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167 results on '"Salas-Alanis, Julio C"'

4. Epithelial HMGB1 Delays Skin Wound Healing and Drives Tumor Initiation by Priming Neutrophils for NET Formation

Author

Hoste, Esther, Maueröder, Christian, van Hove, Lisette, Catrysse, Leen, Vikkula, Hanna-Kaisa, Sze, Mozes, Maes, Bastiaan, Karjosukarso, Dyah, Martens, Liesbet, Gonçalves, Amanda, Parthoens, Eef, Roelandt, Ria, Declercq, Wim, Fuentes, Ignacia, Palisson, Francis, Gonzalez, Sergio, Salas-Alanis, Julio C., Boon, Louis, Huebener, Peter, Mulder, Klaas Willem, Ravichandran, Kodi, Saeys, Yvan, Schwabe, Robert Felix, and van Loo, Geert

Published
2019
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6. Overexpression of Desmoglein 2 in a Mouse Model of Gorlin Syndrome Enhances Spontaneous Basal Cell Carcinoma Formation through STAT3-Mediated Gli1 Expression

Author

Brennan-Crispi, Donna M., Overmiller, Andrew M., Tamayo-Orrego, Lukas, Marous, Molly R., Sahu, Joya, McGuinn, Kathleen P., Cooper, Felicia, Georgiou, Ioanna Ch., Frankfurter, Maxwell, Salas-Alanis, Julio C., Charron, Frédéric, Millar, Sarah E., Mahoney, Mỹ G., and Riobo-Del Galdo, Natalia A.

Published
2019
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7. Mutations in the Cholesterol Transporter Gene ABCA5 Are Associated with Excessive Hair Overgrowth

Author

DeStefano, Gina M, Kurban, Mazen, Anyane-Yeboa, Kwame, Dall'Armi, Claudia, Di Paolo, Gilbert, Feenstra, Heather, Silverberg, Nanette, Rohena, Luis, López-Cepeda, Larissa D, Jobanputra, Vaidehi, Fantauzzo, Katherine A, Kiuru, Maija, Tadin-Strapps, Marija, Sobrino, Antonio, Vitebsky, Anna, Warburton, Dorothy, Levy, Brynn, Salas-Alanis, Julio C, and Christiano, Angela M

Subjects
Biological Sciences, Genetics, Clinical Research, Neurosciences, Pediatric, Congenital Structural Anomalies, 2.1 Biological and endogenous factors, Aetiology, ATP-Binding Cassette Transporters, Child, Preschool, Cholesterol, Chromosome Deletion, Female, Genetic Diseases, X-Linked, Hair, Humans, Hypertrichosis, Infant, Keratinocytes, Mutation, Pedigree, Phenotype, RNA Splicing, Sequence Deletion, Developmental Biology
Abstract

Inherited hypertrichoses are rare syndromes characterized by excessive hair growth that does not result from androgen stimulation, and are often associated with additional congenital abnormalities. In this study, we investigated the genetic defect in a case of autosomal recessive congenital generalized hypertrichosis terminalis (CGHT) (OMIM135400) using whole-exome sequencing. We identified a single base pair substitution in the 5' donor splice site of intron 32 in the ABC lipid transporter gene ABCA5 that leads to aberrant splicing of the transcript and a decrease in protein levels throughout patient hair follicles. The homozygous recessive disruption of ABCA5 leads to reduced lysosome function, which results in an accumulation of autophagosomes, autophagosomal cargos as well as increased endolysosomal cholesterol in CGHT keratinocytes. In an unrelated sporadic case of CGHT, we identified a 1.3 Mb cryptic deletion of chr17q24.2-q24.3 encompassing ABCA5 and found that ABCA5 levels are dramatically reduced throughout patient hair follicles. Collectively, our findings support ABCA5 as a gene underlying the CGHT phenotype and suggest a novel, previously unrecognized role for this gene in regulating hair growth.

Published
2014

9. Characterization of individuals at high risk of developing melanoma in Latin America: bases for genetic counseling in melanoma

Author

Puig, Susana, Potrony, Miriam, Cuellar, Francisco, Puig-Butille, Joan Anton, Carrera, Cristina, Aguilera, Paula, Nagore, Eduardo, Garcia-Casado, Zaida, Requena, Celia, Kumar, Rajiv, Landman, Gilles, Costa Soares de Sá, Bianca, Gargantini Rezze, Gisele, Facure, Luciana, de Avila, Alexandre Leon Ribeiro, Achatz, Maria Isabel, Carraro, Dirce Maria, Duprat Neto, João Pedreira, Grazziotin, Thais C., Bonamigo, Renan R., Rey, Maria Carolina W., Balestrini, Claudia, Morales, Enrique, Molgo, Montserrat, Bakos, Renato Marchiori, Ashton-Prolla, Patricia, Giugliani, Roberto, Larre Borges, Alejandra, Barquet, Virginia, Pérez, Javiera, Martínez, Miguel, Cabo, Horacio, Cohen Sabban, Emilia, Latorre, Clara, Carlos-Ortega, Blanca, Salas-Alanis, Julio C, Gonzalez, Roger, Olazaran, Zulema, Malvehy, Josep, and Badenas, Celia

Published
2016
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10. Supplementary Data from Identification of Rigosertib for the Treatment of Recessive Dystrophic Epidermolysis Bullosa–Associated Squamous Cell Carcinoma

Author

Atanasova, Velina S., primary, Pourreyron, Celine, primary, Farshchian, Mehdi, primary, Lawler, Michael, primary, Brown, Christian A., primary, Watt, Stephen A., primary, Wright, Sheila, primary, Warkala, Michael, primary, Guttmann-Gruber, Christina, primary, Hofbauer, Josefina Piñón, primary, Fuentes, Ignacia, primary, Prisco, Marco, primary, Rashidghamat, Elham, primary, Has, Cristina, primary, Salas-Alanis, Julio C., primary, Palisson, Francis, primary, Hovnanian, Alain, primary, McGrath, John A., primary, Mellerio, Jemima E., primary, Bauer, Johann W., primary, and South, Andrew P., primary

Published
2023
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11. Supplementary Figure 2 from Fibroblast-Derived Dermal Matrix Drives Development of Aggressive Cutaneous Squamous Cell Carcinoma in Patients with Recessive Dystrophic Epidermolysis Bullosa

Author

Ng, Yi-Zhen, primary, Pourreyron, Celine, primary, Salas-Alanis, Julio C., primary, Dayal, Jasbani H.S., primary, Cepeda-Valdes, Rodrigo, primary, Yan, Wenfei, primary, Wright, Sheila, primary, Chen, Mei, primary, Fine, Jo-David, primary, Hogg, Fiona J., primary, McGrath, John A., primary, Murrell, Dedee F., primary, Leigh, Irene M., primary, Lane, E. Birgit, primary, and South, Andrew P., primary

Published
2023
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12. Supplementary Figure 3 from Fibroblast-Derived Dermal Matrix Drives Development of Aggressive Cutaneous Squamous Cell Carcinoma in Patients with Recessive Dystrophic Epidermolysis Bullosa

Author

Ng, Yi-Zhen, primary, Pourreyron, Celine, primary, Salas-Alanis, Julio C., primary, Dayal, Jasbani H.S., primary, Cepeda-Valdes, Rodrigo, primary, Yan, Wenfei, primary, Wright, Sheila, primary, Chen, Mei, primary, Fine, Jo-David, primary, Hogg, Fiona J., primary, McGrath, John A., primary, Murrell, Dedee F., primary, Leigh, Irene M., primary, Lane, E. Birgit, primary, and South, Andrew P., primary

Published
2023
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13. Supplementary Table 1 from Fibroblast-Derived Dermal Matrix Drives Development of Aggressive Cutaneous Squamous Cell Carcinoma in Patients with Recessive Dystrophic Epidermolysis Bullosa

Author

Ng, Yi-Zhen, primary, Pourreyron, Celine, primary, Salas-Alanis, Julio C., primary, Dayal, Jasbani H.S., primary, Cepeda-Valdes, Rodrigo, primary, Yan, Wenfei, primary, Wright, Sheila, primary, Chen, Mei, primary, Fine, Jo-David, primary, Hogg, Fiona J., primary, McGrath, John A., primary, Murrell, Dedee F., primary, Leigh, Irene M., primary, Lane, E. Birgit, primary, and South, Andrew P., primary

Published
2023
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14. Data from Fibroblast-Derived Dermal Matrix Drives Development of Aggressive Cutaneous Squamous Cell Carcinoma in Patients with Recessive Dystrophic Epidermolysis Bullosa

Author

Ng, Yi-Zhen, primary, Pourreyron, Celine, primary, Salas-Alanis, Julio C., primary, Dayal, Jasbani H.S., primary, Cepeda-Valdes, Rodrigo, primary, Yan, Wenfei, primary, Wright, Sheila, primary, Chen, Mei, primary, Fine, Jo-David, primary, Hogg, Fiona J., primary, McGrath, John A., primary, Murrell, Dedee F., primary, Leigh, Irene M., primary, Lane, E. Birgit, primary, and South, Andrew P., primary

Published
2023
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15. Supplementary Methods from Fibroblast-Derived Dermal Matrix Drives Development of Aggressive Cutaneous Squamous Cell Carcinoma in Patients with Recessive Dystrophic Epidermolysis Bullosa

Author

Ng, Yi-Zhen, primary, Pourreyron, Celine, primary, Salas-Alanis, Julio C., primary, Dayal, Jasbani H.S., primary, Cepeda-Valdes, Rodrigo, primary, Yan, Wenfei, primary, Wright, Sheila, primary, Chen, Mei, primary, Fine, Jo-David, primary, Hogg, Fiona J., primary, McGrath, John A., primary, Murrell, Dedee F., primary, Leigh, Irene M., primary, Lane, E. Birgit, primary, and South, Andrew P., primary

Published
2023
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16. Supplementary Figure 4 from Fibroblast-Derived Dermal Matrix Drives Development of Aggressive Cutaneous Squamous Cell Carcinoma in Patients with Recessive Dystrophic Epidermolysis Bullosa

Author

Ng, Yi-Zhen, primary, Pourreyron, Celine, primary, Salas-Alanis, Julio C., primary, Dayal, Jasbani H.S., primary, Cepeda-Valdes, Rodrigo, primary, Yan, Wenfei, primary, Wright, Sheila, primary, Chen, Mei, primary, Fine, Jo-David, primary, Hogg, Fiona J., primary, McGrath, John A., primary, Murrell, Dedee F., primary, Leigh, Irene M., primary, Lane, E. Birgit, primary, and South, Andrew P., primary

Published
2023
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17. Supplementary Table 2 from Fibroblast-Derived Dermal Matrix Drives Development of Aggressive Cutaneous Squamous Cell Carcinoma in Patients with Recessive Dystrophic Epidermolysis Bullosa

Author

Ng, Yi-Zhen, primary, Pourreyron, Celine, primary, Salas-Alanis, Julio C., primary, Dayal, Jasbani H.S., primary, Cepeda-Valdes, Rodrigo, primary, Yan, Wenfei, primary, Wright, Sheila, primary, Chen, Mei, primary, Fine, Jo-David, primary, Hogg, Fiona J., primary, McGrath, John A., primary, Murrell, Dedee F., primary, Leigh, Irene M., primary, Lane, E. Birgit, primary, and South, Andrew P., primary

Published
2023
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18. Supplementary Figure 1 from Fibroblast-Derived Dermal Matrix Drives Development of Aggressive Cutaneous Squamous Cell Carcinoma in Patients with Recessive Dystrophic Epidermolysis Bullosa

Author

Ng, Yi-Zhen, primary, Pourreyron, Celine, primary, Salas-Alanis, Julio C., primary, Dayal, Jasbani H.S., primary, Cepeda-Valdes, Rodrigo, primary, Yan, Wenfei, primary, Wright, Sheila, primary, Chen, Mei, primary, Fine, Jo-David, primary, Hogg, Fiona J., primary, McGrath, John A., primary, Murrell, Dedee F., primary, Leigh, Irene M., primary, Lane, E. Birgit, primary, and South, Andrew P., primary

Published
2023
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19. Bowen's disease

Author

Moreno-Treviño, María G., Salas-Alanís, Julio C., Salas-Garza, Mauricio, Treviño-Alanís, Ma.G., Orozco-Pasadas, David I., and Rivera-Silva, Gerardo

Published
2025
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21. Keratoderma palmoplantaris varians

Author

Rivera-Silva, Gerardo, Blanco-Ortega, Luis F.P., Moreno-Treviño, María G., Salas-Alanís, Julio C., Treviño-Alanís, Ma. Guadalupe, and Silva-Hernández, José G.

Published
2024
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23. Secondary syphilis

Author

Salas-Alanís, Julio C., Salas-Garza, Mauricio, Moreno-Treviño, María G., Gómez-Barraza, Ana C., and Rivera-Silva, Gerardo

Published
2024
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24. Calcinosis cutis

Author

Salas-Alanís, Julio C., Rivera-Silva, Gerardo, Silva-Hernández, Jose G., and Moreno-Treviño, María G.

Published
2024
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29. Multidisciplinary care of epidermolysis bullosa during the COVID-19 pandemic—Consensus: Recommendations by an international panel of experts

Author

Murrell, Dedee F., Lucky, Anne W., Salas-Alanis, Julio C., Woodley, David T., Palisson, Francis, Natsuga, Ken, Nikolic, Milos, Ramirez-Quizon, Mae, Paller, Amy S., Lara-Corrales, Irene, Barzegar, Mohammadreza Amir, Sprecher, Eli, Has, Cristina, Laimer, Martin, Bruckner, Anna L., Bilgic, Asli, Nanda, Arti, Purvis, Diana, Hovnanian, Alain, Murat-Sušić, Slobodna, Bauer, Johannes, Kern, Johannes S., Bodemer, Christine, Martin, Linda K., Mellerio, Jemima, Kowaleski, Cezary, Robertson, Susan J., Bruckner-Tuderman, Leena, Pope, Elena, Marinkovich, M. Peter, Tang, Jean Y., Su, John, Uitto, Jouni, Eichenfield, Lawrence F., Teng, Joyce, Aan Koh, Mark Jean, Lee, Sang Eun, Khuu, Phuong, Rishel, Heather I., Sommerlund, Mette, Wiss, Karen, Hsu, Chao-Kai, Chiu, Tor Wo, and Martinez, Anna E.

Published
2020
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34. Ancestral patterns of recessive dystrophic epidermolysis bullosa mutations in Hispanic populations suggest sephardic ancestry

Author

Warshauer, Emily Mira, primary, Brown, Adam, additional, Fuentes, Ignacia, additional, Shortt, Jonathan, additional, Gignoux, Chris, additional, Montinaro, Francesco, additional, Metspalu, Mait, additional, Youssefian, Leila, additional, Vahidnezhad, Hassan, additional, Jacków, Joanna, additional, Christiano, Angela M., additional, Uitto, Jouni, additional, Fajardo‐Ramírez, Óscar R., additional, Salas‐Alanis, Julio C., additional, McGrath, John A., additional, Consuegra, Liliana, additional, Rivera, Carolina, additional, Maier, Paul A., additional, Runfeldt, Goran, additional, Behar, Doron M., additional, Skorecki, Karl, additional, Sprecher, Eli, additional, Palisson, Francis, additional, Norris, David A., additional, Bruckner, Anna L., additional, Kogut, Igor, additional, Bilousova, Ganna, additional, and Roop, Dennis R., additional

Published
2021
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36. Whole-Transcriptome Analysis by RNA Sequencing for Genetic Diagnosis of Mendelian Skin Disorders in the Context of Consanguinity

Author

Youssefian, Leila, primary, Saeidian, Amir Hossein, additional, Palizban, Fahimeh, additional, Bagherieh, Atefeh, additional, Abdollahimajd, Fahimeh, additional, Sotoudeh, Soheila, additional, Mozafari, Nikoo, additional, Farahani, Rahele A, additional, Mahmoudi, Hamidreza, additional, Babashah, Sadegh, additional, Zabihi, Masoud, additional, Zeinali, Sirous, additional, Fortina, Paolo, additional, Salas-Alanis, Julio C, additional, South, Andrew P, additional, Vahidnezhad, Hassan, additional, and Uitto, Jouni, additional

Published
2021
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37. Identification of C7orf11 (TTDN1) gene mutations and genetic heterogeneity in nonphotosensitive trichothiodystrophy

Author

Nakabayashi, Kazuhiko, Amann, Daniela, Ren, Yan, Saarialho-Kere, Ulpu, Avidan, Nili, Gentles, Simone, MacDonald, Jeffrey R., Puffenberger, Erik G., Christiano, Angela M., Martinez-Mir, Amalia, Salas-Alanis, Julio C., Rizzo, Renata, Vamos, Esther, Raams, Anja, Les, Clifford, Seboun, Eric, Jaspers, Nicolaas G.J., Beckmann, Jacques S., Jackson, Charles E., and Scherer, Stephen W.

Subjects
Genetic disorders -- Research, Genetics -- Research, Biological sciences
Published
2005

42. Identification of Rigosertib for the Treatment of Recessive Dystrophic Epidermolysis Bullosa–Associated Squamous Cell Carcinoma

Author

Atanasova, Velina S., primary, Pourreyron, Celine, additional, Farshchian, Mehdi, additional, Lawler, Michael, additional, Brown, Christian A., additional, Watt, Stephen A., additional, Wright, Sheila, additional, Warkala, Michael, additional, Guttmann-Gruber, Christina, additional, Hofbauer, Josefina Piñón, additional, Fuentes, Ignacia, additional, Prisco, Marco, additional, Rashidghamat, Elham, additional, Has, Cristina, additional, Salas-Alanis, Julio C., additional, Palisson, Francis, additional, Hovnanian, Alain, additional, McGrath, John A., additional, Mellerio, Jemima E., additional, Bauer, Johann W., additional, and South, Andrew P., additional

Published
2019
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43. Cutaneous adverse effects due to personal protective measures during COVID‐19 pandemic: a study of 101 patients.

Author

Mushtaq, Sabha, Terzi, Erdinc, Recalcati, Sebastiano, Salas‐Alanis, Julio C., Amin, Sanober, and Faizi, Nafis

Subjects
COVID-19 pandemic, COVID-19, MEDICAL personnel, PERSONAL belongings, SARS-CoV-2
Abstract

Background: Coronavirus Disease 2019 (COVID‐19) is a viral illness caused by the novel coronavirus SARS‐CoV‐2 which spreads via droplets from an infected person. There has been an unprecedented rise in the use of personal protective equipment and practice of personal hygiene measures against COVID‐19. The extended use of protective measures (PM) can lead to ill effects on the skin. Our aim was to investigate PM‐induced dermatoses amongst healthcare workers and the general population during the COVID‐19 pandemic. Methods: A cross‐sectional study was conducted over a period of 2 months. The study subjects were patients who presented to dermatology outpatient clinics or sought teleconsultation for skin problems related to the use of PMs against COVID‐19. A detailed history was obtained and cutaneous examination was documented for all the patients in a pre‐set proforma. Diagnoses of the adverse skin effects were formulated based upon history and clinical examination. Results: A total of 101 cases with cutaneous adverse effects due to the use of PMs against COVID‐19 were included in the study. The general population and healthcare workers were affected similarly, comprising of 54.5% and 45.5%, respectively. The mean age of the study participants was 36.71 ± 15.72 years. The most common culprit material was soap and water (56.4%). Contact dermatitis was found to be the most common adverse effect in the majority of our patients (72.3%). The most common symptom reported was pruritus (45.5%). The wearing of personal protective equipment for a longer duration was significantly associated with multiple symptoms (P = 0.026). Conclusion: The enhanced use of different PMs against COVID‐19 can result in a variety of adverse skin effects. In our study, the use of soap and water was the most common culprit PM, and contact dermatitis was the most common adverse effect noted. [ABSTRACT FROM AUTHOR]

Published
2021
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44. Epithelial HMGB1 Delays Skin Wound Healing and Drives Tumor Initiation by Priming Neutrophils to NETosis

Author

Hoste, Esther, primary, Hove, Lisette van, additional, Catrysse, Leen, additional, Vikkula, Hanna-­Kaisa, additional, Roelandt, Ria, additional, Declercq, Wim, additional, Fuentes, Ignacia, additional, Palisson, Francis, additional, Gonzalez, Sergio, additional, Salas-­Alanis, Julio C., additional, Huebener, Peter, additional, Schwabe, Robert F., additional, and Loo, Geert van, additional

Published
2019
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45. APOBEC mutation drives early-onset squamous cell carcinomas in recessive dystrophic epidermolysis bullosa

Author

Cho, Raymond J., primary, Alexandrov, Ludmil B., additional, den Breems, Nicoline Y., additional, Atanasova, Velina S., additional, Farshchian, Mehdi, additional, Purdom, Elizabeth, additional, Nguyen, Tran N., additional, Coarfa, Cristian, additional, Rajapakshe, Kimal, additional, Prisco, Marco, additional, Sahu, Joya, additional, Tassone, Patrick, additional, Greenawalt, Evan J., additional, Collisson, Eric A., additional, Wu, Wei, additional, Yao, Hui, additional, Su, Xiaoping, additional, Guttmann-Gruber, Christina, additional, Hofbauer, Josefina Piñón, additional, Hashmi, Raabia, additional, Fuentes, Ignacia, additional, Benz, Stephen C., additional, Golovato, Justin, additional, Ehli, Erik A., additional, Davis, Christel M., additional, Davies, Gareth E., additional, Covington, Kyle R., additional, Murrell, Dedee F., additional, Salas-Alanis, Julio C., additional, Palisson, Francis, additional, Bruckner, Anna L., additional, Robinson, William, additional, Has, Cristina, additional, Bruckner-Tuderman, Leena, additional, Titeux, Matthias, additional, Jonkman, Marcel F., additional, Rashidghamat, Elham, additional, Lwin, Su M., additional, Mellerio, Jemima E., additional, McGrath, John A., additional, Bauer, Johann W., additional, Hovnanian, Alain, additional, Tsai, Kenneth Y., additional, and South, Andrew P., additional

Published
2018
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47. Preclinical comparison of proteasome and ubiquitin E1 enzyme inhibitors in cutaneous squamous cell carcinoma: The identification of mechanisms of differential sensitivity

Author

McHugh, Angela, Fernandes, Kenneth, South, Andrew P., Mellerio, Jemima E., Salas-Alanis, Julio C., Proby, Charlotte M., Leigh, Irene M., Saville, Mark K., McHugh, Angela, Fernandes, Kenneth, South, Andrew P., Mellerio, Jemima E., Salas-Alanis, Julio C., Proby, Charlotte M., Leigh, Irene M., and Saville, Mark K.

Abstract

Proteasome inhibitors have distinct properties and the biochemical consequences of suppressing ubiquitin E1 enzymes and the proteasome differ. We compared the effects of the proteasome inhibitors bortezomib, ixazomib and carfilzomib and the ubiquitin E1 enzyme inhibitor MLN7243/TAK-243 on cell viability and cell death in normal keratinocytes and cutaneous squamous cell carcinoma (cSCC) cell lines. The effects of both a pulse of treatment and more extended incubation were investigated. This is relevant to directly-delivered therapy (topical treatment/intratumoral injection) where the time of exposure can be controlled and a short exposure may better reflect systemically-delivered inhibitor pharmacokinetics. These agents can selectively kill cSCC cells but there are variations in the pattern of cSCC cell line sensitivity/resistance. Variations in the responses to proteasome inhibitors are associated with differences in the specificity of the inhibitors for the three proteolytic activities of the proteasome. There is greater selectivity for killing cSCC cells compared to normal keratinocytes with a pulse of proteasome inhibitor treatment than with a more extended exposure. We provide evidence that c-MYC-dependent NOXA upregulation confers susceptibility to a short incubation with proteasome inhibitors by priming cSCC cells for rapid BAK-dependent death. We observed that bortezomib-resistant cSCC cells can be sensitive to MLN7243-induced death. Low expression of the ubiquitin E1 UBA1/UBE1 participates in conferring susceptibility to MLN7243 by increasing sensitivity to MLN7243-mediated attenuation of ubiquitination. This study supports further investigation of the potential of proteasome and ubiquitin E1 inhibition for cSCC therapy. Direct delivery of inhibitors could facilitate adequate exposure of skin cancers.

Published
2018

48. Innate sensing of microbial products promotes wound-induced skin cancer

Author

Hoste, Esther, Arwert, Esther N., Lal, Rohit, South, Andrew P., Salas Alanis, Julio C., Murrell, Dedee F., Donati, Giacomo, and Watt, Fiona M.

Subjects
Genetics and Molecular Biology (all), Male, Skin Neoplasms, Mice, Transgenic, Crosses, Inbred C57BL, Biochemistry, Transgenic, Article, Physics and Astronomy (all), Mice, Genetic, INFLAMMATION, ADAPTER PROTEIN, Medicine and Health Sciences, Animals, Humans, IMMUNE-RESPONSE, HMGB1 Protein, Crosses, Genetic, Skin, TUMOR-NECROSIS-FACTOR, Inflammation, integumentary system, Anti-Bacterial Agents, Disease Models, Animal, Female, Flagellin, Hematopoiesis, Mice, Inbred C57BL, Myeloid Differentiation Factor 88, Signal Transduction, Toll-Like Receptor 5, Wounds and Injuries, Biochemistry, Genetics and Molecular Biology (all), Chemistry (all), Animal, CHROMATIN PROTEIN HMGB1, CARCINOGENESIS, Biology and Life Sciences, EPIDERMAL-CELLS, FACTOR RECEPTOR, Disease Models, EPIDERMOLYSIS-BULLOSA, MYD88
Abstract

The association between tissue damage, chronic inflammation and cancer is well known. However, the underlying mechanisms are unclear. Here we characterize a mouse model in which constitutive epidermal extracellular-signal-regulated kinase-MAP-kinase signalling results in epidermal inflammation, and skin wounding induces tumours. We show that tumour incidence correlates with wound size and inflammatory infiltrate. Ablation of tumour necrosis factor receptor (TNFR)-1/-2, Myeloid Differentiation primary response gene 88 or Toll-like receptor (TLR)-5, the bacterial flagellin receptor, but not other innate immune sensors, in radiosensitive leukocytes protects against tumour formation. Antibiotic treatment inhibits, whereas injection of flagellin induces, tumours in a TLR-5-dependent manner. TLR-5 is also involved in chemical-induced skin carcinogenesis in wild-type mice. Leukocytic TLR-5 signalling mediates upregulation of the alarmin HMGB1 (High Mobility Group Box 1) in wound-induced papillomas. HMGB1 is elevated in tumours of patients with Recessive Dystrophic Epidermolysis Bullosa, a disease characterized by chronic skin damage. We conclude that in our experimental model the combination of bacteria, chronic inflammation and wounding cooperate to trigger skin cancer., Inflammation and wounding can promote cancer development, but the underlying mechanisms are unclear. Here Hoste et al. show that leukocytes sensing flagellin, a component of bacteria, play a key role in inducing skin cancer in the context of wounding and chronic inflammation.

Published
2015
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