, such that animals whose plasma captured more virus were infected with a higher number of T/F strains. Capture also correlated with results of Env binding assays, indicating that greater immunogenicity resulted in greater capture. Although vaccination elicited negligible neutralizing activity against the challenge strain (50% inhibitory dilutions of >1/80 in all cases), animals with low capture and whose plasma, at a fixed dilution, inhibited a higher fraction of virus were infected at a lower rate than animals with high capture and low neutralization (P = 0.039); only animals with the low capture/high neutralization response profile were protected compared with unvaccinated control animals (P = 0.026). In a sieve analysis, high capture and low capture were distinguishable on the basis of polymorphisms in the V1 loop of Env at amino acids 144 and 145. Our results indicate that vaccine-induced antibody that binds to and captures infectious virus but does not inhibit its infectivity may enhance the likelihood of infection following rectal challenge with SIVmac251. Higher immunogenicity resulting in better antibody capture but similar anti-infectivity may not improve vaccine efficacy.ImportanceVaccines generally prevent viral infections by eliciting antibodies that inhibit virus infectivity. However, antibodies, including those induced by vaccination, have the potential to enhance, rather than prevent infection. We measured the ability of vaccine-induced antibodies to capture infectious simian immunodeficiency virus (SIV) and explored the relationship between virus capture and infection outcomes. We found that capture correlated with the number of SIV variants that established infection, such that animals whose plasma captured more virus were infected with a higher number of unique strains. In addition, animals whose sera had high capture but weak anti-infectivity activity were infected at a higher rate than were animals with low capture and stronger anti-infectivity activity. These results suggest that vaccines that induce antibodies that bind to and capture infectious virus but do not inhibit virus infectivity will not be effective in preventing infection.

Published
2016

13. Boosting of ALVAC-SIV Vaccine-Primed Macaques with the CD4-SIVgp120 Fusion Protein Elicits Antibodies to V2 Associated with a Decreased Risk of SIVmac251 Acquisition

Author

Gordon, Shari N, Liyanage, Namal PM, Doster, Melvin N, Vaccari, Monica, Vargas-Inchaustegui, Diego A, Pegu, Poonam, Schifanella, Luca, Shen, Xiaoying, Tomaras, Georgia D, Rao, Mangala, Billings, Erik A, Schwartz, Jennifer, Prado, Ilia, Bobb, Kathryn, Zhang, Wenlei, Montefiori, David C, Foulds, Kathryn E, Ferrari, Guido, Robert-Guroff, Marjorie, Roederer, Mario, Phan, Tran B, Forthal, Donald N, Stablein, Donald M, Phogat, Sanjay, Venzon, David J, Fouts, Timothy, and Franchini, Genoveffa

Subjects
HIV/AIDS, Vaccine Related (AIDS), Vaccine Related, Prevention, Immunization, Biotechnology, Infectious Diseases, 3.4 Vaccines, Prevention of disease and conditions, and promotion of well-being, Infection, Good Health and Well Being, Animals, Antibodies, Viral, CD4 Antigens, Cell Line, Gene Products, env, Macaca mulatta, SAIDS Vaccines, Simian Acquired Immunodeficiency Syndrome, Viral Vaccines, Immunology
Abstract

The recombinant ALVAC vaccine coupled with the monomeric gp120/alum protein have decreased the risk of HIV and SIV acquisition. Ab responses to the V1/V2 regions have correlated with a decreased risk of virus acquisition in both humans and macaques. We hypothesized that the breadth and functional profile of Abs induced by an ALVAC/envelope protein regimen could be improved by substituting the monomeric gp120 boost, with the full-length single-chain (FLSC) protein. FLSC is a CD4-gp120 fusion immunogen that exposes cryptic gp120 epitopes to the immune system. We compared the immunogenicity and relative efficiency of an ALVAC-SIV vaccine boosted either with bivalent FLSC proteins or with monomeric gp120 in alum. FLSC was superior to monomeric gp120 in directing Abs to the C3 α2 helix, the V5 loop, and the V3 region that contains the putative CCR5 binding site. In addition, FLSC boosting elicited significantly higher binding Abs to V2 and increased both the Ab-dependent cellular cytotoxicity activity and the breadth of neutralizing Abs. However, the FLSC vaccine regimen demonstrated only a trend in vaccine efficacy, whereas the monomeric gp120 regimen significantly decreased the risk of SIVmac251 acquisition. In both vaccine regimens, anti-V2 Abs correlated with a decreased risk of virus acquisition but differed with regard to systemic or mucosal origin. In the FLSC regimen, serum Abs to V2 correlated, whereas in the monomeric gp120 regimen, V2 Abs in rectal secretions, the site of viral challenge, were associated with efficacy.

Published
2016

14. Adjuvant-dependent innate and adaptive immune signatures of risk of SIVmac251 acquisition

Author

Vaccari, Monica, Gordon, Shari N, Fourati, Slim, Schifanella, Luca, Liyanage, Namal PM, Cameron, Mark, Keele, Brandon F, Shen, Xiaoying, Tomaras, Georgia D, Billings, Erik, Rao, Mangala, Chung, Amy W, Dowell, Karen G, Bailey-Kellogg, Chris, Brown, Eric P, Ackerman, Margaret E, Vargas-Inchaustegui, Diego A, Whitney, Stephen, Doster, Melvin N, Binello, Nicolo, Pegu, Poonam, Montefiori, David C, Foulds, Kathryn, Quinn, David S, Donaldson, Mitzi, Liang, Frank, Loré, Karin, Roederer, Mario, Koup, Richard A, McDermott, Adrian, Ma, Zhong-Min, Miller, Christopher J, Phan, Tran B, Forthal, Donald N, Blackburn, Matthew, Caccuri, Francesca, Bissa, Massimiliano, Ferrari, Guido, Kalyanaraman, Vaniambadi, Ferrari, Maria G, Thompson, DeVon, Robert-Guroff, Marjorie, Ratto-Kim, Silvia, Kim, Jerome H, Michael, Nelson L, Phogat, Sanjay, Barnett, Susan W, Tartaglia, Jim, Venzon, David, Stablein, Donald M, Alter, Galit, Sekaly, Rafick-Pierre, and Franchini, Genoveffa

Subjects
Biomedical and Clinical Sciences, Immunology, Good Health and Well Being, Adaptive Immunity, Adjuvants, Immunologic, Alum Compounds, Animals, Immunity, Innate, Immunity, Mucosal, Immunogenicity, Vaccine, Immunoglobulin G, Interleukin-17, Lymphocytes, Macaca mulatta, Membrane Glycoproteins, Random Allocation, SAIDS Vaccines, Signal Transduction, Simian Acquired Immunodeficiency Syndrome, Simian Immunodeficiency Virus, Transcriptome, Viral Envelope Proteins, Viral Vaccines, ras Proteins, Simian immunodeficiency virus, Medical and Health Sciences, Biomedical and clinical sciences, Health sciences
Abstract

A recombinant vaccine containing Aventis Pasteur's canarypox vector (ALVAC)-HIV and gp120 alum decreased the risk of HIV acquisition in the RV144 vaccine trial. The substitution of alum with the more immunogenic MF59 adjuvant is under consideration for the next efficacy human trial. We found here that an ALVAC-simian immunodeficiency virus (SIV) and gp120 alum (ALVAC-SIV + gp120) equivalent vaccine, but not an ALVAC-SIV + gp120 MF59 vaccine, was efficacious in delaying the onset of SIVmac251 in rhesus macaques, despite the higher immunogenicity of the latter adjuvant. Vaccine efficacy was associated with alum-induced, but not with MF59-induced, envelope (Env)-dependent mucosal innate lymphoid cells (ILCs) that produce interleukin (IL)-17, as well as with mucosal IgG to the gp120 variable region 2 (V2) and the expression of 12 genes, ten of which are part of the RAS pathway. The association between RAS activation and vaccine efficacy was also observed in an independent efficacious SIV-vaccine approach. Whether RAS activation, mucosal ILCs and antibodies to V2 are also important hallmarks of HIV-vaccine efficacy in humans will require further studies.

Published
2016

15. Chemical carcinogen safety testing: OECD expert group international consensus on the development of an integrated approach for the testing and assessment of chemical non-genotoxic carcinogens

Author

Jacobs, Miriam N., Colacci, Annamaria, Corvi, Raffaella, Vaccari, Monica, Aguila, M. Cecilia, Corvaro, Marco, Delrue, Nathalie, Desaulniers, Daniel, Ertych, Norman, Jacobs, Abigail, Luijten, Mirjam, Madia, Federica, Nishikawa, Akiyoshi, Ogawa, Kumiko, Ohmori, Kiyomi, Paparella, Martin, Sharma, Anoop Kumar, and Vasseur, Paule

Published
2020
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16. Disruptive environmental chemicals and cellular mechanisms that confer resistance to cell death

Author

Narayanan, Kannan Badri, Ali, Manaf, Barclay, Barry J, Cheng, Qiang Shawn, D'Abronzo, Leandro, Dornetshuber-Fleiss, Rita, Ghosh, Paramita M, Gonzalez Guzman, Michael J, Lee, Tae-Jin, Leung, Po Sing, Li, Lin, Luanpitpong, Suidjit, Ratovitski, Edward, Rojanasakul, Yon, Romano, Maria Fiammetta, Romano, Simona, Sinha, Ranjeet K, Yedjou, Clement, Al-Mulla, Fahd, Al-Temaimi, Rabeah, Amedei, Amedeo, Brown, Dustin G, Ryan, Elizabeth P, Colacci, Annamaria, Hamid, Roslida A, Mondello, Chiara, Raju, Jayadev, Salem, Hosni K, Woodrick, Jordan, Scovassi, A Ivana, Singh, Neetu, Vaccari, Monica, Roy, Rabindra, Forte, Stefano, Memeo, Lorenzo, Kim, Seo Yun, Bisson, William H, Lowe, Leroy, and Park, Hyun Ho

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, 2.1 Biological and endogenous factors, Aetiology, Generic health relevance, Animals, Carcinogenesis, Carcinogens, Environmental, Cell Death, Environmental Exposure, Hazardous Substances, Homeostasis, Humans, Neoplasms, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

Cell death is a process of dying within biological cells that are ceasing to function. This process is essential in regulating organism development, tissue homeostasis, and to eliminate cells in the body that are irreparably damaged. In general, dysfunction in normal cellular death is tightly linked to cancer progression. Specifically, the up-regulation of pro-survival factors, including oncogenic factors and antiapoptotic signaling pathways, and the down-regulation of pro-apoptotic factors, including tumor suppressive factors, confers resistance to cell death in tumor cells, which supports the emergence of a fully immortalized cellular phenotype. This review considers the potential relevance of ubiquitous environmental chemical exposures that have been shown to disrupt key pathways and mechanisms associated with this sort of dysfunction. Specifically, bisphenol A, chlorothalonil, dibutyl phthalate, dichlorvos, lindane, linuron, methoxychlor and oxyfluorfen are discussed as prototypical chemical disruptors; as their effects relate to resistance to cell death, as constituents within environmental mixtures and as potential contributors to environmental carcinogenesis.

Published
2015

17. The effect of environmental chemicals on the tumor microenvironment

Author

Casey, Stephanie C, Vaccari, Monica, Al-Mulla, Fahd, Al-Temaimi, Rabeah, Amedei, Amedeo, Barcellos-Hoff, Mary Helen, Brown, Dustin G, Chapellier, Marion, Christopher, Joseph, Curran, Colleen S, Forte, Stefano, Hamid, Roslida A, Heneberg, Petr, Koch, Daniel C, Krishnakumar, PK, Laconi, Ezio, Maguer-Satta, Veronique, Marongiu, Fabio, Memeo, Lorenzo, Mondello, Chiara, Raju, Jayadev, Roman, Jesse, Roy, Rabindra, Ryan, Elizabeth P, Ryeom, Sandra, Salem, Hosni K, Scovassi, A Ivana, Singh, Neetu, Soucek, Laura, Vermeulen, Louis, Whitfield, Jonathan R, Woodrick, Jordan, Colacci, Annamaria, Bisson, William H, and Felsher, Dean W

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Stem Cell Research, Cancer, Prevention, 2.2 Factors relating to the physical environment, Aetiology, 2.1 Biological and endogenous factors, Animals, Carcinogenesis, Environmental Exposure, Hazardous Substances, Humans, Neoplasms, Tumor Microenvironment, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

Potentially carcinogenic compounds may cause cancer through direct DNA damage or through indirect cellular or physiological effects. To study possible carcinogens, the fields of endocrinology, genetics, epigenetics, medicine, environmental health, toxicology, pharmacology and oncology must be considered. Disruptive chemicals may also contribute to multiple stages of tumor development through effects on the tumor microenvironment. In turn, the tumor microenvironment consists of a complex interaction among blood vessels that feed the tumor, the extracellular matrix that provides structural and biochemical support, signaling molecules that send messages and soluble factors such as cytokines. The tumor microenvironment also consists of many host cellular effectors including multipotent stromal cells/mesenchymal stem cells, fibroblasts, endothelial cell precursors, antigen-presenting cells, lymphocytes and innate immune cells. Carcinogens can influence the tumor microenvironment through effects on epithelial cells, the most common origin of cancer, as well as on stromal cells, extracellular matrix components and immune cells. Here, we review how environmental exposures can perturb the tumor microenvironment. We suggest a role for disrupting chemicals such as nickel chloride, Bisphenol A, butyltins, methylmercury and paraquat as well as more traditional carcinogens, such as radiation, and pharmaceuticals, such as diabetes medications, in the disruption of the tumor microenvironment. Further studies interrogating the role of chemicals and their mixtures in dose-dependent effects on the tumor microenvironment could have important general mechanistic implications for the etiology and prevention of tumorigenesis.

Published
2015

18. Transient Increase of Interferon-Stimulated Genes and No Clinical Benefit by Chloroquine Treatment During Acute Simian Immunodeficiency Virus Infection of Macaques

Author

Vaccari, Monica, Fenizia, Claudio, Ma, Zhong-Min, Hryniewicz, Anna, Boasso, Adriano, Doster, Melvin N, Miller, Christopher J, Lindegardh, Niklas, Tarning, Joel, Landay, Alan L, Shearer, Gene M, and Franchini, Genoveffa

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, HIV/AIDS, Prevention, Infectious Diseases, Genetics, Vaccine Related, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Infection, Good Health and Well Being, Animals, Chloroquine, Immunologic Factors, Macaca mulatta, Simian Acquired Immunodeficiency Syndrome, Simian Immunodeficiency Virus, Treatment Outcome, Simian immunodeficiency virus, Clinical Sciences, Virology, Clinical sciences
Abstract

Simian immunodeficiency virus (SIV) infection leads to AIDS in experimentally infected Rhesus macaques similarly to HIV-infected humans. In contrast, SIV infection of natural hosts is characterized by a down-regulation of innate acute responses to the virus within a few weeks of infection and results in limited pathology. Chloroquine (CQ) has been used in the treatment or prevention of malaria and has recently been shown to cause a decrease of immune activation and CD4 cell loss in HIV-infected individuals treated with antiretroviral therapy. Here, we treated Rhesus macaques with CQ during the acute phase of SIVmac251 infection with the intent to decrease viral-induced immune activation and possibly limit disease progression. Contrary to what was expected, CQ treatment resulted in a temporary increased expression of interferon (IFN)-stimulating genes and it worsened the recovery of CD4(+) T cells in the blood. Our findings confirm recent results observed in asymptomatic HIV-infected patients and suggest that CQ does not provide an obvious benefit in the absence of antiretroviral therapy.

Published
2014

19. In Vivo Treatment with Insulin-like Growth Factor 1 Reduces CCR5 Expression on Vaccine-Induced Activated CD4+ T-Cells

Author

Bissa, Massimiliano, primary, Galli, Veronica, additional, Schifanella, Luca, additional, Vaccari, Monica, additional, Rahman, Mohammad Arif, additional, Gorini, Giacomo, additional, Binello, Nicolò, additional, Sarkis, Sarkis, additional, Gutowska, Anna, additional, Silva de Castro, Isabela, additional, Doster, Melvin N., additional, Moles, Ramona, additional, Ferrari, Guido, additional, Shen, Xiaoying, additional, Tomaras, Georgia D., additional, Montefiori, David C., additional, N’guessan, Kombo F., additional, Paquin-Proulx, Dominic, additional, Kozlowski, Pamela A., additional, Venzon, David J., additional, Choo-Wosoba, Hyoyoung, additional, Breed, Matthew W., additional, Kramer, Joshua, additional, and Franchini, Genoveffa, additional

Published
2023
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20. TGF-β blockade drives a transitional effector phenotype in T cells reversing SIV latency and decreasing SIV reservoirsin vivo

Author

Kim, Jinhee, primary, Bose, Deepanwita, additional, Araínga, Mariluz, additional, Haque, Muhammad R., additional, Fennessey, Christine M, additional, Caddell, Rachel A, additional, Thomas, Yanique, additional, Ferrell, Douglas E, additional, Ali, Syed, additional, Grody, Emanuelle, additional, Goyal, Yogesh, additional, Cicala, Claudia, additional, Arthos, James, additional, Keele, Brandon F, additional, Vaccari, Monica, additional, Lorenzo-Redondo, Ramon, additional, Hope, Thomas J, additional, Villinger, Francois, additional, and Martinelli, Elena, additional

Published
2023
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22. Preclinical Evaluation of HIV Eradication Strategies in the Simian Immunodeficiency Virus-Infected Rhesus Macaque: A Pilot Study Testing Inhibition of Indoleamine 2,3-Dioxygenase

Author

Dunham, Richard M, Gordon, Shari N, Vaccari, Monica, Piatak, Michael, Huang, Yong, Deeks, Steven G, Lifson, Jeffrey, Franchini, Genoveffa, and McCune, Joseph M

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Sexually Transmitted Infections, HIV/AIDS, Mental Health, Infectious Diseases, Infection, Good Health and Well Being, Administration, Oral, Animals, DNA, Viral, Disease Models, Animal, Enzyme Inhibitors, Indoleamine-Pyrrole 2, 3, -Dioxygenase, Macaca mulatta, Pilot Projects, Plasma, RNA, Viral, Simian Acquired Immunodeficiency Syndrome, Simian Immunodeficiency Virus, Treatment Outcome, Tryptophan, Viral Load, Simian immunodeficiency virus, Clinical Sciences, Virology, Clinical sciences
Abstract

Even in the setting of maximally suppressive antiretroviral therapy (ART), HIV persists indefinitely. Several mechanisms might contribute to this persistence, including chronic inflammation and immune dysfunction. In this study, we have explored a preclinical model for the evaluation of potential interventions that might serve to eradicate or to minimize the level of persistent virus. Given data that metabolic products of the inducible enzyme indoleamine 2,3-dioxygeanse (IDO) might foster inflammation and viral persistence, chronically simian immunodeficiency virus (SIV)-infected, ART-treated rhesus macaques were treated with the IDO inhibitor 1-methyl tryptophan (1mT). Orally administered 1mT achieved targeted plasma levels, but did not impact tryptophan metabolism or decrease viral RNA or DNA in plasma or in intestinal tissues beyond levels achieved by ART alone. Animals treated with 1mT showed no difference in the levels of T cell activation or differentiation, or in the kinetics or magnitude of viral rebound following cessation of ART. Notwithstanding these negative results, our observations suggest that the chronically SIV-infected rhesus macaque on suppressive ART can serve as a tractable model in which to test and to prioritize the selection of other potential interventions designed to eradicate HIV in vivo. In addition, this model might be used to optimize the route and dose by which such interventions are administered and the methods by which their effects are monitored.

Published
2013

24. In Vivo Treatment with Insulin-like Growth Factor 1 Reduces CCR5 Expression on Vaccine-Induced Activated CD4 + T-Cells.

Author

Bissa, Massimiliano, Galli, Veronica, Schifanella, Luca, Vaccari, Monica, Rahman, Mohammad Arif, Gorini, Giacomo, Binello, Nicolò, Sarkis, Sarkis, Gutowska, Anna, Silva de Castro, Isabela, Doster, Melvin N., Moles, Ramona, Ferrari, Guido, Shen, Xiaoying, Tomaras, Georgia D., Montefiori, David C., N'guessan, Kombo F., Paquin-Proulx, Dominic, Kozlowski, Pamela A., and Venzon, David J.

Subjects
SOMATOMEDIN C, CHEMOKINE receptors, T cells, VACCINE effectiveness, CD4 antigen
Abstract

At the heart of the DNA/ALVAC/gp120/alum vaccine's efficacy in the absence of neutralizing antibodies is a delicate balance of pro- and anti-inflammatory immune responses that effectively decreases the risk of SIVmac251 acquisition in macaques. Vaccine efficacy is linked to antibodies recognizing the V2 helical conformation, DC-10 tolerogenic dendritic cells eliciting the clearance of apoptotic cells via efferocytosis, and CCR5 downregulation on vaccine-induced gut homing CD4+ cells. RAS activation is also linked to vaccine efficacy, which prompted the testing of IGF-1, a potent inducer of RAS activation with vaccination. We found that IGF-1 changed the hierarchy of V1/V2 epitope recognition and decreased both ADCC specific for helical V2 and efferocytosis. Remarkably, IGF-1 also reduced the expression of CCR5 on vaccine-induced CD4+ gut-homing T-cells, compensating for its negative effect on ADCC and efferocytosis and resulting in equivalent vaccine efficacy (71% with IGF-1 and 69% without). [ABSTRACT FROM AUTHOR]

Published
2023
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27. Balance of cellular and humoral immunity determines the level of protection by HIV vaccines in rhesus macaque models of HIV infection

Author

Fouts, Timothy R., Bagley, Kenneth, Prado, Ilia J., Bobb, Kathryn L., Schwartz, Jennifer A., Xu, Rong, Zagursky, Robert J., Egan, Michael A., Eldridge, John H., LaBranche, Celia C., Montefiori, David C., Le Buanec, Hélène, Zagury, Daniel, Pal, Ranajit, Pavlakis, George N., Felber, Barbara K., Franchini, Genoveffa, Gordon, Shari, Vaccari, Monica, Lewis, George K., DeVico, Anthony L., and Gallo, Robert C.

Published
2015

29. Modulation of type I interferon responses potently inhibits SARS-CoV-2 replication and inflammation in rhesus macaques

Author

Hoang, Timothy N., primary, Viox, Elise G., additional, Upadhyay, Amit A., additional, Strongin, Zachary, additional, Tharp, Gregory K., additional, Pino, Maria, additional, Nchioua, Rayhane, additional, Hirschenberger, Maximilian, additional, Gagne, Matthew, additional, Nguyen, Kevin, additional, Harper, Justin L., additional, Marciano, Shir, additional, Boddapati, Arun K., additional, Pellegrini, Kathryn L., additional, Tisoncik-Go, Jennifer, additional, Whitmore, Leanne S., additional, Karunakaran, Kirti A., additional, Roy, Melissa, additional, Kirejczyk, Shannon, additional, Curran, Elizabeth H., additional, Wallace, Chelsea, additional, Wood, Jennifer S., additional, Connor-Stroud, Fawn, additional, Kasturi, Sudhir P., additional, Levit, Rebecca D., additional, Gale, Michael, additional, Vanderford, Thomas H., additional, Silvestri, Guido, additional, Busman-Sahay, Kathleen, additional, Estes, Jacob D., additional, Vaccari, Monica, additional, Douek, Daniel C., additional, Sparrer, Konstantin M.J., additional, Kirchhoff, Frank, additional, Johnson, R. Paul, additional, Schreiber, Gideon, additional, Bosinger, Steven E., additional, and Paiardini, Mirko, additional

Published
2022
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30. Comparative analysis of SIV-specific cellular immune responses induced by different vaccine platforms in rhesus macaques

Author

Valentin, Antonio, McKinnon, Katherine, Li, Jinyao, Rosati, Margherita, Kulkarni, Viraj, Pilkington, Guy R., Bear, Jenifer, Alicea, Candido, Vargas-Inchaustegui, Diego A., Jean Patterson, L., Pegu, Poonam, Liyanage, Namal P.M., Gordon, Shari N., Vaccari, Monica, Wang, Yichuan, Hogg, Alison E., Frey, Blake, Sui, Yongjun, Reed, Steven G., Sardesai, Niranjan Y., Berzofsky, Jay A., Franchini, Genoveffa, Robert-Guroff, Marjorie, Felber, Barbara K., and Pavlakis, George N.

Published
2014
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31. Memory T Cells in Rhesus Macaques

Author

Vaccari, Monica, Franchini, Genoveffa, Back, Nathan, editor, Cohen, Irun R., editor, Lajtha, Abel, editor, Lambris, John D., editor, Paoletti, Rodolfo, editor, Zanetti, Maurizio, editor, and Schoenberger, Stephen P., editor

Published
2010
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38. Progress towards an OECD reporting framework for transcriptomics and metabolomics in regulatory toxicology

Author

Harrill, Joshua A., Viant, Mark R., Yauk, Carole L., Sachana, Magdalini, Gant, Timothy W., Auerbach, Scott S., Beger, Richard D., Bouhifd, Mounir, O'Brien, Jason, Burgoon, Lyle, Caiment, Florian, Carpi, Donatella, Chen, Tao, Chorley, Brian N., Colbourne, John, Corvi, Raffaella, Debrauwer, Laurent, O'Donovan, Claire, Ebbels, Timothy M.D., Ekman, Drew R., Faulhammer, Frank, Gribaldo, Laura, Hilton, Gina M., Jones, Stephanie P., Kende, Aniko, Lawson, Thomas N., Leite, Sofia B., Leonards, Pim E.G., Luijten, Mirjam, Martin, Alberto, Moussa, Laura, Rudaz, Serge, Schmitz, Oliver, Sobanski, Tomasz, Strauss, Volker, Vaccari, Monica, Vijay, Vikrant, Weber, Ralf J.M., Williams, Antony J., Williams, Andrew, Thomas, Russell S., and Whelan, Maurice

Published
2021
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41. Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead

Author

Goodson, William H., III, Lowe, Leroy, Carpenter, David O., Gilbertson, Michael, Manaf Ali, Abdul, Lopez de Cerain Salsamendi, Adela, Lasfar, Ahmed, Carnero, Amancio, Azqueta, Amaya, Amedei, Amedeo, Charles, Amelia K., Collins, Andrew R., Ward, Andrew, Salzberg, Anna C., Colacci, Annamaria, Olsen, Ann-Karin, Berg, Arthur, Barclay, Barry J., Zhou, Binhua P., Blanco-Aparicio, Carmen, Baglole, Carolyn J., Dong, Chenfang, Mondello, Chiara, Hsu, Chia-Wen, Naus, Christian C., Yedjou, Clement, Curran, Colleen S., Laird, Dale W., Koch, Daniel C., Carlin, Danielle J., Felsher, Dean W., Roy, Debasish, Brown, Dustin G., Ratovitski, Edward, Ryan, Elizabeth P., Corsini, Emanuela, Rojas, Emilio, Moon, Eun-Yi, Laconi, Ezio, Marongiu, Fabio, Al-Mulla, Fahd, Chiaradonna, Ferdinando, Darroudi, Firouz, Martin, Francis L., Van Schooten, Frederik J., Goldberg, Gary S., Wagemaker, Gerard, Nangami, Gladys, Calaf, Gloria M., Williams, Graeme, Wolf, Gregory T., Koppen, Gudrun, Brunborg, Gunnar, Kim Lyerly, H., Krishnan, Harini, Ab Hamid, Hasiah, Yasaei, Hemad, Sone, Hideko, Kondoh, Hiroshi, Salem, Hosni K., Hsu, Hsue-Yin, Park, Hyun Ho, Koturbash, Igor, Miousse, Isabelle R., Scovassi, A.Ivana, Klaunig, James E., Vondráček, Jan, Raju, Jayadev, Roman, Jesse, Wise, John Pierce, Sr., Whitfield, Jonathan R., Woodrick, Jordan, Christopher, Joseph A., Ochieng, Josiah, Martinez-Leal, Juan Fernando, Weisz, Judith, Kravchenko, Julia, Sun, Jun, Prudhomme, Kalan R., Narayanan, Kannan Badri, Cohen-Solal, Karine A., Moorwood, Kim, Gonzalez, Laetitia, Soucek, Laura, Jian, Le, D’Abronzo, Leandro S., Lin, Liang-Tzung, Li, Lin, Gulliver, Linda, McCawley, Lisa J., Memeo, Lorenzo, Vermeulen, Louis, Leyns, Luc, Zhang, Luoping, Valverde, Mahara, Khatami, Mahin, Romano, Maria Fiammetta, Chapellier, Marion, Williams, Marc A., Wade, Mark, Manjili, Masoud H., Lleonart, Matilde, Xia, Menghang, Gonzalez, Michael J., Karamouzis, Michalis V., Kirsch-Volders, Micheline, Vaccari, Monica, Kuemmerle, Nancy B., Singh, Neetu, Cruickshanks, Nichola, Kleinstreuer, Nicole, van Larebeke, Nik, Ahmed, Nuzhat, Ogunkua, Olugbemiga, Krishnakumar, P.K., Vadgama, Pankaj, Marignani, Paola A., Ghosh, Paramita M., Ostrosky-Wegman, Patricia, Thompson, Patricia, Dent, Paul, Heneberg, Petr, Darbre, Philippa, Sing Leung, Po, Nangia-Makker, Pratima, Cheng, Qiang (Shawn), Robey, R.Brooks, Al-Temaimi, Rabeah, Roy, Rabindra, Andrade-Vieira, Rafaela, Sinha, Ranjeet K., Mehta, Rekha, Vento, Renza, Di Fiore, Riccardo, Ponce-Cusi, Richard, Dornetshuber-Fleiss, Rita, Nahta, Rita, Castellino, Robert C., Palorini, Roberta, Abd Hamid, Roslida, Langie, Sabine A.S., Eltom, Sakina, Brooks, Samira A., Ryeom, Sandra, Wise, Sandra S., Bay, Sarah N., Harris, Shelley A., Papagerakis, Silvana, Romano, Simona, Pavanello, Sofia, Eriksson, Staffan, Forte, Stefano, Casey, Stephanie C., Luanpitpong, Sudjit, Lee, Tae-Jin, Otsuki, Takemi, Chen, Tao, Massfelder, Thierry, Sanderson, Thomas, Guarnieri, Tiziana, Hultman, Tove, Dormoy, Valérian, Odero-Marah, Valerie, Sabbisetti, Venkata, Maguer-Satta, Veronique, Rathmell, W.Kimryn, Engström, Wilhelm, Decker, William K., Bisson, William H., Rojanasakul, Yon, Luqmani, Yunus, Chen, Zhenbang, and Hu, Zhiwei

Published
2015
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42. Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: focus on the cancer hallmark of tumor angiogenesis

Author

Hu, Zhiwei, Brooks, Samira A., Dormoy, Valérian, Hsu, Chia-Wen, Hsu, Hsue-Yin, Lin, Liang-Tzung, Massfelder, Thierry, Rathmell, W. Kimryn, Xia, Menghang, Al-Mulla, Fahd, Al-Temaimi, Rabeah, Amedei, Amedeo, Brown, Dustin G., Prudhomme, Kalan R., Colacci, Annamaria, Hamid, Roslida A., Mondello, Chiara, Raju, Jayadev, Ryan, Elizabeth P., Woodrick, Jordan, Scovassi, A. Ivana, Singh, Neetu, Vaccari, Monica, Roy, Rabindra, Forte, Stefano, Memeo, Lorenzo, Salem, Hosni K., Lowe, Leroy, Jensen, Lasse, Bisson, William H., and Kleinstreuer, Nicole

Published
2015
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43. Metabolic reprogramming and dysregulated metabolism: cause, consequence and/or enabler of environmental carcinogenesis?

Author

Brooks Robey, R., Weisz, Judith, Kuemmerle, Nancy, Salzberg, Anna C., Berg, Arthur, G. Brown, Dustin, Kubik, Laura, Palorini, Roberta, Al-Mulla, Fahd, Al-Temaimi, Rabeah, Colacci, Annamaria, Mondello, Chiara, Raju, Jayadev, Woodrick, Jordan, Scovassi, A. Ivana, Singh, Neetu, Vaccari, Monica, Roy, Rabindra, Forte, Stefano, Memeo, Lorenzo, Salem, Hosni K., Amedei, Amedeo, Hamid, Roslida A., Williams, Graeme P., Lowe, Leroy, Meyer, Joel, Martin, Francis L., Bisson, William H., Chiaradonna, Ferdinando, and Ryan, Elizabeth P.

Published
2015
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44. Chemical compounds from anthropogenic environment and immune evasion mechanisms: potential interactions

Author

Kravchenko, Julia, Corsini, Emanuela, Williams, Marc A., Decker, William, Manjili, Masoud H., Otsuki, Takemi, Singh, Neetu, Al-Mulla, Faha, Al-Temaimi, Rabeah, Amedei, Amedeo, Colacci, Anna Maria, Vaccari, Monica, Mondello, Chiara, Scovassi, A. Ivana, Raju, Jayadev, Hamid, Roslida A., Memeo, Lorenzo, Forte, Stefano, Roy, Rabindra, Woodrick, Jordan, Salem, Hosni K., Ryan, Elizabeth P., Brown, Dustin G., Bisson, William H., Lowe, Leroy, and Lyerly, H.Kim

Published
2015
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45. Environmental immune disruptors, inflammation and cancer risk

Author

Thompson, Patricia A., Khatami, Mahin, Baglole, Carolyn J., Sun, Jun, Harris, Shelley, Moon, Eun-Yi, Al-Mulla, Fahd, Al-Temaimi, Rabeah, Brown, Dustin, Colacci, Annamaria, Mondello, Chiara, Raju, Jayadev, Ryan, Elizabeth, Woodrick, Jordan, Scovassi, Ivana, Singh, Neetu, Vaccari, Monica, Roy, Rabindra, Forte, Stefano, Memeo, Lorenzo, Salem, Hosni K., Amedei, Amedeo, Hamid, Roslida A., Lowe, Leroy, Guarnieri, Tiziana, and Bisson, William H.

Published
2015
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46. Causes of genome instability: the effect of low dose chemical exposures in modern society

Author

Langie, Sabine A.S., Koppen, Gudrun, Desaulniers, Daniel, Al-Mulla, Fahd, Al-Temaimi, Rabeah, Amedei, Amedeo, Azqueta, Amaya, Bisson, William H., Brown, Dustin, Brunborg, Gunnar, Charles, Amelia K., Chen, Tao, Colacci, Annamaria, Darroudi, Firouz, Forte, Stefano, Gonzalez, Laetitia, Hamid, Roslida A., Knudsen, Lisbeth E., Leyns, Luc, Lopez de Cerain Salsamendi, Adela, Memeo, Lorenzo, Mondello, Chiara, Mothersill, Carmel, Olsen, Ann-Karin, Pavanello, Sofia, Raju, Jayadev, Rojas, Emilio, Roy, Rabindra, Ryan, Elizabeth, Ostrosky-Wegman, Patricia, Salem, Hosni K., Scovassi, Ivana, Singh, Neetu, Vaccari, Monica, Van Schooten, Frederik J., Valverde, Mahara, Woodrick, Jordan, Zhang, Luoping, van Larebeke, Nik, Kirsch-Volders, Micheline, and Collins, Andrew R.

Published
2015
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47. Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression

Author

Nahta, Rita, Al-Mulla, Fahd, Al-Temaimi, Rabeah, Amedei, Amedeo, Andrade-Vieira, Rafaela, Bay, Sarah, G. Brown, Dustin, Calaf, Gloria M., Castellino, Robert C., Cohen-Solal, Karine A., Colacci, Annamaria, Cruickshanks, Nichola, Dent, Paul, Di Fiore, Riccardo, Forte, Stefano, Goldberg, Gary S., Hamid, Roslida A., Krishnan, Harini, Laird, Dale W., Lasfar, Ahmed, Marignani, Paola A., Memeo, Lorenzo, Mondello, Chiara, Naus, Christian C., Ponce-Cusi, Richard, Raju, Jayadev, Roy, Debasish, Roy, Rabindra, P. Ryan, Elizabeth, Salem, Hosni K., Scovassi, A. Ivana, Singh, Neetu, Vaccari, Monica, Vento, Renza, Vondráček, Jan, Wade, Mark, Woodrick, Jordan, and Bisson, William H.

Published
2015
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48. Disruptive chemicals, senescence and immortality

Author

Carnero, Amancio, Blanco-Aparicio, Carmen, Kondoh, Hiroshi, Lleonart, Matilde E., Martinez-Leal, Juan Fernando, Mondello, Chiara, Ivana Scovassi, A., Bisson, William H., Amedei, Amedeo, Roy, Rabindra, Woodrick, Jordan, Colacci, Annamaria, Vaccari, Monica, Raju, Jayadev, Al-Mulla, Fahd, Al-Temaimi, Rabeah, Salem, Hosni K., Memeo, Lorenzo, Forte, Stefano, Singh, Neetu, Hamid, Roslida A., Ryan, Elizabeth P., Brown, Dustin G., Wise, John Pierce, Sr, Wise, Sandra S., and Yasaei, Hemad

Published
2015
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49. The impact of low-dose carcinogens and environmental disruptors on tissue invasion and metastasis

Author

Ochieng, Josiah, Nangami, Gladys N., Ogunkua, Olugbemiga, Miousse, Isabelle R., Koturbash, Igor, Odero-Marah, Valerie, McCawley, Lisa, Nangia-Makker, Pratima, Ahmed, Nuzhat, Luqmani, Yunus, Chen, Zhenbang, Papagerakis, Silvana, Wolf, Gregory T., Dong, Chenfang, Zhou, Binhua P., Brown, Dustin G., Colacci, Annamaria, Hamid, Roslida A., Mondello, Chiara, Raju, Jayadev, Ryan, Elizabeth P., Woodrick, Jordan, Scovassi, Ivana, Singh, Neetu, Vaccari, Monica, Roy, Rabindra, Forte, Stefano, Memeo, Lorenzo, Salem, Hosni K., Amedei, Amedeo, Al-Temaimi, Rabeah, Al-Mulla, Fahd, Bisson, William H., and Eltom, Sakina E.

Published
2015
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50. The potential for chemical mixtures from the environment to enable the cancer hallmark of sustained proliferative signalling

Author

Engström, Wilhelm, Darbre, Philippa, Eriksson, Staffan, Gulliver, Linda, Hultman, Tove, Karamouzis, Michalis V., Klaunig, James E., Mehta, Rekha, Moorwood, Kim, Sanderson, Thomas, Sone, Hideko, Vadgama, Pankaj, Wagemaker, Gerard, Ward, Andrew, Singh, Neetu, Al-Mulla, Fahd, Al-Temaimi, Rabeah, Amedei, Amedeo, Colacci, Anna Maria, Vaccari, Monica, Mondello, Chiara, Scovassi, A. Ivana, Raju, Jayadev, Hamid, Roslida A., Memeo, Lorenzo, Forte, Stefano, Roy, Rabindra, Woodrick, Jordan, Salem, Hosni K., Ryan, Elizabeth, Brown, Dustin G., and Bisson, William H.

Published
2015
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