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Model parameters confirm fractal dynamics, show age-related deviations below 30, and suggest BRCA1/2 mutations can shift predicted onset about two years earlier.",{"@graph":14,"@context":77},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/research-report/","Research & 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Ovarian Cancers in the Avrami–Dobrzy ´nski Cellular Phase-Transition Model  \nAnna Zawadzka 1, Beata Brzozowska 2, Anna Matyjanka 3, Michał Mikula 1, Joanna Reszczy ´nska 4, Adrianna Tartas 2 and Krzysztof W. Fornalski 3,5, *  \nCitation: Zawadzka, A.; Brzozowska, B.; Matyjanka, A.; Mikula, M.; Reszczy ´nska, J.; Tartas, A.; Fornalski, K.W. The Risk Function of Breast and Ovarian Cancers in the Avrami–Dobrzy ´nski Cellular Phase-Transition Model. Int. J. Mol. Sci. 2024, 25, 1352. [https://doi.org/](https://doi.org/)[ ](https://doi.org/)[10.3390/ijms25021352](10.3390/ijms25021352)  \nAcademic Editor: Qun Zhou  \nReceived: 8 December 2023  \nRevised: 11 January 2024  \nAccepted: 16 January 2024  \nPublished: 22 January 2024  \nCopyright: © 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://](https://)[ ](https://)[creativecommons.org/licenses/by/](creativecommons.org/licenses/by/)[ ](creativecommons.org/licenses/by/)[4.0/](4.0/)) .  \n1 Maria Skłodowska-Curie National Research Institute of Oncology (NIO-MSCI), 02-781 Warsaw, Poland; [anna.zawadzka.fizyk@nio.gov.pl](anna.zawadzka.fizyk@nio.gov.pl) (A.Z.)  \n2 Faculty of Physics, University of Warsaw, 02-093 Warsaw, Poland; [beata.brzozowska@fuw.edu.pl](beata.brzozowska@fuw.edu.pl) (B.B.)  \n3 Faculty of Physics, Warsaw University of Technology, 00-662 Warsaw, Poland  \n4 Mossakowski Medical Research Institute, Polish Academy of Sciences (IMDiK PAN), 02-106 Warsaw, Poland; [jreszczynska@imdik.pan.pl](jreszczynska@imdik.pan.pl)  \n5 National Centre for Nuclear Research (NCBJ), 05-400 Otwock-´Swierk, Poland  \n* Correspondence: [krzysztof.fornalski@pw.edu.pl](krzysztof.fornalski@pw.edu.pl)  \nAbstract: Specifying the role of genetic mutations in cancer development is crucial for effective screening or targeted treatments for people with hereditary cancer predispositions. Our goal here is to find the relationship between a number of cancerogenic mutations and the probability of cancer induction over the lifetime of cancer patients. We believe that the Avrami–Dobrzy ´nski biophysical model can be used to describe this mechanism. Therefore, clinical data from breast and ovarian cancer patients were used to validate this model of cancer induction, which is based on a purely physical concept of the phase-transition process with an analogy to the neoplastic transformation. The obtained values of model parameters established using clinical data confirm the hypothesis that the carcinogenic process strongly follows fractal dynamics. We found that the model’s theoretical prediction and population clinical data slightly differed for patients with the age below 30 years old, and that might point to the existence of an ancillary protection mechanism against cancer development. Additionally, we reveal that the existing clinical data predict breast or ovarian cancers onset two years earlier for patients with BRCA1/2 mutations.  \nKeywords: Avrami equation; phase transition; cancer; carcinogenesis; neoplastic transformation; cancer physics; breast cancer; ovary cancer; fractal  \n1. Introduction  \nBreast and ovarian cancers (BOCs) are among the most common types of cancer that affect women around the world. According to the latest American Cancer Society report, breast cancer ranks as the second leading cause of cancer-related deaths among women, with an estimated 43,170 patients expected to succumb to the disease in the United States alone in 2024, irrespective of screening or treatment. Ovarian cancer can be more aggressive but the rarer of the two. It ranks fifth in cancer deaths among women.  \nAlthough many cases of these cancers are sporadic, there is a subset of individuals who have a genetic predisposition to developing BOCs due to germinal mutations in the BRCA1/2 DNA repair associated genes. The BRCA1/2 genes play an i","cbCaiamJRDBkD1jG","https://ap.wps.com/l/cbCaiamJRDBkD1jG","pdf",1297565,12,"English","# Abstract\n# Introduction\n## Breast and ovarian cancers in women worldwide\n## Genetic predisposition and BRCA1/2 mutations\n## Molecular diagnostics and screening strategies\n## Founder mutations and differences in risks\n## Broader susceptibility gene panel for hereditary predisposition","[{\"question\":\"What is the primary goal of this study?\",\"answer\":\"To determine the relationship between the number of cancerogenic mutations and the probability of cancer induction over a patient’s lifetime, using a biophysical model validated against clinical data.\"},{\"question\":\"How is the Avrami–Dobrzyński model used in the research?\",\"answer\":\"The Avrami–Dobrzyński biophysical phase-transition model is employed to describe cancer induction, and clinical breast and ovarian cancer data are used to validate its parameter estimates.\"},{\"question\":\"What do the results suggest about fractal dynamics and age effects?\",\"answer\":\"The parameter values support the hypothesis that carcinogenic processes follow fractal dynamics, while theoretical predictions and population clinical data show slight differences for patients below 30 years old, suggesting a possible ancillary protection mechanism.\"},{\"question\":\"How do BRCA1/2 mutations affect predicted cancer onset?\",\"answer\":\"Existing clinical data indicate that breast or ovarian cancer onset is predicted to occur about two years earlier for patients with BRCA1/2 mutations.\"}]","The Risk Function of Breast and Ovarian Cancers in the Avrami–Dobrzyński Cellular Phase-Transition Model | PDF",1789975377]