Modern understanding of the pathogenesis of basal cell skin cancer

Cover Page

Cite item

Full Text

Abstract

The incidence of basal cell skin cancer is increasing worldwide. The initiation and progression of basal cell skin cancer is due to the interaction of environmental factors and the patient's genetic characteristics. Aberrant activation of the transmission of the Hedgehog signaling pathway is the main pathogenetic pathway of carcinogenesis.

Since basal cell skin cancer is manifested by significant variability of morphological structure, aggressiveness and response to treatment, the disclosure of the molecular genetics of pathogenesis will become the basis for developing new approaches and increasing the effectiveness of treatment, as well as overcoming tumor resistance to treatment.

To search for the necessary literature, the PubMed, MedLine, Web of Science and RSCI databases were used.

About the authors

R. R. Saytburkhanov

State Research Center of Dermatovenereology and Cosmetology

Email: rifat03@yandex.ru
ORCID iD: 0000-0001-6132-5632
SPIN-code: 1149-2097

dermatovenereologis

Russian Federation, Moscow

A. A. Kubanov

State Research Center of Dermatovenereology and Cosmetology

Email: alex@cnikvi.ru
ORCID iD: 0000-0002-7625-0503
SPIN-code: 8771-4990

MD, Dr. Sci. (Med.), Professor, Corresponding Member of the Russian Academy of Sciences

Russian Federation, Moscow

I. N. Kondrakhina

State Research Center of Dermatovenereology and Cosmetology

Email: kondrakhina77@gmail.com
ORCID iD: 0000-0003-3662-9954
SPIN-code: 8721-9424

MD, Cand. (Sci.) Med.

Russian Federation, Moscow

X. I. Plakhova

State Research Center of Dermatovenereology and Cosmetology

Author for correspondence.
Email: plahova@cnikvi.ru
ORCID iD: 0000-0003-4169-4128
SPIN-code: 7634-5521

MD, Dr. Sci. (Med.)

Russian Federation, Moscow

References

  1. Каприн А.Д., Старинский В.В., Шахзадова А.О. Злокачественные новообразования в России в 2019 году (заболеваемость и смертность). 2020. [Kaprin AD, Starinskij VV, Shahzadova AO. Zlokachestvennye novoobrazovanija v Rossii v 2019 godu (zabolevaemost' i smertnost'). 2020 (In Russ.)]
  2. Apalla Z, Nashan D, Weller RB, Castellsagué X. Skin Cancer: Epidemiology, Disease Burden, Pathophysiology, Diagnosis, and Therapeutic Approaches. Dermatol Ther (Heidelb). 2017;7(Suppl 1):5–19. doi: 10.1007/s13555-016-0165-y
  3. Sreekantaswamy S, Endo J, Chen A, Butler D, Morrison L, Linos E. Aging and the treatment of basal cell carcinoma. Clin Dermatol. 2019;37(4):373–378. doi: 10.1016/j.clindermatol.2019.06.004
  4. Fania L, Mazzanti C, Campione E, Candi E, Abeni D, Dellambra E. Role of Nicotinamide in Genomic Stability and Skin Cancer Chemoprevention. Int J Mol Sci. 2019;20(23):5946. doi: 10.3390/ijms20235946
  5. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell. 2013;153(6):1194–1217. doi: 10.1016/j.cell.2013.05.039
  6. Snaidr VA, Damian DL, Halliday GM. Nicotinamide for photoprotection and skin cancer chemoprevention: A review of efficacy and safety. Exp Dermatol. 2019;28 Suppl 1:15–22. doi: 10.1111/exd.13819
  7. Кубанов А.А., Жилова М.Б. К вопросу о потенциальных рисках канцерогенности фототерапии у больных псориазом. Вестник дерматологии и венерологии. 2014.5;60–67. [Kubanov AA, Zhilova MB. K voprosu o potencial'nyh riskah kancerogennosti fototerapii u bol'nyh psoriazom . Vestnik dermatologii i venerologii. 2014.5;60–67 (In Russ.)]
  8. Zanetti R, Rosso S, Martinez C, Nieto A, Miranda A, Mercier M, et al. Comparison of risk patterns in carcinoma and melanoma of the skin in men: a multi-centre case-case-control study. Br J Cancer. 2006;94(5):743–751. doi: 10.1038/sj.bjc.6602982
  9. Kricker A, Armstrong BK, English DR, Heenan PJ. (1995). Does intermittent sun exposure cause basal cell carcinoma? A case-control study in Western Australia. International journal of cancer, 60(4)489–494. https://doi.org/10.1002/ijc.2910600411
  10. Gallagher RP, Hill GB, Bajdik CD, Fincham S, Coldman AJ, McLean, DI. et al. Sunlight exposure, pigmentary factors, and risk of nonmelanocytic skin cancer. I. Basal cell carcinoma. Arch Dermatol. 1995;131(2):157–163.
  11. Wehner MR, Shive ML, Chren MM, Han J, Qureshi AA, Linos E. Indoor tanning and non-melanoma skin cancer: systematic review and meta-analysis. BMJ. 2012;345:e5909. doi: 10.1136/bmj.e5909
  12. Ferrucci LM, Cartmel B, Molinaro AM, Leffell DJ, Bale AE, Mayne ST. Indoor tanning and risk of early-onset basal cell carcinoma. J Am Acad Dermatol. 2012;67(4):552–562. doi: 10.1016/j.jaad.2011.11.940
  13. Schmidt SA, Schmidt M, Mehnert F, Lemeshow S, Sørensen HT. Use of antihypertensive drugs and risk of skin cancer. J Eur Acad Dermatol Venereol. 2015;29(8):1545–1554. doi: 10.1111/jdv.12921
  14. Boaventura P, Oliveira R, Pereira D, Soares P, Teixeira-Gomes J. Head and neck basal cell carcinoma prevalence in individuals submitted to childhood X-ray epilation for tinea capitis treatment. Eur J Dermatol. 2012;22(2):225–230. doi: 10.1684/ejd.2012.1670
  15. Lichter MD, Karagas MR, Mott LA, Spencer SK, Stukel TA, Greenberg ER. Therapeutic ionizing radiation and the incidence of basal cell carcinoma and squamous cell carcinoma. The New Hampshire Skin Cancer Study Group. Arch Dermatol. 2000;136(8):1007–1011. doi: 10.1001/archderm.136.8.1007
  16. Shore RE, Moseson M, Xue X, Tse Y, Harley N, Pasternack BS. Skin cancer after X-ray treatment for scalp ringworm. Radiat Res. 2002;157(4):410–418. doi: 10.1667/0033-7587(2002)157[0410:scaxrt]2.0.co;2
  17. Boaventura P, Pereira D, Mendes A, Batista R, da Silva, AF, Guimarães I, et al. Mitochondrial D310 D-Loop instability and histological subtypes in radiation-induced cutaneous basal cell carcinomas. J Dermatol Sci. 2014;73(1):31–39. doi: 10.1016/j.jdermsci.2013.09.002
  18. Flohil SC, van der Leest RJ, Arends LR, de Vries E, Nijsten T. Risk of subsequent cutaneous malignancy in patients with prior keratinocyte carcinoma: a systematic review and meta-analysis. Eur J Cancer. 2013;49(10):2365–2375. doi: 10.1016/j.ejca.2013.03.010
  19. Marcil I, Stern RS. Risk of developing a subsequent nonmelanoma skin cancer in patients with a history of nonmelanoma skin cancer: a critical review of the literature and meta-analysis. Arch Dermatol. 2000;136(12):1524–1530. doi: 10.1001/archderm.136.12.1524
  20. Wehner MR, Linos E, Parvataneni R, Stuart SE, Boscardin WJ, Chren MM. Timing of subsequent new tumors in patients who present with basal cell carcinoma or cutaneous squamous cell carcinoma. JAMA Dermatol. 2015;151(4):382–388. doi: 10.1001/jamadermatol.2014.3307
  21. Ricci F, Paradisi A, Fania L, Pallotta S, DI Lella G, Sobrino L, et al. High melanoma risk in non-melanoma skin cancer patients under age 40: a large retrospective cohort study. Ital J Dermatol Venerol. 2021;156(2):240–243. doi: 10.23736/S0392-0488.19.06276-X
  22. Marzuka AG, Book SE. Basal cell carcinoma: pathogenesis, epidemiology, clinical features, diagnosis, histopathology, and management. Yale J Biol Med. 2015;88(2):167–179.
  23. Correia de Sá TR, Silva R, Lopes JM. Basal cell carcinoma of the skin (part 1): epidemiology, pathology and genetic syndromes. Future Oncol. 2015;11(22):3011–3021. doi: 10.2217/fon.15.246
  24. Ikehata H, Ono T. The mechanisms of UV mutagenesis. J Radiat Res. 2011;52(2):115–125. doi: 10.1269/jrr.10175
  25. Didona D, Paolino G, Bottoni U, Cantisani C. Non Melanoma Skin Cancer Pathogenesis Overview. Biomedicines. 2018;6(1):6.
  26. doi: 10.3390/biomedicines6010006
  27. Epstein EH. Basal cell carcinomas: attack of the hedgehog. Nat Rev Cancer. 2008;8(10):743–754. doi: 10.1038/nrc2503
  28. Ingham PW, McMahon AP. Hedgehog signaling in animal development: paradigms and principles. Genes Dev. 2001;15(23):3059–3087. doi: 10.1101/gad.938601
  29. Varjosalo M, Taipale J. Hedgehog: functions and mechanisms. Genes Dev. 2008;22(18):2454–2472. doi: 10.1101/gad.1693608
  30. Niyaz M, Khan MS, Mudassar S. Hedgehog Signaling: An Achilles' Heel in Cancer. Transl Oncol. 2019;12(10):1334–1344. doi: 10.1016/j.tranon.2019.07.004
  31. Pellegrini C, Maturo MG, Di Nardo L, Ciciarelli V, Gutiérrez García-Rodrigo C, Fargnoli MC. Understanding the Molecular Genetics of Basal Cell Carcinoma. Int J Mol Sci. 2017;18(11):2485. doi: 10.3390/ijms18112485
  32. Bakshi A, Chaudhary SC, Rana M, Elmets CA, Athar M. Basal cell carcinoma pathogenesis and therapy involving hedgehog signaling and beyond. Mol Carcinog. 2017;56(12):2543–2557. doi: 10.1002/mc.22690
  33. Lee J, Platt KA, Censullo P, Ruiz i Altaba A. Gli1 is a target of Sonic hedgehog that induces ventral neural tube development. Development. 1997;124(13):2537–2552.
  34. Xie J, Murone M, Luoh SM, Ryan A, Gu Q, Zhang C, et al. Activating Smoothened mutations in sporadic basal-cell carcinoma. Nature. 1998;391(6662):90–92. doi: 10.1038/34201
  35. Aszterbaum M, Rothman A, Johnson RL, Fisher M, Xie J, Bonifas JM, et al. Identification of mutations in the human PATCHED gene in sporadic basal cell carcinomas and in patients with the basal cell nevus syndrome. J Invest Dermatol. 1998;110(6):885–888. doi: 10.1046/j.1523-1747.1998.00222.x
  36. Danhof R, Lewis K, Brown M. Small Molecule Inhibitors of the Hedgehog Pathway in the Treatment of Basal Cell Carcinoma of the Skin. Am J Clin Dermatol. 2018;19(2):195–207. doi: 10.1007/s40257-017-0319-4
  37. Nilsson M, Undèn AB, Krause D, Malmqwist U, Raza K, Zaphiropoulos PG, et al. Induction of basal cell carcinomas and trichoepitheliomas in mice overexpressing GLI-1. Proc Natl Acad Sci USA. 2000;97(7):3438–3443. doi: 10.1073/pnas.050467397
  38. Sheng H, Goich S, Wang A, Grachtchouk M, Lowe L, Mo R, et al. Dissecting the oncogenic potential of Gli2: deletion of an NH(2)-terminal fragment alters skin tumor phenotype. Cancer Res. 2002;62(18):5308–5316.
  39. Di Magno L, Coni S, Di Marcotullio L, Canettieri G. Digging a hole under Hedgehog: downstream inhibition as an emerging anticancer strategy. Biochim Biophys Acta. 2015;1856(1):62–72. doi: 10.1016/j.bbcan.2015.06.003
  40. Pietrobono S, Gagliardi S, Stecca B. Non-canonical Hedgehog Signaling Pathway in Cancer: Activation of GLI Transcription Factors Beyond Smoothened. Front Genet. 2019;10:556. doi: 10.3389/fgene.2019.00556
  41. Di Magno L, Coni S, Di Marcotullio L, Canettieri G. Digging a hole under Hedgehog: downstream inhibition as an emerging anticancer strategy. Biochim Biophys Acta. 2015;1856(1):62–72. doi: 10.1016/j.bbcan.2015.06.003
  42. Atwood SX, Chang AL, Oro AE. Hedgehog pathway inhibition and the race against tumor evolution. J Cell Biol. 2012;199(2):193–197. doi: 10.1083/jcb.201207140
  43. DiDonato JA, Mercurio F, Karin M. NF-B and the link between inflammation and cancer. Immunol Rev. 2012;246(1):379–400. doi: 10.1111/j.1600-065X.2012.01099.x
  44. Mazzà D, Infante P, Colicchia V, Greco A, Alfonsi R, Siler M, et al. PCAF ubiquitin ligase activity inhibits Hedgehog/Gli1 signaling in p53-dependent response to genotoxic stress. Cell Death Differ. 2013;20(12):1688–1697. doi: 10.1038/cdd.2013.120
  45. Riobó NA, Lu K, Ai X, Haines GM, Emerson CP Jr. Phosphoinositide 3-kinase and Akt are essential for Sonic Hedgehog signaling. Proc Natl Acad Sci U S A. 2006;103(12):4505-4510. doi: 10.1073/pnas.0504337103
  46. Atwood SX, Sarin KY, Whitson RJ, Li JR, Kim G, Rezaee M, et al. Smoothened variants explain the majority of drug resistance in basal cell carcinoma. Cancer Cell. 2015;27(3):342–353. doi: 10.1016/j.ccell.2015.02.002
  47. Zhang H, Pasolli HA, Fuchs E. Yes-associated protein (YAP) transcriptional coactivator functions in balancing growth and differentiation in skin. Proc Natl Acad Sci U S A. 2011;108(6):2270–2275. doi: 10.1073/pnas.1019603108
  48. Zhao B, Li L, Lei Q, Guan KL. The Hippo-YAP pathway in organ size control and tumorigenesis: an updated version. Genes Dev. 2010;24(9):862–874. doi: 10.1101/gad.1909210
  49. Furth N, Aylon Y, Oren M. p53 shades of Hippo. Cell Death Differ. 2018;25(1):81–92. doi: 10.1038/cdd.2017.163
  50. van Amerongen R, Nusse R. Towards an integrated view of Wnt signaling in development. Development. 2009;136(19):3205–3214. doi: 10.1242/dev.033910
  51. Lo Muzio L, Pannone G, Staibano S, Mignogna MD, Grieco M, Ramires P, et al. WNT-1 expression in basal cell carcinoma of head and neck. An immunohistochemical and confocal study with regard to the intracellular distribution of beta-catenin. Anticancer Res. 2002;22(2A):565–576.
  52. El-Bahrawy M, El-Masry N, Alison M, Poulsom R, Fallowfield M. Expression of beta-catenin in basal cell carcinoma. Br J Dermatol. 2003;148(5):964–970. doi: 10.1046/j.1365-2133.2003.05240.x
  53. Watt FM, Estrach S, Ambler CA. Epidermal Notch signalling: differentiation, cancer and adhesion. Curr Opin Cell Biol. 2008;20(2):171–179. doi: 10.1016/j.ceb.2008.01.010
  54. Jayaraman SS, Rayhan DJ, Hazany S, Kolodney MS. Mutational landscape of basal cell carcinomas by whole-exome sequencing. J Invest Dermatol. 2014;134(1):213–220. doi: 10.1038/jid.2013.276
  55. Nicolas M, Wolfer A, Raj K, Kummer JA, Mill P, van Noort M, et al. Notch1 functions as a tumor suppressor in mouse skin. Nat Genet. 2003;33(3):416–421. doi: 10.1038/ng1099
  56. Bartel DP. MicroRNAs: genomics, biogenesis, mechanism, and function. Cell. 2004;116(2):281–297. doi: 10.1016/s0092-8674(04)000455 Friedman RC, Farh KK, Burge CB, Bartel DP. Most mammalian mRNAs are conserved targets of microRNAs. Genome Res. 2009;19(1):92–105. doi: 10.1101/gr.082701.108
  57. Sand M, Sand D, Altmeyer P, Bechara FG. MicroRNA in non-melanoma skin cancer. Cancer Biomark. 2012;11(6):253–257. doi: 10.3233/CBM-2012-0274
  58. Heffelfinger C, Ouyang Z, Engberg A, Leffell DJ, Hanlon AM, Gordon PB, et al. Correlation of Global MicroRNA Expression With Basal Cell Carcinoma Subtype. G3 (Bethesda). 2012;2(2):279–286. doi: 10.1534/g3.111.001115
  59. Sonkoly E, Lovén J, Xu N, Meisgen F, Wei T, Brodin P, et al. MicroRNA-203 functions as a tumor suppressor in basal cell carcinoma. Oncogenesis. 2012;1(3):e3. doi: 10.1038/oncsis.2012.3
  60. Sand M, Bechara FG, Gambichler T, Sand D, Friedländer MR, Bromba M, et al. Next-generation sequencing of the basal cell carcinoma miRNome and a description of novel microRNA candidates under neoadjuvant vismodegib therapy: an integrative molecular and surgical case study. Ann Oncol. 2016;27(2):332–338. doi: 10.1093/annonc/mdv551
  61. Goradel NH, Asghari MH, Moloudizargari M, Negahdari B, Haghi-Aminjan H, Abdollahi M. Melatonin as an angiogenesis inhibitor to combat cancer: Mechanistic evidence. Toxicol Appl Pharmacol. 2017;335:56–63. doi: 10.1016/j.taap.2017.09.022
  62. Veikkola T, Karkkainen M, Claesson-Welsh L, Alitalo K. Regulation of angiogenesis via vascular endothelial growth factor receptors. Cancer Res. 2000;60(2):203–212.
  63. Wang Z, Dabrosin C, Yin X, Fuster MM, Arreola A, Rathmell WK, et al. Broad targeting of angiogenesis for cancer prevention and therapy. Semin Cancer Biol. 2015;35 Suppl(Suppl):S224-S243. doi: 10.1016/j.semcancer.2015.01.001
  64. Coultas L, Chawengsaksophak K, Rossant J. Endothelial cells and VEGF in vascular development. Nature. 2005;438(7070):937–945. doi: 10.1038/nature04479
  65. Angara K, Borin TF, Arbab AS. Vascular Mimicry: A Novel Neovascularization Mechanism Driving Anti-Angiogenic Therapy (AAT) Resistance in Glioblastoma. Transl Oncol. 2017;10(4):650–660. doi: 10.1016/j.tranon.2017.04.007
  66. Chung AS, Ferrara N. Developmental and pathological angiogenesis. Annu Rev Cell Dev Biol. 2011;27:563–584.
  67. doi: 10.1146/annurev-cellbio-092910-154002
  68. Seaman S, Stevens J, Yang MY, Logsdon D, Graff-Cherry C, St Croix B. Genes that distinguish physiological and pathological angiogenesis. Cancer Cell. 2007;11(6):539–554. doi: 10.1016/j.ccr.2007.04.017
  69. Bielenberg DR, Zetter BR. The Contribution of Angiogenesis to the Process of Metastasis. Cancer J. 2015;21(4):267–273. doi: 10.1097/PPO.0000000000000138
  70. Sand M, Bromba A, Sand D, Gambichler T, Hessam S, Becker JC. et al. Dicer Sequencing, Whole Genome Methylation Profiling, mRNA and smallRNA Sequencing Analysis in Basal Cell Carcinoma. Cell Physiol Biochem. 2019;53(5):760–773. doi: 10.33594/000000171
  71. Pakravan K, Babashah S, Sadeghizadeh M, Mowla SJ, Mossahebi-Mohammadi M, Ataei F, et al. MicroRNA-100 shuttled by mesenchymal stem cell-derived exosomes suppresses in vitro angiogenesis through modulating the mTOR/HIF-1/VEGF signaling axis in breast cancer cells. Cell Oncol (Dordr). 2017;40(5):457–470. doi: 10.1007/s13402-017-0335-7
  72. Mogilyansky E, Rigoutsos I. The miR-17/92 cluster: a comprehensive update on its genomics, genetics, functions and increasingly important and numerous roles in health and disease. Cell Death Differ. 2013;20(12):1603–1614. doi: 10.1038/cdd.2013.125
  73. Sand M, Skrygan M, Sand D, Georgas D, Hahn SA, Gambichler T, et al. Expression of microRNAs in basal cell carcinoma. Br J Dermatol. 2012;167(4):847–855. doi: 10.1111/j.1365-2133.2012.11022.x
  74. Ma H, Pan JS, Jin LX, Wu J, Ren YD, Chen P, et al. MicroRNA-17~92 inhibits colorectal cancer progression by targeting angiogenesis. Cancer Lett. 2016;376(2):293–302. doi: 10.1016/j.canlet.2016.04.011
  75. Teh MT, Wong ST, Neill GW, Ghali LR, Philpott MP, Quinn AG. FOXM1 is a downstream target of Gli1 in basal cell carcinomas. Cancer Res. 2002;62(16):4773–4780.
  76. Li Y, Zhang D, Wang X, Yao X, Ye C, Zhang S, et al. Hypoxia-inducible miR-182 enhances HIF1 signaling via targeting PHD2 and FIH1 in prostate cancer. Sci Rep. 2015;5:12495. doi: 10.1038/srep12495
  77. Wan C, Li Y. Integrative analysis of mRNA-miRNA-TFs reveals the key regulatory connections involved in basal cell carcinoma. Arch Dermatol Res. 2020;312(2):133–143. doi: 10.1007/s00403-019-02002-y
  78. Li Y, Cai B, Shen L, Dong Y, Lu Q, Sun S, et al. MiRNA-29b suppresses tumor growth through simultaneously inhibiting angiogenesis and tumorigenesis by targeting Akt3. Cancer Lett. 2017;397:111–119. doi: 10.1016/j.canlet.2017.03.032
  79. Sawada Y, Nakamura M. Daily Lifestyle and Cutaneous Malignancies. Int J Mol Sci. 2021;22(10):5227. doi: 10.3390/ijms22105227
  80. Fania L, Didona D, Morese R, Campana I, Coco V, Di Pietro FR, et al. Basal Cell Carcinoma: From Pathophysiology to Novel Therapeutic Approaches. Biomedicines. 2020;8(11):449. doi: 10.3390/biomedicines8110449
  81. Axelson M, Liu K, Jiang X, He K, Wang J, Zhao H, et al. (2013). U.S. Food and Drug Administration approval: vismodegib for recurrent, locally advanced, or metastatic basal cell carcinoma. Clinical cancer research: an official journal of the American Association for Cancer Research, 19(9); 2289–2293. doi: 10.1158/1078-0432.CCR-12-1956
  82. Casey D, Demko S, Shord S, Zhao H, Chen H, He K, et al. (2017). FDA Approval Summary: Sonidegib for Locally Advanced Basal Cell Carcinoma. Clinical cancer research : an official journal of the American Association for Cancer Research, 23(10), 2377–2381. doi: 10.1158/1078-0432.CCR-16-2051

Supplementary files

Supplementary Files
Action
1. JATS XML
2. Fig. 1. Physiological Hedgehog signaling pathway [79]. Description in text

Download (564KB)
3. Fig. 2. Ligand-dependent or receptor-induced activation of the Hedgehog signaling pathway in the development of basal cell skin cancer. Activated or inactivated pathways are reported in red or green, respectively. Description in text [79]

Download (636KB)
4. Fig. 3. Alternative activation of the Hedgehog signaling pathway in the development of basal cell skin cancer [79]. Activated or inactivated pathways are reported in red or green, respectively. Description in text

Download (786KB)
5. Fig. 4. Mutations in other genes involved in the pathogenesis of basal cell skin cancer [79]. Activated or inactivated pathways are reported in red or green, respectively. Description in text

Download (531KB)

Copyright (c) 2021 Saytburkhanov R.R., Kubanov A.A., Kondrakhina I.N., Plakhova X.I.

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.

Согласие на обработку персональных данных с помощью сервиса «Яндекс.Метрика»

1. Я (далее – «Пользователь» или «Субъект персональных данных»), осуществляя использование сайта https://journals.rcsi.science/ (далее – «Сайт»), подтверждая свою полную дееспособность даю согласие на обработку персональных данных с использованием средств автоматизации Оператору - федеральному государственному бюджетному учреждению «Российский центр научной информации» (РЦНИ), далее – «Оператор», расположенному по адресу: 119991, г. Москва, Ленинский просп., д.32А, со следующими условиями.

2. Категории обрабатываемых данных: файлы «cookies» (куки-файлы). Файлы «cookie» – это небольшой текстовый файл, который веб-сервер может хранить в браузере Пользователя. Данные файлы веб-сервер загружает на устройство Пользователя при посещении им Сайта. При каждом следующем посещении Пользователем Сайта «cookie» файлы отправляются на Сайт Оператора. Данные файлы позволяют Сайту распознавать устройство Пользователя. Содержимое такого файла может как относиться, так и не относиться к персональным данным, в зависимости от того, содержит ли такой файл персональные данные или содержит обезличенные технические данные.

3. Цель обработки персональных данных: анализ пользовательской активности с помощью сервиса «Яндекс.Метрика».

4. Категории субъектов персональных данных: все Пользователи Сайта, которые дали согласие на обработку файлов «cookie».

5. Способы обработки: сбор, запись, систематизация, накопление, хранение, уточнение (обновление, изменение), извлечение, использование, передача (доступ, предоставление), блокирование, удаление, уничтожение персональных данных.

6. Срок обработки и хранения: до получения от Субъекта персональных данных требования о прекращении обработки/отзыва согласия.

7. Способ отзыва: заявление об отзыве в письменном виде путём его направления на адрес электронной почты Оператора: info@rcsi.science или путем письменного обращения по юридическому адресу: 119991, г. Москва, Ленинский просп., д.32А

8. Субъект персональных данных вправе запретить своему оборудованию прием этих данных или ограничить прием этих данных. При отказе от получения таких данных или при ограничении приема данных некоторые функции Сайта могут работать некорректно. Субъект персональных данных обязуется сам настроить свое оборудование таким способом, чтобы оно обеспечивало адекватный его желаниям режим работы и уровень защиты данных файлов «cookie», Оператор не предоставляет технологических и правовых консультаций на темы подобного характера.

9. Порядок уничтожения персональных данных при достижении цели их обработки или при наступлении иных законных оснований определяется Оператором в соответствии с законодательством Российской Федерации.

10. Я согласен/согласна квалифицировать в качестве своей простой электронной подписи под настоящим Согласием и под Политикой обработки персональных данных выполнение мною следующего действия на сайте: https://journals.rcsi.science/ нажатие мною на интерфейсе с текстом: «Сайт использует сервис «Яндекс.Метрика» (который использует файлы «cookie») на элемент с текстом «Принять и продолжить».