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3. Recapitulating thyroid cancer histotypes through engineering embryonic stem cells

Author

Veschi, Veronica, Turdo, Alice, Modica, Chiara, Verona, Francesco, Di Franco, Simone, Gaggianesi, Miriam, Tirrò, Elena, Di Bella, Sebastiano, Iacono, Melania Lo, Pantina, Vincenzo Davide, Porcelli, Gaetana, Mangiapane, Laura Rosa, Bianca, Paola, Rizzo, Aroldo, Sciacca, Elisabetta, Pillitteri, Irene, Vella, Veronica, Belfiore, Antonino, Bongiorno, Maria Rita, Pistone, Giuseppe, Memeo, Lorenzo, Colarossi, Lorenzo, Giuffrida, Dario, Colarossi, Cristina, Vigneri, Paolo, Todaro, Matilde, and Stassi, Giorgio

Published
2023
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6. Analysis by TeloView ® Technology Predicts the Response of Hodgkin's Lymphoma to First-Line ABVD Therapy.

Author

Knecht, Hans, Johnson, Nathalie, Bienz, Marc N., Brousset, Pierre, Memeo, Lorenzo, Shifrin, Yulia, Alikhah, Asieh, Louis, Sherif F., and Mai, Sabine

Subjects
VINBLASTINE, MEDICAL technology, PREDICTION models, RECEIVER operating characteristic curves, CANCER relapse, RESEARCH funding, LOGISTIC regression analysis, TREATMENT effectiveness, MULTIVARIATE analysis, DESCRIPTIVE statistics, BLEOMYCIN, DOXORUBICIN, DACARBAZINE, TELOMERES, PROGRESSION-free survival, HODGKIN'S disease, SENSITIVITY & specificity (Statistics), DISEASE progression, DISEASE risk factors
Abstract

Simple Summary: Three-dimensional (3D) telomere analysis using TeloView v 2.2 has shown promise in quantifying genomic instability and predicting therapy response. In a study of 156 Classic Hodgkin's lymphoma (cHL), we identified significant 3D telomere parameters that predict patient outcomes. A predictive model using four 3D telomere parameters, including the proportion of t-stumps (very short telomeres), achieved an area under curve (AUC) of 0.83, with a sensitivity and specificity of 0.82 and 0.78, respectively. Classic Hodgkin's lymphoma (cHL) is a curable cancer with a disease-free survival rate of over 10 years. Over 80% of diagnosed patients respond favorably to first-line chemotherapy, but few biomarkers exist that can predict the 15–20% of patients who experience refractory or early relapsed disease. To date, the identification of patients who will not respond to first-line therapy based on disease staging and traditional clinical risk factor analysis is still not possible. Three-dimensional (3D) telomere analysis using the TeloView® software platform has been shown to be a reliable tool to quantify genomic instability and to inform on disease progression and patients' response to therapy in several cancers. It also demonstrated telomere dysfunction in cHL elucidating biological mechanisms related to disease progression. Here, we report 3D telomere analysis on a multicenter cohort of 156 cHL patients. We used the cohort data as a training data set and identified significant 3D telomere parameters suitable to predict individual patient outcomes at the point of diagnosis. Multivariate analysis using logistic regression procedures allowed for developing a predictive scoring model using four 3D telomere parameters as predictors, including the proportion of t-stumps (very short telomeres), which has been a prominent predictor for cHL patient outcome in a previously published study using TeloView® analysis. The percentage of t-stumps was by far the most prominent predictor to identify refractory/relapsing (RR) cHL prior to initiation of adriamycin, bleomycin, vinblastine, and dacarbazine (ABVD) therapy. The model characteristics include an AUC of 0.83 in ROC analysis and a sensitivity and specificity of 0.82 and 0.78 respectively. [ABSTRACT FROM AUTHOR]

Published
2024
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8. ARID1A Mutations in Gastric Cancer: A Review with Focus on Clinicopathological Features, Molecular Background and Diagnostic Interpretation.

Author

Angelico, Giuseppe, Attanasio, Giulio, Colarossi, Lorenzo, Colarossi, Cristina, Montalbano, Matteo, Aiello, Eleonora, Di Vendra, Federica, Mare, Marzia, Orsi, Nicolas, and Memeo, Lorenzo

Subjects
ADENOCARCINOMA, STOMACH tumors, IMMUNOTHERAPY, ANTINEOPLASTIC agents, PROGRAMMED death-ligand 1, CELLULAR signal transduction, TRANSCRIPTION factors, NEOVASCULARIZATION inhibitors, TUMOR markers, GENES, GENE expression, IMMUNOHISTOCHEMISTRY, GENETIC mutation, DNA-binding proteins
Abstract

Simple Summary: ARID1A mutations are emerging as a prognostic and predictive factor in gastric cancer. Recent studies suggest their potential role in predicting patient response to novel treatment strategies including immunotherapy, poly(ADP) ribose polymerase (PARP) inhibitors, mammalian target of rapamycin (mTOR) inhibitors, and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) inhibitors. The aim of the present review is to provide a detailed appraisal of the significance of the loss of ARID1A functionality in GCs, and examine its prognostic and therapeutic implications. AT-rich interaction domain 1 (ARID1A) is a pivotal gene with a significant role in gastrointestinal tumors which encodes a protein referred to as BAF250a or SMARCF1, an integral component of the SWI/SNF (SWItch/sucrose non-fermentable) chromatin remodeling complex. This complex is instrumental in regulating gene expression by modifying the structure of chromatin to affect the accessibility of DNA. Mutations in ARID1A have been identified in various gastrointestinal cancers, including colorectal, gastric, and pancreatic cancers. These mutations have the potential to disrupt normal SWI/SNF complex function, resulting in aberrant gene expression and potentially contributing to the initiation and progression of these malignancies. ARID1A mutations are relatively common in gastric cancer, particularly in specific adenocarcinoma subtypes. Moreover, such mutations are more frequently observed in specific molecular subtypes, such as microsatellite stable (MSS) cancers and those with a diffuse histological subtype. Understanding the presence and implications of ARID1A mutations in GC is of paramount importance for tailoring personalized treatment strategies and assessing prognosis, particularly given their potential in predicting patient response to novel treatment strategies including immunotherapy, poly(ADP) ribose polymerase (PARP) inhibitors, mammalian target of rapamycin (mTOR) inhibitors, and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) inhibitors. [ABSTRACT FROM AUTHOR]

Published
2024
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9. Adipose stem cell niche reprograms the colorectal cancer stem cell metastatic machinery

Author

Di Franco, Simone, Bianca, Paola, Sardina, Davide Stefano, Turdo, Alice, Gaggianesi, Miriam, Veschi, Veronica, Nicotra, Annalisa, Mangiapane, Laura Rosa, Lo Iacono, Melania, Pillitteri, Irene, van Hooff, Sander, Martorana, Federica, Motta, Gianmarco, Gulotta, Eliana, Lentini, Vincenzo Luca, Martorana, Emanuele, Fiori, Micol Eleonora, Vieni, Salvatore, Bongiorno, Maria Rita, Giannone, Giorgio, Giuffrida, Dario, Memeo, Lorenzo, Colarossi, Lorenzo, Mare, Marzia, Vigneri, Paolo, Todaro, Matilde, De Maria, Ruggero, Medema, Jan Paul, and Stassi, Giorgio

Published
2021
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10. 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

11. 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

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

Author

Goodson, William H, 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 N, Calaf, Gloria M, Williams, Graeme, Wolf, Gregory T, Koppen, Gudrun, Brunborg, Gunnar, Lyerly, H Kim, 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, 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, and Wade, Mark

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, 2.2 Factors relating to the physical environment, Animals, Carcinogenesis, Carcinogens, Environmental, Environmental Exposure, Hazardous Substances, Humans, Neoplasms, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology.

Published
2015

13. Tumor Infiltrating Lymphocytes (TILS) and PD-L1 Expression in Breast Cancer: A Review of Current Evidence and Prognostic Implications from Pathologist’s Perspective

Author

Angelico, Giuseppe, primary, Broggi, Giuseppe, additional, Tinnirello, Giordana, additional, Puzzo, Lidia, additional, Vecchio, Giada Maria, additional, Salvatorelli, Lucia, additional, Memeo, Lorenzo, additional, Santoro, Angela, additional, Farina, Jessica, additional, Mulé, Antonino, additional, Magro, Gaetano, additional, and Caltabiano, Rosario, additional

Published
2023
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22. Data from 3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma

Author

Maurer, Matthew, primary, Su, Tao, primary, Saal, Lao H., primary, Koujak, Susan, primary, Hopkins, Benjamin D., primary, Barkley, Christina R., primary, Wu, Jiaping, primary, Nandula, Subhadra, primary, Dutta, Bhaskar, primary, Xie, Yuli, primary, Chin, Y. Rebecca, primary, Kim, Da-In, primary, Ferris, Jennifer S., primary, Gruvberger-Saal, Sofia K., primary, Laakso, Mervi, primary, Wang, Xiaomei, primary, Memeo, Lorenzo, primary, Rojtman, Albert, primary, Matos, Tulio, primary, Yu, Jennifer S., primary, Cordon-Cardo, Carlos, primary, Isola, Jorma, primary, Terry, Mary Beth, primary, Toker, Alex, primary, Mills, Gordon B., primary, Zhao, Jean J., primary, Murty, Vundavalli V.V.S., primary, Hibshoosh, Hanina, primary, and Parsons, Ramon, primary

Published
2023
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24. Supplementary Information, Methods, Table 1, Figures 1-7 from 3-Phosphoinositide–Dependent Kinase 1 Potentiates Upstream Lesions on the Phosphatidylinositol 3-Kinase Pathway in Breast Carcinoma

Author

Maurer, Matthew, primary, Su, Tao, primary, Saal, Lao H., primary, Koujak, Susan, primary, Hopkins, Benjamin D., primary, Barkley, Christina R., primary, Wu, Jiaping, primary, Nandula, Subhadra, primary, Dutta, Bhaskar, primary, Xie, Yuli, primary, Chin, Y. Rebecca, primary, Kim, Da-In, primary, Ferris, Jennifer S., primary, Gruvberger-Saal, Sofia K., primary, Laakso, Mervi, primary, Wang, Xiaomei, primary, Memeo, Lorenzo, primary, Rojtman, Albert, primary, Matos, Tulio, primary, Yu, Jennifer S., primary, Cordon-Cardo, Carlos, primary, Isola, Jorma, primary, Terry, Mary Beth, primary, Toker, Alex, primary, Mills, Gordon B., primary, Zhao, Jean J., primary, Murty, Vundavalli V.V.S., primary, Hibshoosh, Hanina, primary, and Parsons, Ramon, primary

Published
2023
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25. Supplementary Figure 1 from PIK3CA Mutations Correlate with Hormone Receptors, Node Metastasis, and ERBB2, and Are Mutually Exclusive with PTEN Loss in Human Breast Carcinoma

Author

Saal, Lao H., primary, Holm, Karolina, primary, Maurer, Matthew, primary, Memeo, Lorenzo, primary, Su, Tao, primary, Wang, Xiaomei, primary, Yu, Jennifer S., primary, Malmström, Per-Olof, primary, Mansukhani, Mahesh, primary, Enoksson, Jens, primary, Hibshoosh, Hanina, primary, Borg, Åke, primary, and Parsons, Ramon, primary

Published
2023
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27. Supplementary Figure 2 from PIK3CA Mutations Correlate with Hormone Receptors, Node Metastasis, and ERBB2, and Are Mutually Exclusive with PTEN Loss in Human Breast Carcinoma

Author

Saal, Lao H., primary, Holm, Karolina, primary, Maurer, Matthew, primary, Memeo, Lorenzo, primary, Su, Tao, primary, Wang, Xiaomei, primary, Yu, Jennifer S., primary, Malmström, Per-Olof, primary, Mansukhani, Mahesh, primary, Enoksson, Jens, primary, Hibshoosh, Hanina, primary, Borg, Åke, primary, and Parsons, Ramon, primary

Published
2023
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30. Supplementary Material from PIK3CA Mutations Correlate with Hormone Receptors, Node Metastasis, and ERBB2, and Are Mutually Exclusive with PTEN Loss in Human Breast Carcinoma

Author

Saal, Lao H., primary, Holm, Karolina, primary, Maurer, Matthew, primary, Memeo, Lorenzo, primary, Su, Tao, primary, Wang, Xiaomei, primary, Yu, Jennifer S., primary, Malmström, Per-Olof, primary, Mansukhani, Mahesh, primary, Enoksson, Jens, primary, Hibshoosh, Hanina, primary, Borg, Åke, primary, and Parsons, Ramon, primary

Published
2023
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33. Destroying the Shield of Cancer Stem Cells: Natural Compounds as Promising Players in Cancer Therapy

Author

Lo Iacono, Melania, primary, Gaggianesi, Miriam, additional, Bianca, Paola, additional, Brancato, Ornella Roberta, additional, Muratore, Giampaolo, additional, Modica, Chiara, additional, Roozafzay, Narges, additional, Shams, Kimiya, additional, Colarossi, Lorenzo, additional, Colarossi, Cristina, additional, Memeo, Lorenzo, additional, Turdo, Alice, additional, Veschi, Veronica, additional, Di Franco, Simone, additional, Todaro, Matilde, additional, and Stassi, Giorgio, additional

Published
2022
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41. STARD3: A Prospective Target for Cancer Therapy

Author

Asif, Kanwal, primary, Memeo, Lorenzo, additional, Palazzolo, Stefano, additional, Frión-Herrera, Yahima, additional, Parisi, Salvatore, additional, Caligiuri, Isabella, additional, Canzonieri, Vincenzo, additional, Granchi, Carlotta, additional, Tuccinardi, Tiziano, additional, and Rizzolio, Flavio, additional

Published
2021
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45. 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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46. 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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47. 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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48. 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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49. 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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50. 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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