Critical evaluation of 2-ethylhexyl acrylate dermal carcinogenicity studies using contemporary criteria.

[1]  C. Thompson,et al.  An Adverse Outcome Pathway (AOP) for forestomach tumors induced by non‐genotoxic initiating events , 2018, Regulatory toxicology and pharmacology : RTP.

[2]  C. Thompson,et al.  Assessment of the mode of action underlying development of forestomach tumors in rodents following oral exposure to ethyl acrylate and relevance to humans , 2018, Regulatory toxicology and pharmacology : RTP.

[3]  C. Thompson,et al.  A review of the genotoxic, mutagenic, and carcinogenic potentials of several lower acrylates. , 2018, Toxicology.

[4]  M. Ståhle,et al.  Transition from inflammation to proliferation: a critical step during wound healing , 2016, Cellular and Molecular Life Sciences.

[5]  Paul Martin,et al.  Wound repair and regeneration: Mechanisms, signaling, and translation , 2014, Science Translational Medicine.

[6]  A. Patel.  Postinflammatory hyperpigmentation: Review of pathogenesis, prevention, and treatment , 2014 .

[7]  Y. Shukla,et al.  New Enlightenment of Skin Cancer Chemoprevention through Phytochemicals: In Vitro and In Vivo Studies and the Underlying Mechanisms , 2014, BioMed research international.

[8]  S. Reddy,et al.  Reactive oxygen species in inflammation and tissue injury. , 2014, Antioxidants & redox signaling.

[9]  L. DiPietro,et al.  Toll-like receptor 4 plays an essential role in early skin wound healing , 2012, The Journal of investigative dermatology.

[10]  T. Koh,et al.  Inflammation and wound healing: the role of the macrophage , 2011, Expert Reviews in Molecular Medicine.

[11]  C. Takiya,et al.  Proinflammatory Clearance of Apoptotic Neutrophils Induces an IL-12lowIL-10high Regulatory Phenotype in Macrophages , 2010, The Journal of Immunology.

[12]  K. Kiguchi,et al.  Multi-stage chemical carcinogenesis in mouse skin: Fundamentals and applications , 2009, Nature Protocols.

[13]  C. Elmets,et al.  Resveratrol enhances cell‐mediated immune response to DMBA through TLR4 and prevents DMBA induced cutaneous carcinogenesis , 2009, Molecular carcinogenesis.

[14]  C. Elmets,et al.  Protective role of Toll-like receptor 4 during the initiation stage of cutaneous chemical carcinogenesis. , 2008, Cancer research.

[15]  M. Feldmann,et al.  Collagen-induced arthritis in C57BL/6 mice is associated with a robust and sustained T-cell response to type II collagen , 2007, Arthritis research & therapy.

[16]  D. Hattis,et al.  Issues in the Design and Interpretation of Chronic Toxicity and Carcinogenicity Studies in Rodents: Approaches to Dose Selection , 2007, Critical reviews in toxicology.

[17]  M. Mueller.  Inflammation in epithelial skin tumours: old stories and new ideas. , 2006, European journal of cancer.

[18]  J. Sundberg,et al.  Resistance to alopecia areata in C3H/HeJ mice is associated with increased expression of regulatory cytokines and a failure to recruit CD4+ and CD8+ cells. , 2002, The Journal of investigative dermatology.

[19]  T. O'Brien,et al.  Genetic control of polyamine-dependent susceptibility to skin tumorigenesis. , 2002, Genomics.

[20]  F. Marks,et al.  Mouse skin as a model for cancer chemoprevention by nonsteroidal anti-inflammatory drugs. , 2002, Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer.

[21]  T. Goldsworthy,et al.  Quantitation of the Cancer Process in C57BL/6J, B6C3F1 and C3H/HeJ Mice , 2002, Toxicologic pathology.

[22]  A. Gilhar,et al.  Alopecia areata is a T-lymphocyte mediated autoimmune disease: lesional human T-lymphocytes transfer alopecia areata to human skin grafts on SCID mice. , 1999, The journal of investigative dermatology. Symposium proceedings.

[23]  U. Mohr,et al.  Incidence and spectrum of spontaneous neoplasms in Han:NMRI mice of both sexes. , 1997, Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie.

[24]  W. C. Thomas,et al.  Comparison of the maximum tolerated dose (MTD) dermal response in three strains of mice following repeated exposure to acrylic acid. , 1995, Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association.

[25]  W. Mellert,et al.  2-year carcinogenicity study in the male NMRI mouse with 2-ethylhexyl acrylate by epicutaneous administration. , 1994, Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association.

[26]  H. Brune,et al.  Dermal oncogenicity study of 2-ethylhexyl acrylate by epicutaneous application in male C3H/HeJ mice , 2004, Journal of Cancer Research and Clinical Oncology.

[27]  E. Bomhard.  Frequency of spontaneous tumours in NMRI mice in 21-month studies. , 1993, Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie.

[28]  R. Wenning,et al.  Pathology reevaluation of the Kociba et al. (1978) bioassay of 2,3,7,8-TCDD: implications for risk assessment. , 1991, Journal of toxicology and environmental health.

[29]  D. Zimmerman,et al.  Acute toxicity, genotoxicity, and dermal carcinogenicity assessment of isooctyl acrylate. , 1991, Journal of toxicology and environmental health.

[30]  U. Mohr,et al.  Spontaneous tumors in NMRI mice from carcinogenicity studies. , 1989, Experimental pathology.

[31]  C. S. Weil,et al.  Dermal oncogenicity bioassays of monofunctional and multifunctional acrylates and acrylate-based oligomers. , 1985, Journal of toxicology and environmental health.

[32]  E. H. Fowler,et al.  Dermal oncogenicity bioassays of acrylic acid, ethyl acrylate, and butyl acrylate. , 1984, Journal of toxicology and environmental health.